CoA and CHD Causes
Environ Health Perspect. 2013 Jan 3. [Epub ahead of print]
Traffic-Related Air Pollution and Congenital Anomalies in Barcelona.
Schembari A, Nieuwenhuijsen MJ, Salvador J, de Nazelle A, Cirach M, Dadvand P, Beelen R, Hoek G, Basagaña X, Vrijheid M.
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Abstract
BACKGROUND:
A recent meta-analysis suggested evidence for an effect of exposure to ambient air pollutants on risk of certain congenital heart defects. However, few studies have investigated the effects of traffic-related air pollutants with sufficient spatial accuracy.
OBJECTIVES:
We estimated associations between congenital anomalies and exposure to traffic-related air pollution in Barcelona.
METHOD:
Cases with non-chromosomal anomalies (n = 2247) and controls (n = 2991) were selected from the Barcelona congenital anomaly register between 1994 and 2006. Land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE), were applied to residential addresses at birth to estimate spatial exposure to nitrogen oxides and dioxide (NOx, NO2), particulate matter with diameter ≤ 10 μm (PM10), 10 μm-2.5 μm (PMcoarse), ≤ 2.5 μm (PM2.5), and PM2.5 absorbance. Spatial estimates were adjusted for temporal trends using data from routine monitoring stations for weeks 3 to 8 of each pregnancy. Logistic regression models were used to calculate odds ratios (OR) for 18 congenital anomaly groups associated with an inter-quartile range (IQR) increase in exposure estimates.
RESULTS:
In spatial and spatio-temporal exposure models we estimated statistically significant associations between an IQR increase in NO2 (12.2 μg/m3) and coarctation of the aorta (ORspatio-temporal = 1.15; 95%CI: 1.01, 1.31) and digestive system defects (ORspatio-temporal = 1.11; 95%CI: 1.00, 1.23), and between an IQR increase in PMcoarse (3.6 μg/m3) and abdominal wall defects (ORspatio-temporal = 1 .93; 95%CI: 1.37, 2.73). Other statistically significant increased and decreased ORs were estimated based on the spatial model only or the spatio-temporal model only, but not both.
CONCLUSIONS:
Our results overall do not indicate an association between traffic-related air pollution and most groups of congenital anomalies. Findings for coarctation of the aorta are consistent with the previous meta-analysis.
Paediatr Perinat Epidemiol. 2013 Jul;27(4):329-39. doi: 10.1111/ppe.12055. Epub 2013 Apr 21.
Ambient air pollution and traffic exposures and congenital heart defects in the San Joaquin Valley of California.
Padula AM1, Tager IB, Carmichael SL, Hammond SK, Yang W, Lurmann F, Shaw GM.
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Abstract
BACKGROUND:
Congenital anomalies are a leading cause of infant morbidity and mortality. Studies suggest associations between environmental contaminants and some anomalies, although evidence is limited.
METHODS:
We used data from the California Center of the National Birth Defects Prevention Study and the Children’s Health and Air Pollution Study to estimate the odds of 27 congenital heart defects with respect to quartiles of seven ambient air pollutant and traffic exposures in California during the first 2 months of pregnancy, 1997-2006 (n = 822 cases and n = 849 controls).
RESULTS:
Particulate matter < 10 microns (PM10 ) was associated with pulmonary valve stenosis [adjusted odds ratio (aOR)Fourth Quartile = 2.6] [95% confidence intervals (CI) 1.2, 5.7] and perimembranous ventricular septal defects (aORThird Quartile = 2.1) [95% CI 1.1, 3.9] after adjusting for maternal race/ethnicity, education and multivitamin use. PM2.5 was associated with transposition of the great arteries (aORThird Quartile = 2.6) [95% CI 1.1, 6.5] and inversely associated with perimembranous ventricular septal defects (aORFourth Quartile = 0.5) [95% CI 0.2, 0.9]. Secundum atrial septal defects were inversely associated with carbon monoxide (aORFourth Quartile = 0.4) [95% CI 0.2, 0.8] and PM2.5 (aORFourth Quartile = 0.5) [95% CI 0.3, 0.8]. Traffic density was associated with muscular ventricular septal defects (aORFourth Quartile = 3.0) [95% CI 1.2, 7.8] and perimembranous ventricular septal defects (aORThird Quartile = 2.4) [95% CI 1.3, 4.6], and inversely associated with transposition of the great arteries (aORFourth Quartile = 0.3) [95% CI 0.1, 0.8].
