RESUMEN
BACKGROUND: Several studies have shown that exposure to air pollutants affects lung growth and development and can result in poor respiratory health in early life. METHODS: We included a subsample of 772 Mexican preschoolers whose mothers participated in a Prenatal Omega-3 fatty acid Supplements, GRowth, And Development birth cohort study with the aim to evaluate the impact of prenatal exposure to volatile organic compounds and nitrogen oxides on lung function measured by oscillation tests. The preschoolers were followed until 5 years of age. Anthropometric measurements and forced oscillation tests were performed at 36, 48, and 60 months of age. Information on sociodemographic and health characteristics was obtained during follow up. Prenatal exposure to volatile organic compounds and nitrogen oxides was evaluated using a land use regression models and the association between them was tested using a lineal regression and longitudinal linear mixed effect models adjusting for potential confounders. RESULTS: Overall, the mean (standard deviation) of the measurements of respiratory system resistance and respiratory system reactance at 6, 8, and 10 Hz during the follow-up period was 11.3 (2.4), 11.1 (2.4), 10.3 (2.2) and -5.2 (1.6), -4.8 (1.7), and -4.6 hPa s L-1 (1.6), respectively. We found a significantly positive association between respiratory resistance (ßRrs6 = 0.011; 95%CI: 0.001, 0.023) (P < .05) and prenatal exposure to nitrogen dioxide and a marginally negatively association between respiratory reactance (ßXrs6 = -11.40 95%CI: -25.26, 1.17 and ßXrs8 = -11.91 95%CI: -26.51, 1.43) (P = .07) and prenatal exposure to xylene. CONCLUSION: Prenatal exposure to air pollutants was significantly associated with the alteration of lung function measured by oscillation tests in these preschool children.
Asunto(s)
Contaminantes Atmosféricos/toxicidad , Exposición a Riesgos Ambientales/efectos adversos , Pulmón/efectos de los fármacos , Óxidos de Nitrógeno/toxicidad , Efectos Tardíos de la Exposición Prenatal , Compuestos Orgánicos Volátiles/toxicidad , Contaminantes Atmosféricos/análisis , Preescolar , Estudios de Cohortes , Exposición a Riesgos Ambientales/análisis , Femenino , Humanos , Pulmón/fisiología , Masculino , Intercambio Materno-Fetal , Óxidos de Nitrógeno/análisis , Embarazo , Pruebas de Función Respiratoria , Compuestos Orgánicos Volátiles/análisisRESUMEN
BACKGROUND: The Child-Mother binomial is potentially susceptible to the toxic effects of pollutants because some chemicals interfere with placental transfer of nutrients, thus affecting fetal development, and create an increased the risk of low birth weight, prematurity and intrauterine growth restriction. OBJECTIVE: To evaluate the impact of prenatal exposure to nitrogen oxides (NOx) on birth weight in a cohort of Mexican newborns. METHODOLOGY: We included 745 mother-child pair participants of the POSGRAD cohort study. Information on socio-demographic characteristics, obstetric history, health history and environmental exposure during pregnancy were readily available and the newborns' anthropometric measurements were obtained at delivery. Prenatal NOx exposure assessment was evaluated using a Land-Use Regression predictive models considering local monitoring from 60 sites on the State of Morelos. The association between prenatal exposure to NOx and birth weight was estimated using a multivariate linear regression models. RESULTS: The average birth weight was 3217 ± 439 g and the mean of NOx concentration was 21 ppb (Interquartile range, IQR = 6.95 ppb). After adjusting for maternal age and other confounders, a significant birthweight reduction was observed for each IQR of NOx increase (ß = -39.61 g, 95% CI: -77.00; -2.21; p = 0.04). CONCLUSIONS: Our results provides evidence that prenatal NOx exposure has a negative effect on birth weight, which may influence the growth and future development of the newborn.
