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1.
Environ Sci Pollut Res Int ; 30(43): 98526-98535, 2023 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-37608181

RESUMEN

Infants with low birth weight (LBW) are more likely to have health problems than normal weight infants. In studies examining the associations between particulate matter (PM) exposures and LBW, there is a tendency to focus on PM2.5 as a whole. However, insufficient information is available regarding the effects of different components of PM2.5 on birth weight. This study identified the associations between maternal exposure to 10 metal components of PM2.5 and LBW in offspring based on small area (divided by population size) level data in New Mexico, USA, from 2012 to 2016. This study used a pruned feed-forward neural network (pruned-FNN) approach to estimate the annual average exposure index to each metal component in each small area. The linear regression model was employed to examine the association between maternal PM2.5 metal exposures and LBW rate in small areas, adjusting for the female percentage and race/ethnicity compositions, marriage status, and educational level in the population. An interquartile range increase in maternal exposure to mercury and chromium of PM2.5 increased LBW rate by 0.43% (95% confidence interval (CI): 0.18-0.68%) and 0.63% (95% CI: 0.15-1.12%), respectively. These findings suggest that maternal exposure to metal components of air pollutants may increase the risk of LBW in offspring. With no similar studies in New Mexico, this study also posed great importance because of a higher LBW rate in New Mexico than the national average. These findings provide critical information to inform further epidemiological, biological, and toxicological studies.


Asunto(s)
Exposición Materna , Material Particulado , Lactante , Femenino , Humanos , Recién Nacido , New Mexico , Metales , Peso al Nacer , Recién Nacido de Bajo Peso
2.
Environ Health ; 19(1): 63, 2020 06 05.
Artículo en Inglés | MEDLINE | ID: mdl-32503633

RESUMEN

BACKGROUND: There have been no studies of air pollution and mortality in Lima, Peru. We evaluate whether daily environmental PM2.5 exposure is associated to respiratory and cardiovascular mortality in Lima during 2010 to 2016. METHODS: We analyzed 86,970 deaths from respiratory and cardiovascular diseases in Lima from 2010 to 2016. Estimated daily PM2.5 was assigned based on district of residence. Poisson regression was used to estimate associations between daily district-level PM2.5 exposures and daily counts of deaths. RESULTS: An increase in 10 µg/m3 PM2.5 on the day before was significantly associated with daily cardiorespiratory mortality (RR 1.029; 95% CI: 1.01-1.05) across all ages and in the age group over 65 (RR 1.04; 95% CI: 1.005-1.09) which included 74% of all deaths. We also observed associations with circulatory deaths for all age groups (RR 1.06; 95% CI: 1.01-1.11), and those over 65 (RR 1.06; 95% CI 1.00-1.12). A borderline significant trend was seen (RR 1.05; 95% CI 0.99-1.06; p = 0.10) for respiratory deaths in persons aged over 65. Trends were driven by the highest quintile of exposure. CONCLUSIONS: PM2.5 exposure is associated with daily cardiorespiratory mortality in Lima, especially for older people. Our data suggest that the existing limits on air pollution exposure are too high.


Asunto(s)
Contaminantes Atmosféricos/efectos adversos , Enfermedades Cardiovasculares/mortalidad , Exposición a Riesgos Ambientales/efectos adversos , Material Particulado/efectos adversos , Enfermedades Respiratorias/mortalidad , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Enfermedades Cardiovasculares/inducido químicamente , Niño , Preescolar , Ciudades , Femenino , Humanos , Lactante , Recién Nacido , Masculino , Persona de Mediana Edad , Perú/epidemiología , Enfermedades Respiratorias/inducido químicamente , Adulto Joven
3.
Environ Res ; 176: 108567, 2019 09.
Artículo en Inglés | MEDLINE | ID: mdl-31344533

