Association between maternal exposure to pollutant particulate matter 2.5 and congenital heart defects: a systematic review.

OBJECTIVE: The objective of this review was to determine if there was an association between maternal exposure to pollutant particulate matter 2.5 during the first trimester of pregnancy and congenital heart defects within the first year of life.
INTRODUCTION: The environment is recognized as an important determinant of health for both the individual and population. Air pollution specifically is a major environmental risk factor impacting health with links to asthma, heart disease, obesity, and fetal developmental complications. Of the commonly monitored air pollutants, particulate matter 2.5 has associations with health, especially among vulnerable populations such as children and pregnant women. A congenital heart defect is a fetal complication that impacts 34.3 million infants globally, with more than 80% of the diagnoses having an unknown etiology. Although environmental risk factors such as air pollution are thought to be a risk factor in the diagnosis of a congenital heart defect, epidemiologic research evidence is limited. INCLUSION CRITERIA: This review considered studies that evaluated maternal exposure to the air pollutant particulate matter 2.5 during the first trimester (weeks 1-12) of fetal development. The primary outcome was a diagnosis of a congenital heart defect in an infant within the first year of life.
METHODS: A three-step search strategy was utilized in this review and included 11 databases and two websites. Studies published from January 2002 to September 2018 were eligible for inclusion. Only papers published in English were included. Eligible studies underwent critical appraisal by two independent reviewers using standardized critical appraisal instruments from JBI. Quantitative data were extracted from the included studies independently by two reviewers. Odds ratios (ORs) and 95% confidence intervals (CIs) were extracted for the individual outcome measures, specifically atrial septal defect, ventricular septal defect, and tetralogy of fallot, respectively. The defects were identified and pooled, where possible, in statistical meta-analysis. Where statistical pooling was not possible, findings were reported narratively.
RESULTS: Five studies were identified that met the inclusion criteria, including three cohort and two case-control designs. Each individual study identified at least one statistically significant increase or inverse association between particulate matter 2.5 and a congenital heart defect. An increased risk was identified with more than seven isolated and two groupings of congenital heart defects. An inverse risk was identified with two isolated and one grouping of congenital heart defects. Meta-analysis results were: atrial septal defect, OR = 0.65 (95% CI, 0.37 to 1.15); ventricular septal defect, OR = 1.02 (95% CI, 075 to 1.37); and tetralogy of fallot, OR = 1.16 (95% CI, 0.78 to 1.73), indicating no statistically significant findings.
CONCLUSION: There was no significant evidence to support an association between air pollutant particulate matter 2.5 and a congenital heart defect in the first year of life. However, few studies met the rigorous inclusion criteria, and the studies that did had high heterogeneity, making it difficult to complete a meta-analysis with such a limited number of articles. Further research is needed to standardize the outcomes and pollutant monitoring methods, and provide comparable analysis results so that future synthesis of the literature can be conducted.