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Table 2 Effect of pollutants on IVF outcomes (ICM: Inner cell mass; TE: trophectoderm)

From: Does air pollution play a role in infertility?: a systematic review

Publication

Species

Number of subjects

Air pollutant (s) studied

Methodology

Results

Legro et al., 2010 [34]

Humans

7403 patients in first IVF cycle

PM2.5, PM10, SO2, NO2, O3

Retrospective cohort study Examined association between live birth rate and predicted daily pollutant exposure at the place of residence from first day of ovarian stimulation to day of oocyte retrieval (T1); from oocyte retrieval to embryo transfer (T2); from embryo transfer to pregnancy test (T3) and from embryo transfer to pregnancy outcome(T4)

Odd ratio (95%CI) for live birth associated with 1 SD increment of each pollutant: NO2 at T1: 0.80 (0.71–0.91) NO2 at T2: 0.87 (0.79–0.96) NO2 at T3: 0.76 (0.66–0.86) O3 at T1: 1.26 (1.10–1.44) O3 at T3:1.23 (1.07–1.41) O3 at T4: 0.62 (0.48–0.81)

Perin et al., 2010 [36]

Humans

531 pregnant women

PM10

Retrospective matched (study in infertile (n = 177) and spontaneously conceiving women (n = 354). Measured average exposure for 14 days following date of last menstrual period and association with first trimester pregnancy loss

Odd Ratio (95% CI) for first trimester miscarriage in fourth quartile of PM10 exposure level: -Total population: 2.58 (95% CI: 1.63–4.07); −in Infertile population: 2.32 (1.00–5.43) -Natural conception population: 2.72 (1.51–4.89).

Perin et al., 2010 [35]

Humans

400 women in first IVF cycle for male infertility

PM10

Retrospective study: measured average exposure during 14 days following the date of last menstrual period and association with laboratory outcomes (number of oocytes, fertilization rate, embryo morphology; n = 348), IVF treatment outcomes (n = 348) and pregnancy outcomes (n = 189).

No association between exposure to high concentrations of PM10 and laboratory and IVF treatment outcomes. Odd ratio (95% CI) for clinical early pregnancy loss in fourth quartile of PM10 exposure level: 5.05 (1.04–24.51).

Maluf et al., 2009 [37]

Mice

112

Multiple air pollutants from automobile traffic

3 groups of virgin females exposed to filtered (FA) or ambient air (AA) during prenatal (from date of efficient mating to delivery) and/or postnatal period (from delivery to 6 weeks of age): FA-FA group (n = 40); FA-AA group (n = 36) and AA-AA group (n = 36).

Significant effect of exposure to PM2.5 on blastocyst development.: ICM cell count decreased: FA-AA: 24.45 ± 5.58 AA-AA: 24.08 ± 4.79 FA-FA: 30.06 ± 6.32 TE cell count increased: FA-AA: 102.60 ± 10.82 AA-AA: 95.43 ± 12.28 FA-FA: 90.64 ± 10.11

Januario et al., 2010 [42]

Mice

225 zygotes (exposure 1) and 95 zygotes (exposure 2)

Diesel exhaust particles (DEP)

In vitro embryo culture with Exposure 1: 0, 0.2, 2 and 20 μg/cm2 DEP (10 μg/cm2 relevant to concentrations of ambient air) until day 5 Exposure 2: 0, 0.2, 2 and 20 μg/cm2 DEP until day 8

Exposure 1: ICM cells count decreased with increasing DEP concentrations: 0 μg/cm2:29.9 ± 2.5 0.2 μg/cm2:18.2 ± 3.5 2 μg/cm2:14.6 ± 6.5 20 μg/cm2:10.3 ± 4.1 TE cells count unchanged Exposure 2: Increased apoptotic cells at Day 8 with increasing DEP concentrations: 0 μg/cm2: 8.6% 0.2 μg/cm2:17.2% 2 μg/cm2: 22.1%