Differential embryotoxicity of the organic pollutants in rural and urban air particles

Mesquita, Sofia Raquel; Drooge, Barend L. van; Oliveira, Eva; Grimalt, Joan O.; Barata, Carlos; Vieira, Maria Natividade; Guimarães, Laura; Piña, Benjamı́n

doi:10.1016/j.envpol.2015.08.008

Cited by 36 publications

(20 citation statements)

References 54 publications

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“…Epidemiologic studies have suggested an increased risk of congenital heart defects (CHD) in the offspring of mothers exposed to ambient air pollution and PM2.5 . Zebrafish is an ideal vertebrate animal model for investigating cardiac development, and we and others have shown that extractable organic matter (EOM) from PM2.5 has adverse effects on heart development in zebrafish embryos …”

Section: Introductionmentioning

confidence: 99%

Protective effects of folic acid on PM2.5-induced cardiac developmental toxicity in zebrafish embryos by targeting AhR and Wnt/β-catenin signal pathways

Cong

Zhang

et al. 2017

Environmental Toxicology

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Our previous observations indicated that extractable organic matter (EOM) from PM2.5 induced malformations in the heart of zebrafish embryos by activating AhR and inhibiting canonical Wnt/β-catenin signal pathway. As a nutritional factor, folic acid (FA) is reported to prevent cardiac defects during embryo development. Hence, we hypothesize that FA may prevent PM2.5-induced heart defects by interfering with AhR and Wnt/β-catenin signaling pathways. Our results showed that FA supplementation alleviated the EOM-induced heart defects in zebrafish embryos, and both AhR inhibitor CH223191 and Wnt activator CHIR99021 enhanced the protective efficiency of FA. Furthermore, FA supplementation attenuated the EOM-induced upregulation of AhR and its target genes including Cyp1a1, Cyp1b1, Ahrra, and Ahrrb. EROD assay confirmed that the EOM agonized Cyp1a1 activity was diminished by FA. The EOM-induced downregulation of β-catenin and its target genes including Nkx2.5, Axin2, Sox9b, and Cox2b were recovered or even overexpressed in embryos exposed to EOM plus FA. In conclusion, our study suggested that FA supplementation protected against PM2.5 cardiac development toxicity by targeting AhR and Wnt/β-catenin signal pathways.

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Section: Introductionmentioning

confidence: 99%

Protective effects of folic acid on PM2.5-induced cardiac developmental toxicity in zebrafish embryos by targeting AhR and Wnt/β-catenin signal pathways

Cong

Zhang

et al. 2017

Environmental Toxicology

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“… 3 The carcinogenic potential of PAH has been known since 1776, 22 but their effects on the nervous system, particularly the developing nervous system, have come to light only in the recent past. 23 It has been postulated that PAH may damage the developing fetal brain by increasing oxidative stress 24 , 25 and causing vascular injury. 26 Several epidemiological studies have found an association between in utero exposure to PAH and neurodevelopment and behavior.…”

Section: Introductionmentioning

confidence: 99%

Environmental Pollutants and Neurodevelopment: Review of Benefits From Closure of a Coal-Burning Power Plant in Tongliang, China

Kalia

Perera

Tang

2017

Global Pediatric Health

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Background. Understanding preventable causes of neurodevelopmental disorders is a public health priority. Polycyclic aromatic hydrocarbons (PAH) from combustion of fossil fuel, lead, and mercury are among known neurodevelopmental toxicants. Method. For the first time, we comprehensively review the findings from a study by the Columbia Center for Children’s Environmental Health and Chinese partners that followed 2 groups of mother-child pairs, one from 2002 and another from 2005, in Tongliang County, China. Pregnant mothers in the 2 cohorts experienced different exposure to PAH because a local coal-burning power plant was shut down in 2004. Investigators assessed change in prenatal PAH exposure, measured using a biomarker (benzo[a]pyrene [BaP]-DNA adducts in cord blood). Developmental quotients were measured using the Gesell Developmental Scales at age 2 and IQ was assessed using the Wechsler Intelligence Scale for Children at age 5. Biologic markers of preclinical response were measured in cord blood: methylation status of long interspersed nuclear elements (LINE1), an indicator of genomic stability, and brain-derived neurotrophic factor (BDNF), a neuronal growth promoter. Analyses accounted for co-exposure to lead and mercury. Results. BaP-DNA adducts were significantly inversely associated with Gesell Developmental Scales scores in the first cohort but not in the second cohort; and levels of BDNF and LINE1 methylation were higher in the second cohort. Conclusion. In this study, reduced exposure to PAH was associated with beneficial effects on neurodevelopment as well as molecular changes related to improved brain development and health. These benefits should encourage further efforts to limit exposure to these toxic pollutants.

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“…This is a transcription factor activated by a large number of ligands, including PAHs [82,83,85,86] and involved in many cell processes. For example, extractable organic matter (EOM) from PM2.5 may cause heart malformations and decreased heart rates in zebrafish embryos through the AhR, and these heart defects appear to be counteracted in embryos co-exposed to EOM and an AhR antagonist [87,88]. Concerning the male reproductive system, Izawa et al have reported a decrease in the daily production of spermatozoa, an increase in morphological abnormalities in spermatozoa as well as a significant increase in blood testosterone levels in the group exposed to diesel exhaust combined with a significant increase in the AhR activity index [89].…”

Section: Action As Endocrine Disruptorsmentioning

confidence: 99%

Does air pollution play a role in infertility?: a systematic review

et al. 2017

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Background: Air pollution is involved in many pathologies. These pollutants act through several mechanisms that can affect numerous physiological functions, including reproduction: as endocrine disruptors or reactive oxygen species inducers, and through the formation of DNA adducts and/or epigenetic modifications. We conducted a systematic review of the published literature on the impact of air pollution on reproductive function. Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included (1) ovary or follicle or oocyte or testis or testicular or sperm or spermatozoa or fertility or infertility and (2) air quality or O 3 or NO 2 or PM2.5 or diesel or SO 2 or traffic or PM10 or air pollution or air pollutants. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the search terms and published in English. We have excluded articles whose results did not concern fertility or gamete function and those focused on cancer or allergy. We have also excluded genetic, auto-immune or iatrogenic causes of reduced reproduction function from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on fertility and the molecular pathways involved.

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Differential embryotoxicity of the organic pollutants in rural and urban air particles

Cited by 36 publications

References 54 publications

Protective effects of folic acid on PM2.5-induced cardiac developmental toxicity in zebrafish embryos by targeting AhR and Wnt/β-catenin signal pathways

Protective effects of folic acid on PM2.5-induced cardiac developmental toxicity in zebrafish embryos by targeting AhR and Wnt/β-catenin signal pathways

Environmental Pollutants and Neurodevelopment: Review of Benefits From Closure of a Coal-Burning Power Plant in Tongliang, China

Does air pollution play a role in infertility?: a systematic review

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