Ambient PM2.5 exposures and systemic biomarkers of lipid peroxidation and total antioxidant capacity in early pregnancy.

Evidence for effects of PM2.5 on systemic oxidative stress in pregnant women is limited, especially in early pregnancy. To estimate the associations between ambient PM2.5 exposures and biomarkers of lipid peroxidation and total antioxidant capacity (T-AOC) in women with normal early pregnancy (NEP) and women with clinically recognized early pregnancy loss (CREPL), 206 early pregnant women who had measurements of serum malondialdehyde (MDA) and T-AOC were recruited from a larger case-control study in Tianjin, China from December 2017 to July 2018. Ambient PM2.5 concentrations of eight single-day lags exposure time windows before blood collection at the women's residential addresses were estimated using temporally-adjusted land use regression models. Effects of PM2.5 exposures on percentage change in the biomarkers were estimated using multivariable linear regression models adjusted for month, temperature, relative humidity, gestational age and other covariates. Unconstrained distributed lag models were used to estimate net cumulative effects. Increased serum MDA and T-AOC were significantly associated with increases in PM2.5 at several lag exposure time windows in both groups. The net effects of each interquartile range increase in PM2.5 over the preceding 8 days on MDA were significantly higher (p < 0.001) in CREPL [52% (95% CI: 41%, 62%)] than NEP [22% (95% CI: 9%, 36%)] women. Net effects of each interquartile range increase in PM2.5 over the preceding 5 days on T-AOC were significantly lower (p = 0.010) in CREPL [14% (95% CI: 9%, 19%)] than NEP [24% (95% CI: 18%, 29%)] women. Exposure to ambient PM2.5 may induce systemic lipid peroxidation and antioxidant response in early pregnant women. More severe lipid peroxidation and insufficient antioxidant capacity associated with PM2.5 was found in CREPL women than NEP women. Future studies should focus on mechanisms of individual susceptibility and interventions to reduce PM2.5-related oxidative stress in the first trimester.

Ambient PM2.5 and clinically recognized early pregnancy loss: A case-control study with spatiotemporal exposure predictions.

BACKGROUND: Experimental research suggests that fine particulate matter (PM2.5) exposure might affect embryonic development. However, only few population-based studies have investigated the impact of maternal exposure to PM2.5 on the early pregnancy loss. OBJECTIVES: To estimate associations between clinically recognized early pregnancy loss (CREPL) and exposure to ambient PM2.5 at individual residences during peri-conception periods, with the aim to identify susceptible exposure time windows. METHODS: CREPL cases and normal early pregnancy controls (of similar age and gravidity presenting within one week, a total of 364 pairs) were recruited between July 2017 and July 2018 among women residing in Tianjin, China. Average ambient PM2.5 concentrations of ten exposure windows (4 weeks, 2 weeks and 1 week before conception; the first, second, third and fourth single week, the first and second 2-week periods, and the entire 4-week period after conception) at the women's residential addresses were estimated using temporally-adjusted land use regression models. Associations between PM2.5 exposures at specific peri-conception time windows and CREPL were examined using conditional logistic regression models, adjusted for covariates. RESULTS: Based on adjusted models, CREPL was significantly associated with a 10 µg/m3 increase in PM2.5 exposure during the second week after conception (OR = 1.15; 95% CI: 1.04, 1.27; p = 0.005), independent of effects at other time windows. There was also an association of CREPL with PM2.5 during the entire 4-week period after conception (OR = 1.22; 95% CI: 1.02, 1.46; p = 0.027). There was little evidence for associations with exposure during pre-conception exposure windows. CONCLUSIONS: Maternal exposures to ambient PM2.5 during a critical time window following conception are associated with CREPL, with the second week after conception possibly being the exposure window of most vulnerability. Future studies should focus on replicating these findings and on pathogenic mechanisms.