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Ambient air pollution and risk of congenital anomalies: a systematic review and meta-analysis.

Vrijheid M, Martinez D, Manzanares S, Dadvand P, Schembari A, Rankin J, Nieuwenhuijsen M - Environ. Health Perspect. (2010)

Bottom Line: Summary risk estimates were calculated for a) risk at high versus low exposure level in each study and b) risk per unit increase in continuous pollutant concentration.We found some evidence for an effect of ambient air pollutants on congenital cardiac anomaly risk.Improvements in the areas of exposure assessment, outcome harmonization, assessment of other congenital anomalies, and mechanistic knowledge are needed to advance this field.

View Article: PubMed Central - PubMed

Affiliation: Center for Research in Environmental Epidemiology, Barcelona, Spain. mvrijheid@creal.cat

ABSTRACT

Objective: We systematically reviewed epidemiologic studies on ambient air pollution and congenital anomalies and conducted meta-analyses for a number of air pollutant-anomaly combinations.

Data sources and extraction: From bibliographic searches we extracted 10 original epidemiologic studies that examined the association between congenital anomaly risk and concentrations of air pollutants. Meta-analyses were conducted if at least four studies published risk estimates for the same pollutant and anomaly group. Summary risk estimates were calculated for a) risk at high versus low exposure level in each study and b) risk per unit increase in continuous pollutant concentration.

Data synthesis: Each individual study reported statistically significantly increased risks for some combinations of air pollutants and congenital anomalies, among many combinations tested. In meta-analyses, nitrogen dioxide (NO₂) and sulfur dioxide (SO₂) exposures were related to increases in risk of coarctation of the aorta [odds ratio (OR) per 10 ppb NO₂ = 1.17; 95% confidence interval (CI), 1.00-1.36; OR per 1 ppb SO₂ = 1.07; 95% CI, 1.01-1.13] and tetralogy of Fallot (OR per 10 ppb NO₂ = 1.20; 95% CI, 1.02-1.42; OR per 1 ppb SO₂ = 1.03; 95% CI, 1.01-1.05), and PM₁₀ (particulate matter ≤ 10 µm) exposure was related to an increased risk of atrial septal defects (OR per 10 μg/m³ = 1.14; 95% CI, 1.01-1.28). Meta-analyses found no statistically significant increase in risk of other cardiac anomalies and oral clefts.

Conclusions: We found some evidence for an effect of ambient air pollutants on congenital cardiac anomaly risk. Improvements in the areas of exposure assessment, outcome harmonization, assessment of other congenital anomalies, and mechanistic knowledge are needed to advance this field.

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Related in: MedlinePlus

Forest plots showing risk estimates for individual studies and the combined meta-analysis result. Marker sizes represent the relative weight the study contributed to the summary estimation. (A) NO2 and coarctation of the aorta. (B) NO2 and tetralogy of Fallot. (C) PM10 and ASDs. (D) SO2 and coarctation of the aorta. (E) SO2 and tetralogy of Fallot. (F) O3 and cleft lip with or without cleft palate.
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f1-ehp-119-598: Forest plots showing risk estimates for individual studies and the combined meta-analysis result. Marker sizes represent the relative weight the study contributed to the summary estimation. (A) NO2 and coarctation of the aorta. (B) NO2 and tetralogy of Fallot. (C) PM10 and ASDs. (D) SO2 and coarctation of the aorta. (E) SO2 and tetralogy of Fallot. (F) O3 and cleft lip with or without cleft palate.

Mentions: We conducted meta-analyses for 18 combinations of pollutants and cardiac anomaly groups for which four or more studies published results [for summary results, see Table 2; for full results, see Supplemental Material, Table 2 (doi:10.1289/ehp.1002946)]. The summary risk estimates from these meta-analyses were generally close to one, with a range of summary ORs for continuous exposure from 0.87 to 1.20, and for high versus low exposure from 0.80 to 1.23. Heterogeneity tests showed evidence for heterogeneity among studies (p < 0.10) in fewer than half of the analyses conducted, most consistently related to analyses of VSDs. Egger test p-values were statistically significant for only 3 of the 68 meta-analyses we conducted (see Supplemental Material, Table 2), indicating that wide-scale publication bias is unlikely. We found statistically significantly increased summary risk estimates for continuous NO2 exposure and risk of coarctation of the aorta (OR per 10 ppb = 1.17; 95% CI, 1.01–1.36) and tetralogy of Fallot (OR per 10 ppb = 1.20; 95% CI, 1.02–1.42), for continuous PM10 exposure and atrial septal defect (ASD; OR per 10 μg/m3 = 1.14; 95% CI, 1.01–1.28), and for continuous SO2 exposure and risk of coarctation of the aorta (OR per 1 ppb = 1.07; 95% CI, 1.01–1.13) and tetralogy of Fallot (OR per 1 ppb = 1.03; 95% CI, 1.01–1.05) (Table 2, Figure 1A–E). p-Values for heterogeneity in these analyses showed limited evidence for heterogeneity (p-values between 0.1 and 0.9). Sensitivity analyses excluding the study with the largest weight from each meta-analysis showed that results for NO2 and tetralogy of Fallot and for SO2 and coarctation of the aorta were robust to this exclusion. The results for SO2 were not robust to the inclusion of the first Dadvand study (Dadvand et al. 2011a) instead of the second (Dadvand et al. 2011b) (Table 2); the first study by Dadvand et al. (2011a) also introduced significant heterogeneity. High versus low comparisons did not show evidence for increased risks for any anomaly–pollutant combinations. The summary OR for high compared with low CO exposure and risk of ASDs was significantly reduced (OR per 1 ppm = 0.86; 95% CI, 0.75–0.99).


