Microplastics (MPs) are pervasive environmental contaminants, resulting in unavoidable human exposure. This study identified MPs in follicular fluid and investigated the specific MPs and mechanisms that adversely affect oocytes. MPs in the follicular fluid of 44 infertile women undergoing assisted reproductive technology were measured using Raman microspectroscopy. Differential metabolites in follicular fluid were analyzed via untargeted metabolomics. Female mice were exposed to polyethylene (PE) to validate human findings. MPs, particularly PE, exhibited the highest detection rate (86.4 %) in human follicular fluid and showed a negative correlation with fertilization rates (r = -0.407, P = 0.007). Elevated PE levels altered metabolites primarily involved in metabolic pathways, ferroptosis, and ovarian steroidogenesis. In mice, PE exposure significantly reduced the number of retrieved oocytes (31.5 vs. 36.3, P < 0.05) and fertilization rate (70.8 % vs. 85.2 %, P < 0.001), while increasing the proportion of poor-quality oocytes (28.2 % vs. 16.5 %, P < 0.001) and reactive oxygen species (ROS) production compared to controls. RNA sequencing indicated significant upregulation of inflammation-related genes (Il10ra, Il1a, Il33, Tnfaip8l2, and Tnfrsf1b) in the PE-exposed group. In conclusion, PE exposure impairs oocyte quality possibly by disrupting follicular fluid metabolism, elevating inflammation-related gene expression, and increasing ROS production in oocytes.

Fetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce. A total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE). The full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (− 9.06, − 1.91), 5.57 (− 6.66, − 4.47), and 5.47 (− 6.39, − 4.55), respectively; the mean EFW decreased by 14.49 (− 16.05, − 13.49) grams by Hadlock’s third formula and 13.56 (− 14.71, − 12.50) grams by Shepard’s formula with each 10 μg/m3 increase in PM2.5 exposure. A negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Microplastics (MPs) are becoming one of the most serious environmental threats worldwide. They have been shown to induce male reproductive toxicity in animal studies. However, evidence of their adverse effects on male reproductive health in human is still lacking. In this study, we evaluated the presence of MPs in human semen and explored their associations with semen quality. A total of 45 semen samples from men attending a fertility center were collected. MPs in the semen samples were analyzed by laser direct infrared (LD-IR) spectroscopy. MPs were found in 34 out of 45 semen samples, with an average abundance of 17.0 (42.0) particles/g. The size of MPs ranged from 20.3 μm to 189.7 μm and the majority (57.8%) were smaller than 50 μm. A total of 15 distinct MPs polymers were identified, and polyethylene (PET) accounted for 35.9% of the total amount of MPs, followed by butadiene rubber (BR, 26.4%) and chlorinated polyethylene (CPE, 12.2%). Analysis of the association of MP exposure with semen quality showed that participants exposed to PET MPs experienced a reduction in sperm progressive motility (20.6% ± 12.8% vs. 34.9% ± 15.9%, p = 0.056). However, no significant association was found between MP exposure and sperm concentration or total sperm count. Our findings confirmed the presence of MPs in human semen and suggested that MP exposure might have adverse impacts on male reproductive health. However, further large-scale studies are needed to confirm these findings.

Background: Association between fine particulate matter (PM_2.5) and hypertensive disorders of pregnancy (HDP) is inconsistent and appears to change in each trimester. We aim to investigate the association of exposure to ambient PM_2.5 in early pregnancy with HDP. Methods: A retrospective cohort study was performed among 8776 women with singleton pregnancy who attended the antenatal clinic before 20 gestational weeks in a tertiary women’s hospital during 2014–2015. Land use regression models were used to predict individual levels of PM_2.5 exposure. Results: The average PM_2.5 concentration during the first 20 gestational weeks ranged from 28.6 to 74.8 μg m^− 3 [median, 51.4 μg m^− 3; interquartile range, 47.3–57.8 μg m^− 3]. A total of 440 (5.0%) women was diagnosed with HDP. The restricted cubic spline showed a positive exposure-response relationship between the PM_2.5 concentration and risk of HDP. We observed an association between PM_2.5 exposure during the first trimester with HDP (RR = 3.89 per 10 μg m^− 3, 95% CI: 1.45–10.43), but not during the second trimester (RR = 0.71 per 10 μg m^− 3, 95% CI: 0.40–1.27). Compared with their counterparts, nulliparous women who were exposed to high levels of PM_2.5 in the index pregnancy had a higher risk of developing HDP [the relative excess risk due to interaction was 0.92 (0.46–1.38)]. Conclusion: Our findings suggest that PM_2.5 exposure during the first trimester is associated with the development of HDP. The effect estimate is more obvious for nulliparous women than multiparous women.

Subclinical hypothyroidism (SCH) in pregnancy has drawn an increasing amount of attention over the past two decades. However, the definition of it, including its clinical diagnosis and treatment, i...