Maternal Socioeconomic Status and the Risk of Congenital Heart Defects in Offspring: A Meta-Analysis of 33 Studies

<div><p>Background</p><p>We conducted this meta-analysis to address the open question of a possible association between maternal socioeconomic status and congenital heart defects (CHDs).</p><p>Methods</p><p>We searched MEDLINE and EMBASE from their inception to January 1, 2014 for case-control and cohort studies that assessed the association between maternal socioeconomic status and the risk of CHDs. Study-specific relative risk estimates were polled according to random-effect or fixed-effect models.</p><p>Results</p><p>From 3343 references, a total of 31 case-control studies and 2 cohort studies were enrolled in this meta-analysis, including more than 50,000 cases. We observed that maternal educational attainment, family income and maternal occupation were negatively associated with an 11% (pooled RR = 1.11, 95% CI: 1.03, 1.21), 5% (pooled RR = 1.05, 95% CI: 1.01, 1.09) and 51% (pooled RR = 1.51, 95% CI: 1.02, 2.24) increased risk of CHDs, respectively. In a subgroup analysis by geographic region, the results were inconsistent for the European region (RR = 1.29, 95% CI: 0.99–1.69) and USA/Canada region (RR = 1.06, 95% CI: 0.97, 1.16) in maternal educational attainment.</p><p>Conclusion</p><p>In summary, this meta-analysis suggests that a lower degree of maternal socioeconomic status is modestly associated with an increased risk of CHDs. However, further investigations are needed to confirm the association.</p></div

Estimates (95% CIs) of maternal educational attainment (lowest vs. highest category) and congenital heart defect (CHD) risk.

<p>Estimates (95% CIs) of maternal educational attainment (lowest vs. highest category) and congenital heart defect (CHD) risk.</p

Pooled estimates for socioeconomic category and incidence of CHDs in series of subgroup analyses.

<p>Pooled estimates for socioeconomic category and incidence of CHDs in series of subgroup analyses.</p

References searched and selection of studies in the meta-analysis.

<p>References searched and selection of studies in the meta-analysis.</p

Estimates (95% CIs) of maternal occupational prestige and congenital heart defect (CHD) risk.

<p>A: Level I vs. level IV occupation; B: Level II vs. level IV occupation; C: Level III vs. level IV occupation.</p

Estimates (95% CIs) of income level (lowest vs. highest category) and congenital heart defect (CHD) risk.

<p>Estimates (95% CIs) of income level (lowest vs. highest category) and congenital heart defect (CHD) risk.</p

Overall characteristics of included studies.

<p>Overall characteristics of included studies.</p

Begg's test of studies for maternal educational attainment and congenital heart defects (CHD).

<p>Begg's test of studies for maternal educational attainment and congenital heart defects (CHD).</p

Association of Aminoacyl-tRNA Synthetases Gene Polymorphisms with the Risk of Congenital Heart Disease in the Chinese Han Population

<div><p>Aminoacyl-tRNA synthetases (ARSs) are in charge of cellular protein synthesis and have additional domains that function in a versatile manner beyond translation. Eight core ARSs (<i>EPRS, MRS, QRS, RRS, IRS, LRS, KRS, DRS</i>) combined with three nonenzymatic components form a complex known as multisynthetase complex (MSC).We hypothesize that the single-nucleotide polymorphisms (SNPs) of the eight core ARS coding genes might influence the susceptibility of sporadic congenital heart disease (CHD). Thus, we conducted a case-control study of 984 CHD cases and 2953 non-CHD controls in the Chinese Han population to evaluate the associations of 16 potentially functional SNPs within the eight ARS coding genes with the risk of CHD. We observed significant associations with the risk of CHD for rs1061248 [G/A; odds ratio (OR) = 0.90, 95% confidence interval (CI) = 0.81–0.99; <i>P</i> = 3.81×10⁻²], rs2230301 [A/C; OR = 0.73, 95%CI = 0.60–0.90, <i>P</i> = 3.81×10⁻²], rs1061160 [G/A; OR = 1.18, 95%CI = 1.06–1.31; <i>P</i> = 3.53×10⁻³] and rs5030754 [G/A; OR = 1.39, 95%CI = 1.11–1.75; <i>P</i> = 4.47×10⁻³] of <i>EPRS</i> gene. After multiple comparisons, rs1061248 conferred no predisposition to CHD. Additionally, a combined analysis showed a significant dosage-response effect of CHD risk among individuals carrying the different number of risk alleles (<i>P</i>_trend = 5.00×10⁻⁴). Compared with individuals with “0–2” risk allele, those carrying “3”, “4” or “5 or more” risk alleles had a 0.97-, 1.25- or 1.38-fold increased risk of CHD, respectively. These findings indicate that genetic variants of the <i>EPRS</i> gene may influence the individual susceptibility to CHD in the Chinese Han population.</p></div

Primary information for 16 functional SNPs in ARS-coding genes.

a<p>Derived from the UCSC Genome Browser on Human Feb. 2009 (GRCh37/hg19) Assembly (<a href="http://genome.ucsc.edu/" target="_blank">http://genome.ucsc.edu/</a>);</p>b<p>Derived from an online tool-SNPinfo (<a href="http://snpinfo.niehs.nih.gov/snpfunc.htm" target="_blank">http://snpinfo.niehs.nih.gov/snpfunc.htm</a>);</p>c<p>Major/minor allele;</p>d<p>Hardy-Weinberg equilibrium test among controls;</p>e<p>miRNA: microRNA</p>f<p>Splice sites: Exonic splicing enhancer (ESE) or exonic splicing silencer (ESS) binding sites;</p>g<p>nsSNP: non-synonymous polymorphisms.</p>h<p>TFBS: Transcription factor binding sites;</p><p>Primary information for 16 functional SNPs in ARS-coding genes.</p