Abstract
Purpose of Review
Microplastics in the environment enter the human body through diet, drinking water, and air inhalation. The widespread detection of microplastics in several human tissues was conducted. However, limited knowledge exists on the number of microplastics that can be ingested by humans and the potential adverse effects on various organs. To address these issues, we reviewed the types and abundance of microplastics through different pathways and summarized the average annual intake in humans.
Recent Findings
An adult can ingest about (4.88–5.77) × 105 microplastics/year through the dietary route [including salt (5.00–7.00) × 103, fish (0.50–1.20)×104, fruits (4.48–4.62) × 105, and vegetables (2.96–9.55)×104]. The amount of microplastics ingested via drinking water route was approximately (0.22–1.2)×106 microplastics/year. Inhalation of microplastics via atmospheric environment was nearly (0.21–2.51) × 106 microplastics/year [including indoor (0.16–2.30) × 106 and outdoor (0.46–2.10)×105].
Summary
In conclusion, we found that the human body ingests microplastics most through inhalation, followed by drinking water and diet. We also summarized the types and abundance of microplastics that were enriched in different organs after microplastics entered the human body. Microplastics entering the body would cross the barrier into the target effector organs and cause adverse health effects, mainly including induction of intracellular oxidative stress, genotoxicity, reproductive toxicity, and inflammatory responses. In conclusion, exposure to microplastics can cause many adverse effects on the health of the organism. Thus, an increased awareness of the crisis, urgent discussion, and practical actions are needed to mitigate microplastics contaminants in the environment.
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Introduction
Microplastics are nearly ubiquitous in environments. The presence of microplastics can be detected from the Tibetan Plateau to the Marianas Trench [1] and from the houses we live in every day to the untouched skies over the Pacific Ocean [2, 3]. Since the concept of microplastics was first introduced in the marine environment in 2004 [4], a large number of studies have emerged to investigate microplastics pollution in the ocean. Microplastics in the ocean are mainly from direct emissions of plastic waste, laundry, marine activities, floating plastics, and industrial emissions. Indoor air microplastics are mainly from home decoration, synthetic textiles [5], air conditioning filters [6, 7], and microplastics from the wear and tear of household items and electronics. Outdoor microplastics are mainly from vehicle emissions and tire wear [8], road marking paint, asphalt on roads [9], and street dust [10]. The main sources of microplastics in soil include the casual disposal of discarded plastic products [11,12,13], agricultural plastic films, plastic components added to agricultural supplies such as fertilizers and pesticides [14, 15], artificial fillers in municipal greening and landscape construction projects, and pollution sources such as industrial wastewater, municipal sewage, and garbage microplastics that enter the soil through water flow. The widespread presence of microplastics in the environment inevitably results in people taking in microplastics from the environment through various means (e.g., diet, drinking water, breathing, and skin contact). Therefore, the calculation of microplastics intake are essential for the assessment of human health risks.
Several studies have reported the presence of microplastics in the human skin, lung [16, 17], liver, spleen, kidney [18•], colon [19], feces [20, 21, 22•, 23], blood [24], saliva [25], placenta [26,27,28,29], and breast milk [30]. This suggests that microplastics enter the body through different pathways, reach everywhere through the circulatory system, and are enriched in the target effector organs. A recent study reported the presence of microplastics in human blood clots [31, 32], which proves that the impact of exogenous microplastics on human health cannot be ignored. Therefore, a comprehensive understanding of the absorption, distribution, metabolism, and excretion characteristics of microplastics in humans is essential to investigate the potential toxicological effects of microplastics exposure.
Numerous in vivo cellular and in vitro animal studies have demonstrated that microplastics exposure cause liver fibrosis and metabolic disorders, significant impairment of kidney function, inflammatory response and functional impairment of lung, ecological imbalance and metabolic disorders of intestinal flora, and impairment of neurological function and affects reproduction. However, the adverse effects and main mechanisms of microplastics on different target effector organs and systems have not been systematically elucidated. We analyzed the literature on the potential toxic effects of microplastics exposure on health in recent years to analyze the health hazards of microplastics comprehensively. The effects of microplastics on organism health at different organ levels were also summarized. Then, new ideas and improved methods for environmental management and medical health fields could be provided.
This study aims to estimate the annual intake of microplastics in humans through different routes and review the types and abundance of microplastics in different tissues and organs in the human body. By summarizing the results of available in vitro cellular and in vivo animal experiments, the hazard of microplastics exposure to different organ tissues are explored, and the potential health effects of microplastics exposure are outlined. This review will contribute to the understanding of the health hazards of airborne microplastics and provide a strong basis for the development of laws and regulations related to plastic products in the environment.