RESUMEN

Air pollution is a risk factor for cardiovascular and Alzheimer's disease (AD). Iron-rich, strongly magnetic, combustion- and friction-derived nanoparticles (CFDNPs) are abundant in particulate air pollution. Metropolitan Mexico City (MMC) young residents have abundant brain CFDNPs associated with AD pathology. We aimed to identify if magnetic CFDNPs are present in urbanites' hearts and associated with cell damage. We used magnetic analysis and transmission electron microscopy (TEM) to identify heart CFDNPs and measured oxidative stress (cellular prion protein, PrPC), and endoplasmic reticulum (ER) stress (glucose regulated protein, GRP78) in 72 subjects age 23.8 ±â€¯9.4y: 63 MMC residents, with Alzheimer Continuum vs 9 controls. Magnetite/maghemite nanoparticles displaying the typical rounded crystal morphologies and fused surface textures of CFDNPs were more abundant in MMC residents' hearts. NPs, ∼2-10 × more abundant in exposed vs controls, were present inside mitochondria in ventricular cardiomyocytes, in ER, at mitochondria-ER contact sites (MERCs), intercalated disks, endothelial and mast cells. Erythrocytes were identified transferring 'hitchhiking' NPs to activated endothelium. Magnetic CFDNP concentrations and particle numbers ranged from 0.2 to 1.7 µg/g and ∼2 to 22 × 109/g, respectively. Co-occurring with cardiomyocyte NPs were abnormal mitochondria and MERCs, dilated ER, and lipofuscin. MMC residents had strong left ventricular PrPC and bi-ventricular GRP78 up-regulation. The health impact of up to ∼22 billion magnetic NPs/g of ventricular tissue are likely reflecting the combination of surface charge, ferrimagnetism, and redox activity, and includes their potential for disruption of the heart's electrical impulse pathways, hyperthermia and alignment and/or rotation in response to magnetic fields. Exposure to solid NPs appears to be directly associated with early and significant cardiac damage. Identification of strongly magnetic CFDNPs in the hearts of children and young adults provides an important novel layer of information for understanding CVD pathogenesis emphasizing the urgent need for prioritization of particulate air pollution control.


Asunto(s)
Contaminantes Atmosféricos/metabolismo , Miocardio/metabolismo , Nanopartículas/metabolismo , Contaminación del Aire/estadística & datos numéricos , Ciudades , Chaperón BiP del Retículo Endoplásmico , Exposición a Riesgos Ambientales/estadística & datos numéricos , Fricción , Corazón , Humanos , Fenómenos Magnéticos , México , Material Particulado
4.
Chemosphere ; 212: 418-428, 2018 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-30149315

RESUMEN

Particulate matter driven health problems are strongly associated with its chemical composition. Despite the benefits of using source apportionment models for air quality management, limitations such as collinearity effects, restrict their application or compromise the accurate separation of sources, particularly for particulate matter with similar chemical profiles. Receptors models also depend on the operator expertise to appropriately classified sources, a subjective process that can lead to biased results. For highly correlated sources, the identification of specific markers is still the best way to achieve proper source apportionment. In this study, Resonant Synchrotron X-ray Diffraction has been applied to the analysis of atmospheric particles to determine markers for industrial and vehicular sources in the Region of Greater Vitória, Brazil. Total suspended particulate matter, PM10, and PM2.5 samples were analyzed by Resonant Synchrotron X-ray Diffraction showing high levels of iron-based crystalline phases. In comparison to the use of chemical elemental species, the identification of the crystalline phases provided an enhanced approach to classify specific iron-based source markers. For this study, α-Fe2O3 was identified with iron-based sources such as iron ore, pelletizing, and sintering; metallic Fe was inferred with blast furnaces and steelmaking; FeS2 was correlated with coal deposits; and K2Fe2O4 was associated to sintering emissions. Elemental carbon with different X-ray diffraction patterns enabled the differentiation of industrial and vehicular sources. The attribution of crystal rather than elemental composition in the identification of sources improves the accuracy of source apportionment studies.


Asunto(s)
Contaminantes Atmosféricos/análisis , Monitoreo del Ambiente/métodos , Hierro/análisis , Material Particulado/análisis , Sincrotrones , Emisiones de Vehículos/análisis , Difracción de Rayos X/métodos , Brasil , Industrias , Remodelación Urbana
5.
Toxicol Lett ; 272: 29-37, 2017 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-28279687

RESUMEN

Airborne particulate matter with an aerodynamic diameter ≤10µm (PM10) is considered a risk factor for the development of lung cancer. Little is known about the cellular mechanisms by which PM10 is associated with cancer, but there is evidence that its exposure can lead to an acquired invasive phenotype, apoptosis evasion, inflammasome activation, and cytoskeleton remodeling in lung epithelial cells. Cytoskeleton remodeling occurs through actin stress fiber formation, which is partially regulated through ROCK kinase activation, we aimed to investigate if this protein was activated in response to PM10 exposure in A549 lung epithelial cells. Results showed that 10µg/cm2 of PM10 had no influence on cell viability but increased actin stress fibers, cytoplasmic ROCK expression, and phosphorylation of myosin phosphatase-targeting 1 (MYPT1) and myosin light chain (MLC) proteins, which are targeted by ROCK. The inhibition of ROCK prevented actin stress fiber formation and the phosphorylation of MYPT1 and MLC, suggesting that PM10 activated the ROCK-MYPT1-MLC pathway in lung epithelial cells. The activation of ROCK1 has been involved in the acquisition of malignant phenotypes, and its induction by PM10 exposure could contribute to the understanding of PM10 as a risk factor for cancer development through the mechanisms associated with invasive phenotype.


