A Review of Human Exposure to Microplastics and Insights Into Microplastics as Obesogens.
A Review of Human Exposure to Microplastics and Insights Into Microplastics as Obesogens.
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DOI：
10.3389/fendo.2021.724989
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发表时间：
2021
影响因子：
5.2
通讯作者：
Vimalkumar K
中科院分区：
文献类型：
--
作者：
Kannan K;Vimalkumar K
众所周知，人类通过吸入空气中的颗粒以及摄入灰尘、水和饮食而普遍接触微塑料 (MP)。据估计，人类每年摄入数万至数百万个 MP 颗粒，或每天摄入数毫克左右。现有信息表明，吸入室内空气和摄入塑料瓶装饮用水是 MP 暴露的主要来源。人们对人类饮食中 MP 的存在知之甚少。越来越多的证据表明，奶瓶和医疗设备可能会导致新生儿和婴儿接触 MP。对人类粪便、胎儿和胎盘的生物监测研究提供了婴儿和儿童接触 MP 的直接证据。据报道，<20 µm 的 MP 可以穿过生物膜。尽管塑料曾经被认为是惰性材料，但实验动物接触 MP 与各种形式的炎症、免疫反应、内分泌干扰、脂质和能量代谢的改变以及其他疾病有关。虽然接触 MP 本身就是一个问题，但 MP 也可能是接触塑料添加剂和其他有毒物质的来源。人类细胞系暴露于邻苯二甲酸盐、双酚和有机锡等 MP 添加剂中，会通过激活核受体、过氧化物酶体增殖物激活受体 (PPAR) α、β 和 γ 以及类视黄醇 X 受体 (RXR) 产生不利影响，从而导致氧化应激、细胞毒性、免疫毒性、甲状腺激素破坏以及脂肪生成和能量产生的改变。 MP 的大小、形状、化学成分、表面电荷和疏水性会影响其毒性。 MP 的母体转移至发育中的胎儿已在暴露的实验动物中和通过对人类胎盘的分析得到证实。在实验动物研究中，母亲接触 MP 会改变后代及后代的能量和脂质代谢。此外，随着全球塑料产量的增加，过去五年中人类超重和肥胖的患病率有所增加，并且有证据支持 MP 及其添加剂是潜在致肥胖因素的假设。尽管 MP 暴露无处不在，并且此类暴露的毒性影响令人担忧，但仍然迫切需要对此主题进行系统研究。
The ubiquitous exposure of humans to microplastics (MPs) through inhalation of particles in air and ingestion in dust, water, and diet is well established. Humans are estimated to ingest tens of thousands to millions of MP particles annually, or on the order of several milligrams daily. Available information suggests that inhalation of indoor air and ingestion of drinking water bottled in plastic are the major sources of MP exposure. Little is known on the occurrence of MPs in human diet. Evidence is accumulating that feeding bottles and medical devices can contribute to MP exposure in newborns and infants. Biomonitoring studies of human stool, fetus, and placenta provide direct evidence of MP exposure in infants and children. MPs <20 µm were reported to cross biological membranes. Although plastics were once perceived as inert materials, MP exposure in laboratory animals is linked to various forms of inflammation, immunological response, endocrine disruption, alteration of lipid and energy metabolism, and other disorders. Whereas exposure to MPs itself is a concern, MPs can also be sources of exposure to plastic additives and other toxicants. Exposure of human cell lines to MP additives such as phthalates, bisphenols, and organotins causes adverse effects through the activation of nuclear receptors, peroxisome proliferator-activated receptors (PPARs) α, β, and γ, and retinoid X receptor (RXR), leading to oxidative stress, cytotoxicity, immunotoxicity, thyroid hormone disruption, and altered adipogenesis and energy production. The size, shape, chemical composition, surface charge, and hydrophobicity of MPs influence their toxicity. Maternal transfer of MPs to the developing fetus has been demonstrated in exposed laboratory animals and through the analysis of human placenta. In laboratory animal studies, maternal exposure to MPs altered energy and lipid metabolism in offspring and subsequent generations. Moreover, concomitant with the global increase in plastics production, the prevalence of overweight and obesity in human populations has increased over the past five decades, and there is evidence to support the hypothesis that MPs and their additives are potential obesogens. Even though MP exposures are ubiquitous and toxic effects from such exposures are a concern, systematic studies on this topic remain urgently needed.
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