Ambient air pollution and risk of congenital anomalies: a systematic review and meta-analysis.

Vrijheid M, Martinez D, Manzanares S, Dadvand P, Schembari A, Rankin J, Nieuwenhuijsen M - Environ. Health Perspect. (2010)

Forest plots showing risk estimates for individual studies and the combined meta-analysis result. Marker sizes represent the relative weight the study contributed to the summary estimation. (A) NO2 and coarctation of the aorta. (B) NO2 and tetralogy of Fallot. (C) PM10 and ASDs. (D) SO2 and coarctation of the aorta. (E) SO2 and tetralogy of Fallot. (F) O3 and cleft lip with or without cleft palate.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3094408&req=5

f1-ehp-119-598: Forest plots showing risk estimates for individual studies and the combined meta-analysis result. Marker sizes represent the relative weight the study contributed to the summary estimation. (A) NO2 and coarctation of the aorta. (B) NO2 and tetralogy of Fallot. (C) PM10 and ASDs. (D) SO2 and coarctation of the aorta. (E) SO2 and tetralogy of Fallot. (F) O3 and cleft lip with or without cleft palate.
Mentions: We conducted meta-analyses for 18 combinations of pollutants and cardiac anomaly groups for which four or more studies published results [for summary results, see Table 2; for full results, see Supplemental Material, Table 2 (doi:10.1289/ehp.1002946)]. The summary risk estimates from these meta-analyses were generally close to one, with a range of summary ORs for continuous exposure from 0.87 to 1.20, and for high versus low exposure from 0.80 to 1.23. Heterogeneity tests showed evidence for heterogeneity among studies (p < 0.10) in fewer than half of the analyses conducted, most consistently related to analyses of VSDs. Egger test p-values were statistically significant for only 3 of the 68 meta-analyses we conducted (see Supplemental Material, Table 2), indicating that wide-scale publication bias is unlikely. We found statistically significantly increased summary risk estimates for continuous NO2 exposure and risk of coarctation of the aorta (OR per 10 ppb = 1.17; 95% CI, 1.01–1.36) and tetralogy of Fallot (OR per 10 ppb = 1.20; 95% CI, 1.02–1.42), for continuous PM10 exposure and atrial septal defect (ASD; OR per 10 μg/m3 = 1.14; 95% CI, 1.01–1.28), and for continuous SO2 exposure and risk of coarctation of the aorta (OR per 1 ppb = 1.07; 95% CI, 1.01–1.13) and tetralogy of Fallot (OR per 1 ppb = 1.03; 95% CI, 1.01–1.05) (Table 2, Figure 1A–E). p-Values for heterogeneity in these analyses showed limited evidence for heterogeneity (p-values between 0.1 and 0.9). Sensitivity analyses excluding the study with the largest weight from each meta-analysis showed that results for NO2 and tetralogy of Fallot and for SO2 and coarctation of the aorta were robust to this exclusion. The results for SO2 were not robust to the inclusion of the first Dadvand study (Dadvand et al. 2011a) instead of the second (Dadvand et al. 2011b) (Table 2); the first study by Dadvand et al. (2011a) also introduced significant heterogeneity. High versus low comparisons did not show evidence for increased risks for any anomaly–pollutant combinations. The summary OR for high compared with low CO exposure and risk of ASDs was significantly reduced (OR per 1 ppm = 0.86; 95% CI, 0.75–0.99).

Bottom Line: Summary risk estimates were calculated for a) risk at high versus low exposure level in each study and b) risk per unit increase in continuous pollutant concentration.We found some evidence for an effect of ambient air pollutants on congenital cardiac anomaly risk.Improvements in the areas of exposure assessment, outcome harmonization, assessment of other congenital anomalies, and mechanistic knowledge are needed to advance this field.

View Article: PubMed Central - PubMed

Affiliation: Center for Research in Environmental Epidemiology, Barcelona, Spain. mvrijheid@creal.cat

ABSTRACT

Objective: We systematically reviewed epidemiologic studies on ambient air pollution and congenital anomalies and conducted meta-analyses for a number of air pollutant-anomaly combinations.

Data sources and extraction: From bibliographic searches we extracted 10 original epidemiologic studies that examined the association between congenital anomaly risk and concentrations of air pollutants. Meta-analyses were conducted if at least four studies published risk estimates for the same pollutant and anomaly group. Summary risk estimates were calculated for a) risk at high versus low exposure level in each study and b) risk per unit increase in continuous pollutant concentration.

Data synthesis: Each individual study reported statistically significantly increased risks for some combinations of air pollutants and congenital anomalies, among many combinations tested. In meta-analyses, nitrogen dioxide (NO₂) and sulfur dioxide (SO₂) exposures were related to increases in risk of coarctation of the aorta [odds ratio (OR) per 10 ppb NO₂ = 1.17; 95% confidence interval (CI), 1.00-1.36; OR per 1 ppb SO₂ = 1.07; 95% CI, 1.01-1.13] and tetralogy of Fallot (OR per 10 ppb NO₂ = 1.20; 95% CI, 1.02-1.42; OR per 1 ppb SO₂ = 1.03; 95% CI, 1.01-1.05), and PM₁₀ (particulate matter ≤ 10 µm) exposure was related to an increased risk of atrial septal defects (OR per 10 μg/m³ = 1.14; 95% CI, 1.01-1.28). Meta-analyses found no statistically significant increase in risk of other cardiac anomalies and oral clefts.

Conclusions: We found some evidence for an effect of ambient air pollutants on congenital cardiac anomaly risk. Improvements in the areas of exposure assessment, outcome harmonization, assessment of other congenital anomalies, and mechanistic knowledge are needed to advance this field.

Show MeSH
Related in: MedlinePlus