Asunto(s)
Contaminantes Atmosféricos/toxicidad , Citoesqueleto/efectos de los fármacos , Cadenas Ligeras de Miosina/metabolismo , Fosfatasa de Miosina de Cadena Ligera/metabolismo , Material Particulado/toxicidad , Quinasas Asociadas a rho/metabolismo , Células A549 , Citoesqueleto/metabolismo , Relación Dosis-Respuesta a Droga , Humanos , Tamaño de la Partícula , Transducción de Señal , Fibras de Estrés/metabolismo
6.
Artículo en Inglés | MEDLINE | ID: mdl-27908382

RESUMEN

The in vitro genotoxic effects of organic and water-soluble fractions of airborne particulate matter (PM10) with the cytokinesis blocked micronucleus (MN) test in human alveolar carcinoma cells A549 were investigated. Samples were collected in three different sites of São Paulo State, Brazil, and fifteen soluble metals and the sixteen EPÁs priority polycyclic aromatic hydrocarbons (PAH) were chemically determined. PAHs prevailing were fluoranthene and benzo(ghi)perylene. In the water-soluble extracts, highest concentration of metals was found for zinc, iron, and copper in all places of collection. Although PM10 concentration in all samples was in the range of 33.5-110.1µg/m3, lower than 120µg/m3 (limit established by São Paulo State's legislation for PM10 in 24h), MN results showed that of the 24 samples analyzed, five organic and seven water-soluble extracts presented a significant increase in MN frequency. The frequency of MN correlates with the total PAH concentration of the three sites investigated, and the concentration of PM10 is correlated with the biological effect in two of them. For the water-soluble fraction, all the sites presented a relation between the PM10 concentration and the MN frequency. Again, the genotoxic response showed a correlation with the total concentration of water-soluble metals in two of the three sites. Our results confirm the importance of the soluble fraction of PM10 to the genotoxic effect of airborne PM even at low concentration of water-soluble compounds. Thus, together with chemical analysis, the implementation of the MN protocol for both organic and water-soluble fraction biological monitoring could be used as a strategy in a routine air-quality monitoring program, complementing other usual analyses for air pollution control and protection of populations.


Asunto(s)
Células Epiteliales/efectos de los fármacos , Pulmón/efectos de los fármacos , Material Particulado/efectos adversos , Material Particulado/química , Agua/química , Células A549 , Contaminantes Atmosféricos/efectos adversos , Brasil , Línea Celular Tumoral , Monitoreo del Ambiente/métodos , Humanos , Pruebas de Micronúcleos/métodos , Mutágenos/efectos adversos , Mutágenos/química , Tamaño de la Partícula , Hidrocarburos Policíclicos Aromáticos/efectos adversos , Hidrocarburos Policíclicos Aromáticos/química
7.
Environ Pollut ; 214: 646-656, 2016 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-27131825

RESUMEN

Atmospheric particulate matter with aerodynamic diameter ≤10 µm (PM10) is a risk factor for the development of lung cancer, but cellular pathways are not completely understood. STAT3 is a p21(Waf1/Cip1) transcription factor and is associated with proliferation and cell survival and is upregulated in lung cancer. PM10 exposure induces p21(Waf1/Cip1) expression, which could be related to STAT3 activation. The aims of this work were to investigate whether STAT3 was activated on lung epithelial cells after PM10 exposure and to determine whether or not STAT3 could have an impact on cell cycle distribution and cell survival. Our results showed that PM10 induced STAT3 activation through Src and PKCζ kinases, and it is partially responsible for the p21(Waf1/Cip1) induction that was also observed. Moreover, PM10 induced G1-G0 cell cycle arrest. The inhibition of STAT3 phosphorylation prevented cell cycle arrest and triggered apoptosis. These results suggest that PM10 exposure might activate a survival pathway related to STAT3 activation, similar to what has been described as part of the immune system and apoptosis evasion during tumor promotion and development.


Asunto(s)
Apoptosis/efectos de los fármacos , Puntos de Control del Ciclo Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Neoplasias Pulmonares/etiología , Pulmón/efectos de los fármacos , Material Particulado/farmacología , Factor de Transcripción STAT3/metabolismo , Ciclo Celular/efectos de los fármacos , División Celular , Línea Celular Tumoral , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/metabolismo , Humanos , Pulmón/citología , Pulmón/metabolismo , Neoplasias Pulmonares/metabolismo , Tamaño de la Partícula , Proteína Quinasa C/metabolismo , Activación Transcripcional , Familia-src Quinasas/metabolismo
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