Results
Human Microplastics Exposure Through Different Routes
Plastic products bring great convenience to our life, and they also lead to the emergence of plastic waste and pollution. Not properly treated plastic waste will gradually decompose into plastic particles under environmental or human factors. These microplastics will enter into the human body through different ways and cause exposure risks to human health (Fig. 1).
Human Microplastics Exposure Through Dietary Route
Microplastics in Salt and Human Intake
Numerous studies have detected microplastics in table salt extracted from oceans, lake, well, and rock salts in various countries around the world. Salt is an essential food for humans every day. In 2018, global salt consumption reached 300 Mt, of which 11.6% was used for salt and food processing. In sea salt, PET was the most common microplastics, followed by PE and ST. Fragments smaller than 200 µm and fibrous microplastics accounted for 55% of the total microplastics. In lake and well salts, ST is the most common microplastics. ST is an organic cellulose-based polymer that is often used as a release agent in food and cigarette packaging and utilized in the manufacture of fiberglass and rubber products. In general, lake, rock, and well salts have low contamination levels of microplastics compared with sea salt. This condition may be closely related to the local population density and economic development level.
The World Health Organization (WHO) estimates that adults consume approximately 9–12 g of salt per day. Water evaporates during salt crystallization, but microplastics are not removed and remain enriched and retained in the salt body. Salt serves as an important carrier of microplastics intake in humans, and microplastics can be internal and cause health risks during people’s daily salt intake. Based on the data collected from 11 representative papers (Table 1), an adult can ingest about (5.00–7.00) × 103 microplastics from salt in a year.
Microplastics in Aquatic Products and Human Intake
Microplastics in the aquatic environment can be transferred from the environment to the organism and subsequently enter the food web and eventually enrich in the human body. Microplastics have been found in many edible shellfish (mussels, oysters, clams, field snails, and scallops [2, 3, 52, 81,82,83], commercial fish [84], mollusks, and even mammals. PET, PP, PA, PE, and nylon are the main components of microplastics detected in commercial fish, with fibers being the predominant form. By contrast, shellfish (bivalves) are mainly PP, PE, PS, and PET [81]. The reason for the higher percentage of microplastics in the fibrous form in commercial fish species may be that fishing nets are mainly made of synthetic or natural fibers. On the contrary, shellfish culture often uses filter feeding, which leads to its microplastic content in the form of films and fragments. In general, the abundance of microplastics is higher in commercial fish than in shellfish. The reason may be the influence of wider dietary choices and higher nutritional levels in fish, which leads to a higher intake of microplastics in carnivorous and omnivorous fish.
Some research statistics claim that each person consumes about 2.4–4.8 kg of mollusks and 7.3–13.7 kg of lean meat or fish aquatic products per year. Based on the data collected in 18 representative papers (Table 1), an adult can consume approximately (0.50–1.20) × 104 microplastics a year from aquatic products.
Microplastics in Crops and Human Intake
At least 473,000 t of plastic waste is estimated to be released into the soil each year in European Union countries [12]. The presence of microplastics was detected in terrestrial ecosystems such as agricultural fields and river floodplains. Microplastics in soil can be heavily absorbed and enriched by plant roots through processes such as adhesion and uptake. They can migrate upward from the roots and accumulate in the stems and leaves that can be directly consumed. Microplastics can accumulate in crops such as arabidopsis, lettuce, wheat [85], and rice [86]. Studies comparing the number and size of microplastics in fruits and vegetables (carrots, lettuce, broccoli, potatoes, apples, and pears) found that apples were the most contaminated fruit samples, while carrots were the most contaminated vegetables [80••].
Standardized procedures for collecting, fractionating, characterizing, and quantifying polymer particles need to be established due to the inadequacy of current detection methods and instruments. Relatively few studies are available on measuring microplastics content in agricultural crops (fruits and vegetables); currently, only one article reports the daily intake of microplastics from fruits of approximately 4.48–4.62 × 105 and from vegetables of 2.96–9.55 × 104 for adults [80••] (Table 1).
Human Microplastics Exposure Through Drinking Water Route
Surface freshwater (including rivers, lakes, and reservoir water) and groundwater are the main raw materials for drinking water. Microplastics in surface water mainly originate from washing and bathing wastewater produced in human production and life [87, 88•], followed by direct degradation of plastic products in the environment, wear and tear of plastic products, and deposition of microplastics in the atmosphere. Microplastics in groundwater mainly come from contaminated soil leachate and direct injection from surface loss streams. Microplastics contamination in drinking water is more dangerous than other pathways (e.g., fish and seafood) because the amount of water consumed daily by humans far exceeds the amount consumed by fish and seafood.
