The current study |
China |
2011–2013 |
Cohort |
Average of daily concentration of pollutants measured at nearest monitoring station |
O3 exposure and CHDs overall, and VSD and TF individually |
O3
|
72.4 μg/m3
|
1 μg/m3
|
31.9 μg/m3
|
63.6 μg/m3
|
106 μg/m3
|
334.3 μg/m3
|
74.1 μg/m3
|
(36.9 ppb) |
(0.5 ppb) |
(16.3 ppb) |
(32.4 ppb) |
(54 ppb) |
(170 ppb) |
(37.7 ppb) |
SO2
|
38.5 μg/m3
|
2 μg/m3
|
18 μg/m3
|
32.6 μg/m3
|
53.9 μg/m3
|
261 μg/m3
|
35.9 μg/m3
|
(14.7 ppb) |
(0.8 ppb) |
(6.9 ppb) |
(12.5 ppb) |
(20.6 ppb) |
(99.6 ppb) |
(13.7 ppb) |
NO2
|
59.6 μg/m3
|
7.1 μg/m3
|
38 μg/m3
|
55.8 μg/m3
|
77 μg/m3
|
174 μg/m3
|
39 μg/m3
|
(31.7 ppb) |
(3.8 ppb) |
(20.2 ppb) |
(29.6 ppb) |
(40.9 ppb) |
(92.5 ppb) |
(20.7 ppb) |
CO |
1.0 mg/m3
|
0.02 mg/m3
|
0.71 mg/m3
|
1 mg/m3
|
1.3 mg/m3
|
4.3 mg/m3
|
0.59 mg/m3
|
(0.91 ppm) |
(0.01 ppm) |
(0.62 ppm) |
(0.85 ppm) |
(1.1 ppm) |
(3.8 ppm) |
(0.48 ppm) |
Gianicolo et al.34
|
Southern Italy |
2001–2010 |
Case-control |
Daily average exposure measured by 3 monitoring stations over week 3-8 of pregnancy |
Exposure to the 90th percentile of SO2 to be associated with CHDs |
SO2
|
2.8μg/m3 |
— |
— |
— |
— |
— |
— |
Schembari et al.6
|
Barcelona |
1994–2006 |
Case-control |
Daily spatio-temperal air pollutants estimates over week 3–8 of pregnancy |
A significant association between NO2 and coarctation of the aorta |
NO2
|
— |
— |
— |
55.7 μg/m3
|
— |
— |
12.2 μg/m3
|
Stingone et al.15
|
Nine U.S.states |
1997–2006 |
Case-control |
Daily maximum concentrations using the closest air monitor within 50 km to their residence |
NO2 was associated with coarctation of the aorta and pulmonary valve stenosis. |
O3
|
— |
— |
32.2ppb |
42.9ppb |
51.8ppb |
— |
— |
SO2
|
— |
— |
— |
9.7ppb |
— |
— |
|
NO2
|
— |
— |
— |
33.3ppb |
— |
— |
— |
CO |
— |
— |
— |
1.16ppm |
— |
— |
— |
Agay-Shay et al.11
|
Israel |
2000–2006 |
Cohort |
Geographic Information System-based spatiotemporal approach with weekly inverse distance weighting modeling |
No significant association had been revealed |
O3
|
— |
0.45ppb |
7.8ppb |
26.5ppb |
39.1ppb |
128ppb |
— |
SO2
|
— |
0.33ppb |
1.5ppb |
2.1ppb |
3.3ppb |
51.4ppb |
— |
NO2
|
— |
0.2ppb |
15.6ppb |
23.1ppb |
32.3ppb |
104.5ppb |
— |
CO |
— |
0.15ppm |
0.7ppm |
0.9ppm |
1.3ppm |
13.5ppm |
|
Padula et al.26
|
San Joaquin Valley of California |
1997–2006 |
Case-control |
Daily average concentration during the first two months from from more than 20 locations with a maximum interpolation radius of 50 km. |
No significant association had been revealed |
O3(8-h maximum) |
— |
10.49ppb |
29.05ppb |
46.94ppb |
62.64ppb |
91.92ppb |
— |
NO2
|
— |
2.4 ppb |
13.36 ppb |
16.81 ppb |
20.53 ppb |
38.93 ppb |
