**3.3 Environment or lifestyle factors**

Evidence of teratogenic contamination in certain environments and workplaces is sporadic, albeit environmental factors are a more common cause for multifactorial inheritance CHD. Definitive evidence for the causal relationship between certain exposure and CHD is still unavailable. Available evidence suggests the finding of the higher incidence of CHD babies from women who reside in area with drinking water contaminated by trichloroethylene, dichloroethylene and chromium. While maternal exposure to paint, lacquer, agricultural chemicals, organic solvents, dyes and lead have also been occasionally found statistically associated with CHD. Ingestion of heavy metals and lifetime accumulation of a considerable amount of heavy metals through diet also affects CHD development in babies (table 6).


64 Congenital Heart Disease – Selected Aspects

 **Caffeine;** Caffeine can cross the placenta, and the concern that caffeine may causes birth defects prompted the FDA to caution pregnant women to limit their caffeine intake. Today, there is no evidence associating caffeine ingestion during pregnancy and

 **Cocaine;** Maternal cocaine ingestion was reported to induce coronary thrombosis in the developing fetal heart leading to formation of a single ventricle, other defects were also reported, such as Ebstein's anomaly, VSD, heterotaxy (Linn et al., 1982; Kueh &

 **Cigarette Smoking;** Smoking during pregnancy enhances the risk of adverse pregnancy outcomes such as low birth weight. The relationship between gestational smoking and congenital heart defects has been studied, however the information is inconclusive. Some studies have reported associations between maternal smoking and ASD, AVSD, TOF (Alverson et al., 2011; Malik et al., 2008; Kallen, 1999). A recent study in Greece found that periconceptional tobacco smoking was associated with increased risk of CHD in the offspring (OR=2.7) and has been associated with a quantity of cigarette smoking (Karatza et al., 2011). However, no associations were found (Kallen, 1999) so

Evidence of teratogenic contamination in certain environments and workplaces is sporadic, albeit environmental factors are a more common cause for multifactorial inheritance CHD. Definitive evidence for the causal relationship between certain exposure and CHD is still unavailable. Available evidence suggests the finding of the higher incidence of CHD babies from women who reside in area with drinking water contaminated by trichloroethylene, dichloroethylene and chromium. While maternal exposure to paint, lacquer, agricultural chemicals, organic solvents, dyes and lead have also been occasionally found statistically associated with CHD. Ingestion of heavy metals and lifetime accumulation of a considerable amount of heavy metals through diet also affects CHD development in babies (table 6). **Organic Solvents;** A few studies reported increased risk of HLH, Coarc, PS, TGA with intact ventricular septum, TOF, TAPVR, non-chromosomal AVSD and Ebstein's anomaly. Other reports of occupational exposure to organic solvents have been associated with an increased risk of VSD (Tikkanen & Heinonen, 1991, 1992; Shaw et al., 2003). However the precise links are difficult to clarify, because solvent composition

 **Pesticides & Other Toxic Substances;** A study by Adam et al suggests an association of maternal employment in the agricultural industry with an increased risk of conotruncal defects that suggests a possible association with chemicals used in agriculture (Adams

Loffredo, 2002; Lipshultz et al., 1991; Martin & Khoury, 1992).

research on large population-based studies is required to evaluate.

varies between different commercial preparations.

teratogenicity of congenital heart disease (Pejtsik et al., 1992; Linn et al., 1982). A**lcohol;** Maternal alcohol use during pregnancy is associated with fetal alcohol syndrome which comprise a spectrum of abnormal face, growth restriction, central nervous system abnormality and cardiac defects with VSDs occurring most commonly (Pejtsik et al., 1992; Carmichael et al, 2003; Burd et al., 2007; Loser et al., 1992). In Spain, a case-control study by Martinez-Frias et al. reported that a higher risk of developing CHDs was found in the group with the highest-level daily doses of alcohol consumption (the absolute alcohol ingestion was more than 92 gram per day. However, mechanism in teratogenic effect of alcohol on the developing heart malformation is as

of now unclear.

**3.3 Environment or lifestyle factors** 


(Ref: 1Lisowski et al., 2010; 2Corrigan et al., 2009; 3Wren et al., 2003; 4Rouse & Azen, 2004; 5Buyon et al., 2009; 6Clancy & Buyon, 2004; 7Row, 1973; 8De Santis et al., 2006; 9Webster, 1998; 10Botto et al., 2001; 11Carmichael & Shaw, 2000; 12Adam et al., 1989; 13Cedergren & Kallen, 2003; 14Mills et al., 2010; 15Oddy et al., 2009; 16Gilboa et al., 2010; 17Cohen et al., 1994; 18Jacobson et al., 1992; 19Rothman et al., 1995; 20Botto et al., 2001; 21Lammer et al., 1985; 22Willhite et al., 1986; 23Rischbieth, 1979; 24O'Brien & Gilmour-White, 1993; 25Sonoda et al., 1993; 26Winter et al., 1987; 27Hou, 2004; 28Smithells & Newman, 1992; 29Ericson & Kallen, 2001; 30Czeizel et al., 2001; 31Newman & Correy, 1983; 32Crider et al., 2009; 33Cooper et al., 2006; 34Kallen & Otterblad Olausson, 2006; 35Bar-Oz et al., 2007; 36Berard et al., 2007; 37Pejtsil et al., 1992; 38Carmichael et al., 2003; 39Burd et al., 2007; 40Loser et al., 1992; 41Alverson et al., 2011; 42Malik et al., 1999; 43Kallen, 1999; 44Linn et al., 1982; 45Kuehl & Loffredo, 2002; 46Lipshultz et al., 1991; 47Martin & Khoury, 1992; 48Tikkanen & Heinonen, 1991; 49Shaw et al., 2003; 50Tikkanen et al., 1992; 51Gilboa et al., 2005; 52Dadvand et al., 2011)

Table 6. Risk factors that are known or believed to be associated with the congenital heart defects.

possible cardiac defects using fetal echocardiography during pregnancy when warranted by reports of prenatal maternal illnesses or exposures. The need for screening any individual should be made on an individual basis from the type, likelihood, and level of potential exposure, as well as the time of gestation during which it occurred. This decision typically will be made as a result of the obstetrical history. Because congenital heart defects represent some of the more prevalent birth defects, that result in significant lifelong morbidity, and are an important cause of mortality attributed to birth defects, the development of effective

The number of patients, both children and adults, with CHD has continued to rise. The most common reasons for CHD are associated with multiple factors. Epidemiology studies reveal underestimated cases of CHD, and together with the etiology the studies help to define potential risk factors for CHD. The epidemiology and etiology of CHD also help prioritize the areas needed for intervention and additional regulations the public health officers may impose. Patients and parents of babies with CHD must understand the significance of routine medical checkups, which can be accomplished though an effective transition

The authors thank Sarah Hof and Randall Jones for their supports in proofreading.

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**5. Conclusion** 

**6. Acknowledgement** 

**7. References** 

et al., 1989). In the Baltimore-Washington Infant Study (BWIS), potential exposure to herbicides and rodenticides was associated with an increased risk of TGA, while potential exposure to pesticides was associated with TAPVR and VSD. A case-control study of various end-product uses reported an increased risk of conotruncal defects with maternal reports of exposure to insecticides (Shaw et al., 1999).

