scholarly journals Effects of early life exposure to traffic-related air pollution on brain development in juvenile Sprague-Dawley rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kelley T. Patten ◽  
Eduardo A. González ◽  
Anthony Valenzuela ◽  
Elizabeth Berg ◽  
Christopher Wallis ◽  
...  
Author(s):  
Qi Zhao ◽  
Iana Markevych ◽  
Dietrich Berdel ◽  
Andrea Berg ◽  
Monika Gappa ◽  
...  

2015 ◽  
Vol 2015 (1) ◽  
pp. 2865
Author(s):  
Florence Guida ◽  
Karin Van Veldhoven ◽  
Gianluca Campanella ◽  
Paul Elliott ◽  
John Gulliver ◽  
...  

2013 ◽  
Vol 121 (3) ◽  
pp. 387-392 ◽  
Author(s):  
Inmaculada Aguilera ◽  
Marie Pedersen ◽  
Raquel Garcia-Esteban ◽  
Ferran Ballester ◽  
Mikel Basterrechea ◽  
...  

2013 ◽  
Vol 16 (8) ◽  
pp. 1885-1892 ◽  
Author(s):  
Richard M. O'Connor ◽  
Susan Grenham ◽  
Timothy G. Dinan ◽  
John F. Cryan

Abstract Early-life stress is a main contributory factor to the onset of depression. Treatments remain inadequate and as such, a large unmet medical need for novel therapeutics remains. Impeding advancement is the poor understanding of the molecular pathology. microRNAs (miRNAs) are novel regulators of gene expression. A paucity of information regarding their role in depressive pathology and antidepressant action remains. This study investigated changes to hippocampal miRNA levels induced via early-life stress in Sprague–Dawley rats and whether antidepressant treatments could reverse these changes. Investigated were the selective serotonin reuptake inhibitor fluoxetine, the rapid acting N-methyl-d-aspartate receptor antagonist ketamine and electroconvulsive shock therapy (ECT). Microarray analysis revealed early-life stress affected the expression of multiple hippocampal miRNAs. Antidepressant treatments reversed some of these effects including a stress-induced change to miR-451. Ketamine and ECT possessed the highest number of common targets suggesting convergence on common pathways. Interestingly all three treatments possessed miR-598-5p as a common target. This demonstrates that changes to hippocampal miRNA expression may represent an important component of stress-induced pathology and antidepressant action may reverse these.


2017 ◽  
Vol 184 (2) ◽  
pp. 409-421 ◽  
Author(s):  
Safa Ben Mimouna ◽  
Marouane Chemek ◽  
Sana Boughammoura ◽  
Mohamed Banni ◽  
Imed Messaoudi

2019 ◽  
Vol 18 (2) ◽  
pp. 77-95
Author(s):  
Rashesh Shrestha

In this paper, I study the impact of early life exposure to air pollution caused by the 1997 Indonesian forest fires on cognitive ability, an important determinant of success in the labor market. To isolate the effect of pollution exposure, I use a difference-in-differences approach where exposure to pollution is determined by timing and region of birth. The results suggest that pollution lowered cognitive test score at age 8–9 years by 6 percent. I also estimate how this might translate into lost earnings on a different but comparable sample. The estimates suggest that natural disasters can reduce earnings by 5 to 8 percent by hampering cognitive ability. Lost earnings due to interrupted cognitive development could be an additional cost of exposure to air pollution.


2019 ◽  
Vol 48 (4) ◽  
pp. 1125-1141 ◽  
Author(s):  
Nihit Goyal ◽  
Mahesh Karra ◽  
David Canning

Abstract Background Many low- and middle-income countries are experiencing high and increasing exposure to ambient fine particulate air pollution (PM2.5). The effect of PM2.5 on infant and child mortality is usually modelled using concentration response curves extrapolated from studies conducted in settings with low ambient air pollution, which may not capture its full effect. Methods We pool data on more than half a million births from 69 nationally representative Demographic and Health Surveys that were conducted in 43 low- and middle-income countries between 1998 and 2014, and we calculate early-life exposure (exposure in utero and post partum) to ambient PM2.5 using high-resolution calibrated satellite data matched to the child’s place of residence. We estimate the association between the log of early-life PM2.5 exposure, both overall and separated by type, and the odds of neonatal and infant mortality, adjusting for child-level, parent-level and household-level characteristics. Results We find little evidence that early-life exposure to overall PM2.5 is associated with higher odds of mortality relative to low exposure to PM2.5. However, about half of PM2.5 is naturally occurring dust and sea-salt whereas half is from other sources, comprising mainly carbon-based compounds, which are mostly due to human activity. We find a very strong association between exposure to carbonaceous PM2.5 and infant mortality, particularly neonatal mortality, i.e. mortality in the first 28 days after birth. We estimate that, at the mean level of exposure in the sample to carbonaceous PM2.5—10.9 µg/m3—the odds of neonatal mortality are over 50% higher than in the absence of pollution. Conclusion Our results suggest that the current World Health Organization guideline of limiting the overall ambient PM2.5 level to less than 10 µg/m³ should be augmented with a lower limit for harmful carbonaceous PM2.5.


2019 ◽  
Vol 123 ◽  
pp. 444-450 ◽  
Author(s):  
Baoting He ◽  
Jian V. Huang ◽  
Man Ki Kwok ◽  
Shiu Lun Au Yeung ◽  
Lai Ling Hui ◽  
...  

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