— |
CO |
— |
0.13 ppm |
0.39 ppm |
0.52 ppm |
0.71 ppm |
1.37 ppm |
— |
Vinikoor-Imler et al.16
|
North Carolina |
2003–2005 |
Cohort |
Estimated averaged concentration across weeks 3 through 8 for 12 km x 12 km grid. |
No significant association had been revealed |
O3
|
40.7 ppb |
— |
— |
42.15 ppb |
— |
— |
30.19 ppb |
Dadvand et al.19
|
Northeast England |
1993–2003 |
Case-control |
Weekly average of pollutants at nearest of 6 monitors to maternal residence |
No significant association between SO2 and CHDs |
SO2
|
— |
— |
17.6 μg/m3
|
— |
31.2 μg/m3
|
— |
— |
Dadvand et al.22
|
Northeast England |
1985–1996 |
Case-control |
Two-stage spaiotemporal modeling of weekly exposure levels at maternal residence |
Exposure to CO to be associated with VS,DCSM and CPVS. NO was associated with TF. |
O3
|
— |
— |
33.2 μg/m3
|
— |
42.4 μg/m3
|
— |
— |
NO2
|
— |
— |
29.2 μg/m3
|
— |
38.4 μg/m3
|
— |
— |
CO |
— |
— |
0.39 mg/m3
|
— |
0.64 mg/m3
|
— |
— |
Dolk et al.3
|
England |
1991–1999 |
Cohort |
Estimated annual mean of air pollution for 1 km x 1 km grid |
A significant association between SO2 and TF |
SO2
|
— |
— |
— |
7.86 μg/m3
|
— |
— |
— |
NO2
|
— |
— |
— |
35.11μg/m3
|
— |
— |
— |
Hansen et al.35
|
Brisbane, Australia |
1997–2004 |
Case-control |
Daily averaged measurements of air pollution at 18 nearest monitoring stations. |
O3 was associated with an increased risk of pulmonary artery and valve defects, SO2 was associated with an increased risk of aortic artery and valve defects |
O3
|
25.8 ppb |
4.3 ppb |
— |
— |
— |
54.4 ppb |
— |
SO2
|
1.5 ppb |
0 ppb |
— |
— |
— |
7.1 ppb |
— |
|
NO2
|
8.2 ppb |
1.4 ppb |
— |
— |
— |
22.7 ppb |
— |
|
CO |
1.1 ppm |
0.02 ppm |
— |
— |
— |
7 ppm |
— |
|
|
|
|
|
|
Rankin et al.36
|
Northern region, UK |
1985–1990 |
Case-control |
Daily average concentration during the first trimester from 62 monitors within 10 km of the mother’s residence. |
No significant association between SO2 exposure and CHDs |
SO2
|
|
|
2.7 μg/m3
|
|
4.4 μg/m3
|
|
|
Strickland et al.35
|
Atlanta, USA |
1986–2003 |
Cohort |
Average of daily measuremtns of pollutants from one central monitoring station |
No significant association between SO2, O3, NO2, and CO exposure and CHDs |
O3
|
— |
— |
— |
— |
— |
— |
29.9 ppb |
SO2
|
— |
— |
— |
— |
— |
— |
4.0 ppb |
NO2
|
— |
— |
— |
— |
— |
— |
5.7 ppb |
CO |
— |
— |
— |
— |
— |
— |
0.3 ppm |
Ritz et al.9
|
California, USA |
1987–1993 |
Case-control |
Average of 24-hr measurements of pollutants at nearest monitoring station |
Second-month CO exposure was associated with an increased risk of VSD |
O3
|
— |
— |
1.06 pphm |
1.94 pphm |
2.84 pphm |
— |
— |
CO |
— |
— |
1.14 ppm |
1.6 ppm |
2.47 ppm |
— |
— |