In utero exposure to air pollution lowers erythrocyte antioxidant defense and decreases weight in adult mice

2011 ◽  
Vol 32 (2) ◽  
pp. 315-318
Author(s):  
Karina Camasmie Abe ◽  
Letícia de Campos Brandão ◽  
Sérgio Tufik ◽  
Paulo Hilário do Nascimento Saldiva ◽  
Vânia D’Almeida
Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Victor P Long ◽  
Vineeta Tanwar ◽  
Matthew W Gorr ◽  
Stephen H Baine ◽  
Ingrid M Bonilla ◽  
...  

Introduction: In utero exposure to particulate matter through perinatal development has been demonstrated to produce cardiac dysfunction during adulthood. It is unknown what effect exposure to air pollution during the in utero period alone has on cardiac dysfunction and electrical remodeling in adulthood. We tested the hypothesis that adult mice exposed to concentrated particulate matter in utero would demonstrate global cardiac dysfunction as well as cellular electrical remodeling at adulthood. Methods: Female FVB mice were exposed either to filtered air (FA) or particulate matter with diameter less than 2.5 μm (PM2.5) at a concentration of ~ 51.69 μg/m3 for 6 h/day, 7 days/wk (consistent with exposure in a large metropolitan city) beginning at plug formation throughout pregnancy. Cardiac function was assessed via ECHO in male offspring at 12 wks of age, followed by sacrifice and isolation of ventricular cardiomyocytes from both groups of mice for electrophysiological recordings. Results: ECHO identified increased LVESd (2.25 ± 0.20 FA, 2.61 ± 0.35 PM2.5, P=0.0001) and LVEDd (3.89 ± 0.03 FA, 3.99 ± 0.038 PM2.5, P=0.04) dimensions and reduced PWTs (1.40 ± 0.05 FA, 1.26 ± 0.04 PM2.5, P=0.04) in mice exposed in utero to PM2.5. Morphological alterations were associated with lower systolic function as indicated by reduced fractional shortening% (43.6 ± 2.1 FA, 33.2 ± 1.6 PM2.5, P=0.0009) in PM2.5 exposed mice compared to FA controls. Electrophysiological recordings revealed significant prolongation of the action potential at 90% repolarization (APD90) in PM2.5 exposed mice compared to FA. (FIGURE) Conclusions: In utero exposure to relevant levels of particulate matter results in dilated cardiomyopathy and electrical remodeling. Future studies are warranted to determine the causes of, and the exposure thresholds resulting in this adverse cardiac remodeling.


2017 ◽  
Vol 125 (1) ◽  
pp. 82-88 ◽  
Author(s):  
Matthew J. Meier ◽  
Jason M. O’Brien ◽  
Marc A. Beal ◽  
Beverly Allan ◽  
Carole L. Yauk ◽  
...  

2017 ◽  
Vol 105 ◽  
pp. 126-132 ◽  
Author(s):  
Narjes Madhloum ◽  
Bram G. Janssen ◽  
Dries S. Martens ◽  
Nelly D. Saenen ◽  
Esmée Bijnens ◽  
...  

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Yun Kyung Lee ◽  
Vivek Nerurkar ◽  
Jennifer E Frank ◽  
Pratibha Nerurkar

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Karina Camasmie Abe ◽  
Letícia Campos Brandão ◽  
Sérgio Tufik ◽  
Bruno Frederico Aguilar Calegare ◽  
Paulo Hilário Nascimento Saldiva ◽  
...  

2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Bram Janssen* ◽  
Nelly Saenen ◽  
Harry Roels ◽  
Narjes Madhloum ◽  
Wilfried Gyselaers ◽  
...  

Author(s):  
Susanne Steinle ◽  
Helinor J. Johnston ◽  
Miranda Loh ◽  
William Mueller ◽  
Sotiris Vardoulakis ◽  
...  

In high-income countries, and increasingly in lower- and middle-income countries, chronic non-communicable diseases (NCDs) have become the primary health burden. It is possible that in utero exposure to environmental pollutants such as particulate matter (PM) may have an impact on health later in life, including the development of NCDs. Due to a lack of data on foetal growth, birth weight is often used in epidemiologic studies as a proxy to assess impacts on foetal development and adverse birth outcomes since it is commonly recorded at birth. There are no research studies with humans that directly link PM exposure in utero to birth weight (BW) and subsequently, the effects of lower BW on health outcomes in old age. It is, however, plausible that such associations exist, and it is thus important to assess the potential public health impacts of PM across the life course, and it is plausible to use birth weight as an indicator of risk. We therefore split this narrative review into two parts. In the first part, we evaluated the strength of the evidence on the impact of PM exposure during the entire pregnancy on birth weight outcomes in ten meta-analyses. In the second part, we reviewed the literature linking lower birth weight to childhood and adult chronic cardiovascular disease to explore the potential implications of PM exposure in utero on health later in life. Within the reviewed meta-studies on birth weight, there is sufficient evidence that PM pollution is associated with lower birth weight, i.e., the majority of meta-studies found statistically significant reductions in birth weight. From the second part of the review, it is evident that there is good evidence of associations between lower birth weight and subsequent cardiovascular disease risk. It is thus plausible that in utero exposure to PM is associated with lower birth weight and persisting biological changes that could be associated with adverse health effects in adulthood. Based on the reviewed evidence, however, the magnitude of later life cardiovascular health impacts from in utero exposure and its impact on BW are likely to be small compared to health effects from exposure to particulate air pollution over a whole lifetime.


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