Environmental pollution and the development of congenital heart disease: A scoping review

Abstract

Introduction: Congenital heart disease (CHD) is the most common congenital anomaly in infancy affecting 1% of all live births worldwide of which the etiology in most affected children is unknown. The role of environmental pollutants from various sources is increasingly gaining attention. To explore the existing breadth of knowledge on this topic, we undertook a scoping review of studies examining the role of environmental pollution in relation to the development of CHD. Methods: We searched various databases for studies reporting CHD and exposures to chemicals using Medical Subject Headings (MeSH) and non-MeSH including criteria pollutants (e.g. CO, SO2 NO2), occupational, non-occupational, industrial chemicals and emissions reported in pollutant release and transfer registries (PRTR) from 1980 to 2018. Results: We identified 70 studies that were grouped into the categories of outdoor industrial chemical pollution; urban air pollution; occupational; and non-occupational exposures. There were no marked differences in proportions of studies in the first three categories, which ranged between 29-33%. Non-occupational exposures accounted for 7% of the studies. Proximity to industrial facilities and hazardous waste sites was associated with CHD in a modest number of studies that used PRTR. Urban criteria pollutants were consistently associated with CHD. Maternal occupational exposures were more commonly studied compared to paternal exposures and organic solvents were associated with CHD in these studies. There were limited studies that examined non-occupational and multipollutant exposures. Conclusion: We identified associations between various chemicals and CHD, employing diverse methods of exposure assessment. Most studies examined single pollutant exposures and have demonstrated inconclusive findings. Future studies should examine multiple pollutant exposures and CHD. In addition to monitored data, exploratory studies could exploit PRTR in countries where such registries exist. Furthermore, multicenter studies that examine larger populations of affected patients could facilitate the discovery of the relationship between specific chemicals and CHD subtypes.