CONCLUSIONS:
PM10 and traffic density may contribute to the occurrence of pulmonary valve stenosis and ventricular septal defects, respectively. The results were mixed for other poll
Pediatr Cardiol. 2014 Apr;35(4):559-68. doi: 10.1007/s00246-014-0870-1. Epub 2014 Jan 23.
Potential effects of environmental chemical contamination in congenital heart disease.
Gorini F1, Chiappa E, Gargani L, Picano E.
Author information
- 1Institute of Clinical Physiology, National Council of Research (CNR), via Moruzzi, 1, 56124, Pisa, Italy, fgorini@ifc.cnr.it.
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Abstract
There is compelling evidence that prenatal exposures to environmental xenobiotics adversely affect human development and childhood. Among all birth defects, congenital heart disease (CHD) is the most prevalent of all congenital malformations and remains the leading cause of death. It has been estimated that in most cases the causes of heart defects remain unknown, while a growing number of studies have indicated the potential role of environmental agents as risk factors in CHD occurrence. In particular, maternal exposure to chemicals during the first trimester of pregnancy represents the most critical window of exposure for CHD. Specific classes of xenobiotics (e.g. organochlorine pesticides, organic solvents, air pollutants) have been identified as potential risk factors for CHD. Nonetheless, the knowledge gained is currently still incomplete as a consequence of the frequent heterogeneity of the methods applied and the difficulty in estimating the net effect of environmental pollution on the pregnant mother. The presence of multiple sources of pollution, both indoor and outdoor, together with individual lifestyle factors, may represent a further confounding element for association with the disease. A future new approach for research should probably focus on individual measurements of professional, domestic, and urban exposure to physical and chemical pollutants in order to accurately retrace the environmental exposure of parents of affected offspring during the pre-conceptional and pregnancy periods.
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Rev Environ Health. 2008 Jul-Sep;23(3):167-202.
Environmental risk factors for heart disease.
O’Toole TE1, Conklin DJ, Bhatnagar A.
Author information
- 1Institute of Molecular Cardiology, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, Louisville, KY 40202, United States of America.
Abstract
In this review, we discuss current evidence linking environmental pollutants to cardiovascular disease (CVD). Extensive evidence indicates that environmental factors contribute to CVD risk, incidence, and severity. Migrant studies show that changes in the environment could substantially alter CVD risk in a genetically stable population. Additionally, CVD risk is affected by changes in nutritional and lifestyle choices. Recent studies in the field of environmental cardiology suggest that environmental toxins also influence CVD. Exposure to tobacco smoke is paradigmatic of such environmental risk and is strongly and positively associated with increased cardiovascular morbidity and mortality. In animal models of exposure, tobacco smoke induces endothelial dysfunction and prothrombotic responses and exacerbates atherogenesis and myocardial ischemic injury. Similar mechanism may be engaged by other pollutants or food constituents. Several large population-based studies indicate that exposure to fine or ultrafine particulate air pollution increases CVD morbidity and mortality, and the plausibility of this association is supported by data from animal studies. Exposure to other chemicals such as polyaromatic hydrocarbons, aldehydes, and metals has also been reported to elevate CVD risk by affecting atherogenesis, thrombosis, or blood pressure regulation. Maternal exposure to drugs, toxins, and infection has been linked with cardiac birth defects and premature CVD in later life. Collectively, the data support the notion that chronic environmental stress is an important determinant of CVD risk. Further work is required to assess the magnitude of this risk fully and to delineate specific mechanisms by which environmental toxins affect CVD.
PMID: 19119685 [PubMed – indexed for MEDLINE]
Expert Rev Cardiovasc Ther. 2005 Nov;3(6):1125-30.
Genetic and environmental influences on malformations of the cardiac outflow tract.
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Abstract
Congenital cardiovascular malformations are the most common form of birth defect recorded. Specific malformations of the outflow portions of the heart are termed conotruncal malformations and arise from the septation of the common conotruncus of the heart. There are multiple lines of evidence that point towards genetic-environmental interactions in the genesis of conotruncal congenital cardiovascular malformations. In particular, environmental exposures that involve vitamin A, retinol, folic acid or retinol receptors are identified as cardiac teratogens. Other environmental agents for which there is evidence of cardiac teratogenicity for outflow tract malformations include nitrofen, ambient air pollution, chlorinated hydrocarbons and pesticides. Genetic polymorphisms of xenobiotic metabolism are clearly differentiating in the effect of potential teratogens. Work in this field is at a new cusp, with the ability to measure xenobiotic exposure, document xenobiotic metabolizing genetic polymorphisms and integrate these data into models of cardiac teratogenesis.
PMID: 16293002 [PubMed – indexed for MEDLINE]
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