Table 6.

Impacts of microplastics on pregnancy and maternal exposure to progeny or offspring and associated molecular mechanisms

Biological effects during pregnancy	Mechanism	Reference
Alteration in the serum triglyceride, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels in the mice's first filial offspring Alteration in the hepatic total cholesterol and triglyceride levels Changes in serum metabolites (amino acids and acyl-carnitines) between gender Changes of free carnitine (C0)/(palmitoylcarnitine, C16 C + stearoylcarnitine, C18) as an indicator of the potential risk of fatty acid metabolism disorder	Microplastic could affect the hepatic lipid metabolism Female and male offsprings react differently to maternal microplastic exposure during gestation (the specific mechanism is unknown) Peroxisome proliferator-activated receptors (PPARs) were key regulators of lipid and carbohydrate metabolism and in the modulation of inflammatory responses	Luo et al. (2019)
Polystyrene nanoplastics delivered to offspring increased brain and body weight of postnatal progeny Reduced the number of Kiel-67 + proliferative cells by more than 60%, lower progenitor cells positively labelled with nestin (a specific marker for neural stem cells) in the hippocampus Polystyrene nanoplastic exposure results in neurophysiological abnormalities and cognitive deficits in a gender-dependent manner	Acetylcholinesterase (AChE) inhibition and enhanced lipid oxidation (LPO) in the brain are two ways for microplastics to cause neurotoxicity Significant anomalies in brain development are caused by high doses of polystyrene nanoplastic (more than 500 g/day)	Jeong et al. (2022)
Reduced in number and diameter of uterine arterioles Reduced decidual natural killer cells percentage Increased helper T cells in the placenta Reverse M1 macrophage/M2 macrophage ratios Cytokine secretion shifts	The uterine blood flow is lessened because there are fewer and smaller uterine arterioles The macrophage subtype 1/subtype 2 ratio drastically changed to a dominant subtype 2 Cytokines switched to an immunosuppressive condition	Hu et al. (2021b)
Decreased birth and postnatal body weight Reduced liver weight Reduced testis weight, seminiferous epithelium, and sperm count Induced testicular oxidative injury	Microplastics either cause immunological and inflammatory responses or cell damage Unknown mechanisms contribute to the fertility rate declining over time	Huang et al. (2021b)
Reduced neurite length, the number of primary neurites, and the number of neurite branches Reduced the size of the hippocampal cell body Decreased neuronal viability and neuronal density in the hippocampus Impaired learning/memory Dysregulation of the expression of autism spectrum disorder-related genes in the hippocampus	Exposure of ospreys of both sexes to Bisphenol A caused longer neurites, more primary neurites, and more neurite branches but smaller hippocampus cell bodies. But bisphenol A exposure during pregnancy reduced the number of neurons and their viability in the hippocampus	Thongkorn et al. (2019)
Nano polystyrene deposition in the foetal liver, heart, kidney, and brain, as well as migration from the maternal lungs to the foetal compartment during exposure in late late-stage pregnancy	After exposure to nanoplastics through the mother's lungs, the foetal tissues may get affected There is conflicting evidence regarding how the blood–brain barrier develops and works in pregnancy. Thus, the blood–brain barrier may not have fully developed, leaving the foetal brain vulnerable to particle sedimentation	Fournier et al. (2020)

Maternal exposure to microplastics during pregnancy can negatively impact maternal and foetal health through various mechanisms, including inflammation and disruption of hormonal balance. Further research is needed to fully understand the extent of these effects and identify strategies to minimise exposure to microplastics during pregnancy.