Asunto(s)
Exposición a Riesgos Ambientales , Retardo del Crecimiento Fetal , Exposición Materna , Óxidos de Nitrógeno/toxicidad , Nacimiento Prematuro , Efectos Tardíos de la Exposición Prenatal , Adulto , Peso al Nacer/efectos de los fármacos , Estudios de Cohortes , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Exposición a Riesgos Ambientales/prevención & control , Femenino , Desarrollo Fetal/efectos de los fármacos , Retardo del Crecimiento Fetal/inducido químicamente , Retardo del Crecimiento Fetal/epidemiología , Retardo del Crecimiento Fetal/prevención & control , Humanos , Recién Nacido , Masculino , Exposición Materna/efectos adversos , Exposición Materna/prevención & control , Exposición Materna/estadística & datos numéricos , México/epidemiología , Evaluación de Necesidades , Embarazo , Nacimiento Prematuro/inducido químicamente , Nacimiento Prematuro/epidemiología , Nacimiento Prematuro/prevención & control , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Efectos Tardíos de la Exposición Prenatal/epidemiología , Medición de RiesgoRESUMEN
BACKGROUND, AIM, AND SCOPE: Atmospheric pollution is a worldwide problem. Exposure to atmospheric pollutants causes toxic cellular effects. One of the mechanisms of toxicity by these pollutants is the promotion of oxidative stress. Several signaling pathways control cellular redox homeostasis. In this respect, nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor in the cell's response to oxidative stress. MAIN FEATURES: In cellular animal models, exposure to atmospheric pollutants activates Nrf2, attenuating its toxic and even its carcinogenic effects. Therefore, we have reviewed the scientific literature in order to indicate that air pollutants, such as particulate matter, polycyclic aromatic hydrocarbons, and gaseous matter, are Nrf2 pathway inductors, triggering self-defense through the establishment of proinflammatory and antioxidant responses. RESULTS AND DISCUSSION: Exposure to reactive molecules as atmospheric pollutants causes the activation of Nrf2 and the subsequent regulation of the expression of cytoprotective and detoxifying enzymes, as well as antioxidants. Moreover, induction of Nrf2 prior to exposure reduces the harmful effects of pollutants. The present article discusses the protective role of the Nrf2 pathway against different atmospheric pollutant insults. CONCLUSIONS: Nrf2 regulates the expression of numerous cytoprotective genes that function to detoxify reactive species produced during atmospheric pollutant metabolic reactions. From the papers highlighted in this review, we conclude that Nrf2 has an important role in the defense against atmospheric pollutant-induced toxicity. PERSPECTIVES: Further studies are needed to understand the signaling events that turn on the system in response to atmospheric pollutant stress. This could allow for the possibility of targeting the pathway for prevention benefits in the near future.
Asunto(s)
Contaminantes Atmosféricos/toxicidad , Factor 2 Relacionado con NF-E2/metabolismo , Transducción de Señal/efectos de los fármacos , Monóxido de Carbono/toxicidad , Humanos , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Óxidos de Nitrógeno/toxicidad , Estrés Oxidativo/efectos de los fármacos , Ozono/toxicidad , Material Particulado/toxicidad , Hidrocarburos Policíclicos Aromáticos/toxicidad , Compuestos Orgánicos Volátiles/toxicidadRESUMEN
Atmospheric pollution is a topic of extensive discussion the world over. The clinical repercussions of exposure to the principal atmospheric pollutants are summarized herein. According to the American Environmental Protection Agency, air quality standards for these agents are set based on their primary and half-life values. The respiratory effects of the burning of fossil fuels and biomass are succinctly presented, with a special focus on alerting health care professionals of the increased morbidity related to environmental pollution.
Asunto(s)
Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/efectos adversos , Enfermedades Cardiovasculares/inducido químicamente , Exposición a Riesgos Ambientales/efectos adversos , Enfermedades Respiratorias/inducido químicamente , Brasil , Monóxido de Carbono/toxicidad , Enfermedad Crónica , Combustibles Fósiles/toxicidad , Humanos , Concentración Máxima Admisible , Óxidos de Nitrógeno/toxicidad , Ozono/toxicidad , Material Particulado/toxicidad , Factores de Riesgo , Dióxido de Azufre/toxicidadRESUMEN
Heliotropium curassavicum var. argentinum is widely employed in gout, rheumatism, neuralgias, arteriosclerotic disorders, muscular algias, phlebitis, varix and other illnesses. In order to analyze the genotoxic effect produced in vitro by this medicinal plant, chromosomal aberrations (CA), mitotic index (MI) and anaphase delay (AD) were studied in the CHO cell line, with and without the addition of S9 mix. Prepared according to the Argentine pharmacopeia 0.1, 1, 10 and 100 micrograms/ml plant decoction (aqueous extract) were assayed. One hundred cells per culture were studied for CA and AD, while MI was calculated for 2000 nuclei. The results revealed a significant increase in the percentage of abnormal metaphases (p less than 0.001) and in total aberrations (p less than 0.001). Both the MI and the AD affected the cell cycle. All results were enhanced by the addition of an S9 fraction. The toxic effect could be associated with pyrrolizidine alkaloids and their N-oxides, which through a process of in vitro metabolism become activated by microsomal oxidation and change into pyrrolic derivatives.