Abstract

Epidemiological studies strongly suggest that parental air pollutants exposure during the periconceptional period may play a major role in causing fetal/newborn malformations, including a frequent heterogeneity in the methods applied and a difficulty in estimating the clear effect of environmental toxicants. Moreover, only some couples exposed to toxicants during the pre-conception period give birth to a child with congenital anomalies. The reasons for such phenomena remain elusive but they can be explained by the individual, innate ability to metabolize these contaminants that eventually defines the ultimate dose of a biological active toxicant. In this paper, we reviewed the major evidence regarding the role of parental air pollutant exposure on congenital heart disease (CHD) risk as well as the modulating effect on detoxification systems. Finally, major epigenetic alterations induced by adverse environment contaminants have been revised as possible mechanisms altering a correct heart morphogenesis.

Highlights

  • IntroductionAir pollution is a universal issue and a major public health concern since it can affect everyone and can cause numerous heterogeneous adverse health events including asthma attacks, cancer and cardiovascular diseases [1,2,3]

  • Air pollution is a universal issue and a major public health concern since it can affect everyone and can cause numerous heterogeneous adverse health events including asthma attacks, cancer and cardiovascular diseases [1,2,3].Environmental noxae have effects on all age groups but fetuses are definitely the most vulnerable

  • Epidemiological studies show a total lack of interaction between exposure to toxicant and individual genetic susceptibility, which could explain why only some couples exposed to air contaminants give birth to a child with congenital heart anomalies [44]

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Summary

Introduction

Air pollution is a universal issue and a major public health concern since it can affect everyone and can cause numerous heterogeneous adverse health events including asthma attacks, cancer and cardiovascular diseases [1,2,3]. The other 80% has an unknown etiology that follows a multifactorial inheritance model, in which genetic factors are implicated and where environmental factors contribute heavily [9]. From this prospective, clear information on the impact of the environment is fundamental, firstly because the fraction of cases with CHD attributable to identifiable and potentially modifiable factors might be as high as 30% [10]. AAddddiittiioonnaallllyy,, tthheerree iiss ccoommppeelllliinngg eevviiddeennccee tthhaatt ppeerriiccoonncceeppttiioonnaall eexxppoossuurree ttoo eennvviirroonnmmeennttaall xxeennoobbiioottiiccss aaddvveerrsseellyy aaffffeeccttss ffeettaall ddeevveellooppmmeenntt tthhrroouugghh aalltteerraattiioonnss iinn eeppiiggeenneettiicc mmeecchhaanniissmmss[[1144]],, wwhhiicchh pprroodduuccee hheerriittaabbllee mmooddiiffiiccaattiioonnss iinn ggeennee eexxpprreessssiioonn wwiitthhoouutt cchhaannggeess iinn DDNNAA sseeqquueennccee.

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Study Design
Maternal Susceptibility to Air Pollution and CHD Risk
Findings
Conclusions
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