Microplastics (MPs) are emerging environmental pollutants. Pregnancy and infancy are sensitive windows for environmental exposure. However, few studies have investigated the presence of MPs in mother–infant pairs, or the exposure source. In this study, nine mother–infant pairs were recruited, and samples of placenta, cord blood, and meconium were collected. Information about the living environment and dietary habits were collected to determine the source of exposure during pregnancy. Micro-Raman spectroscopy was applied to identify MPs. In total, 9, 4, and 14 types of MPs were identified in the placenta, cord blood, and meconium samples, with particle counts of 34, 14, and 80, respectively. More than 80.47% of MPs detected in samples had a size of 100–400 μm. The abundance of MPs exhibited the order of meconium > placenta > cord blood (Hc = 14.959, p < 0.01). We found that the abundance of MPs in meconium from women who drank tea ≥ 3 times/week during pregnancy was lower than in those who drank less (p = 0.048). Our study presents evidence of MPs transfer via the placenta–cord blood–meconium pathway. We also found that the habit of drinking tea among pregnant women might be related to the abundance of MPs in meconium.

It remains unclear whether type 2 diabetes and the complication of arthritis are causally related to the PM_2.5 pollutant. Therefore, we aimed to investigate the associations of long-term PM_2.5 exposure with type 2 diabetes and with arthritis in type 2 diabetes patients. This study used data from the China Health and Retirement Longitudinal Survey (CHARLS) implemented during 2011-2018. The associations were analyzed by Cox proportional hazards regression models, and the population-attributable fraction (PAF) was calculated to assess the burden of type 2 diabetes and arthritis-attributable to PM_2.5. A total of 21,075 participants were finally included, with 19,121 analyzed for PM_2.5 and type 2 diabetes risk and 12,427 analyzed for PM_2.5 and arthritis risk, of which 1,382 with newly-diagnosed type 2 diabetes and 1,328 with arthritis during the follow-up. Overall, each 10 μg/m³ increment in PM_2.5 concentration was significantly associated with an increase in the risk of type 2 diabetes (HR = 1.26, 95 %CI1.22 to 1.31), and the PAF of type 2 diabetes attributable to PM_2.5 was 13.54 %. In type 2 diabetes patients, each 10 μg/m³ increment in PM_2.5 exposure was associated with an increase in arthritis (HR = 1.42, 95 %CI: 1.28 to 1.57), and the association was significantly greater than that (H = 1.23, 95 %CI: 1.19 to 1.28) in adults without type 2 diabetes. The PAFs of arthritis-attributable to PM_2.5 in participants with and without type 2 diabetes were 18.54 % and 10.69 %, respectively. Long-term exposure to PM_2.5 may increase the risk of type 2 diabetes and make type 2 diabetes patients susceptible to arthritis.

PFAS (per- and polyfluoroalkyl substances) have been extensively used across numerous industries and consumer goods. Due to their high persistence and mobility, they are ubiquitous in the environment. Exposure to PFAS occurs in people via multiple pathways such as dermal contact, water supply, air inhalation, and dietary intake. Even if some PFAS are being phased out because of their persistent presence in the environment and harmful impacts on human health, mixes of replacement and legacy PFAS will continue to pollute the ecosystem. Numerous toxicological investigations have revealed harmful effects of PFAS exposure on female reproductive health, e.g., polycystic ovaries syndrome, premature ovarian failure, endometriosis, reproductive system tumors, pregnancy complications, and adverse pregnancy outcomes. Despite extensive epidemiological studies on the reproductive toxicity of PFAS, research findings remain inconsistent, and the underlying mechanisms are not well understood. In this review, we give an in-depth description of the sources and pathways of PFAS, and then review the reproductive toxicity of PFAS and its possible mechanisms.