Since the first detection of microplastics in tap water by Kosuth et al. in 2018 [69, 89], a large number of studies have successively reported the presence of microplastics in bottled water and beverages, beer [68, 90], tea [68, 90], and functional drinks [68]. The main reason for the higher levels of microplastics in bottled water and beverages than in tap water is the presence of plastic products in the production, processing, and packaging of bottled water and the wear and tear of production equipment, which makes the sources of microplastics contaminant in bottled water more widespread. Fragments are the most common particulate form in bottled water (65%). PP and PET are the most common types of polymers in bottled water, both of which may come from common plastics used in the manufacture of caps and bottles. Different packaging materials have different microplastics contamination in bottled water [89]. Schymanski’s team used micro-Raman spectroscopy to compare drinking water in plastic bottles, glass bottles, and beverage cartons. They found that the microplastics content in glass bottles was lower than that in plastic bottles, and disposable plastic bottles and cartons of beverages had lower microplastics content than recyclable plastic bottles. The repeated use of these plastic products increases the wear and tear of the packaging material and produces more particles of microplastics.
The amount of water consumed by an adult varies according to gender, climate, diet, and physical activity and the WHO guideline value of 2 L per day for an adult (default weight of 60 kg). Based on the data collected from 8 representative papers (Table 1), an adult can consume approximately (0.22–1.20) × 106 microplastics through drinking water routes in a year.
Human Microplastics Exposure Through Air Inhalation Route
Microplastics, as a new type of atmospheric environmental pollutant, are nearly everywhere. The sources and distribution of microplastics in the air have their own characteristics indoors and outdoors. Among them, indoor microplastics are mainly derived from synthetic textiles [5], air conditioning filter [6, 7], and indoor dust, and their main components are PP, PE, and PET [70, 71, 78]. Outdoor microplastics are mainly derived from tire wear [8], road marking coatings, asphalt on the road [9], and street dust [10], and their main components are PET and PE [2, 3, 70, 75••, 76, 78]. The main forms of indoor and outdoor microplastics are not only fibers (95%) [5] but also debris (4%) and foam and film (less than 1%). The reason why fibers account for such a large proportion may be due to the good mechanical properties, wear resistance, and chemical stability of fibers, which are widely used in various industries around the world.
The concentration of microplastics in indoor air is much higher than that in the outdoors [71]. The reason is that outdoor air has more circulation than indoor air, which is conducive to the diffusion of pollutants. Meanwhile, microplastics in indoor air are more widely available than in outdoor sources. Under different indoor environmental conditions, the abundance of microplastics in the air is also different. For example, nail salons have a concentration of microplastics in indoor air (46 ± 55 microplastics/m3) 1.6 times that in outdoor air (28 ± 24 microplastics/m3) [6, 7]. The reason is that the materials used in nail art involve more microplastics. Another example is that the concentration of microplastics in the air of rooms with clothes dryers in the home (1.6 ± 1.8 blue fibers/m3) is higher than that in rooms without dryers (0.17 ± 0.27 blue fibers/m3). This condition may be due to the fact that synthetic textiles themselves are the source of microplastics on the one hand, and the heating and ventilation function of the dryer accelerates the spread of microplastics on the other hand.
The main ways for microplastics in the atmosphere to enter the human body are respiratory inhalation. According to statistics, adults consume around 10–20 m3 of air per day. According to relevant literature, people spend nearly 87% of the day indoors and only 13% outdoors. Based on the data collected in 9 representative papers, the amount of microplastics exposed by inhalation per person per year was about (0.21–2.51) × 106 microplastics/year, including about (0.16–2.30) × 106 microplastics inhaled indoors and (0.46–2.10) × 105 microplastics inhaled outdoors (Table 1).
Accumulation of Microplastics in the Human Body
The human body ingests microplastics from the environment on a daily basis through atmospheric inhalation, diet, drinking water, and skin contact. Microplastics smaller than 10 µm can cross cell membranes, enter the human circulatory system, and diffuse and transfer through various organs and tissues in the human body by adsorption, migration, and transformation. Table 2 summarizes the current studies related to the size, category, content, and abundance of microplastics in various tissues that have been detected in different countries, regions, and populations. In two recent studies, PP, PET, and PS were found to be the top three most abundant microplastics detected in feces, and their detected sizes were also broadly similar, which were mainly in the range of 20–800 µm [21, 22•, 23]. PP, which is the most abundant microplastics in food, is mainly used for food packaging. PET is commonly used for the packaging of daily necessities and containers for drinking water. PS is commonly used for manufacturing building materials, toys, and stationery. Since people are exposed to more of these three plastics on a daily basis, it is not surprising that they are found in the highest amounts in human feces. However, a study by the team of Wibowo in 2021 found the highest levels of HDPE microplastics in stool samples [20], and the main reason for this difference was the high concentration of HDPE in the toothpaste used by the subjects. Therefore, human intake of microplastics from toothpaste may also be an important source of microplastics contamination in the body.
Zhang’s team found significantly higher concentrations of PET in infants’ feces than in adults, and PET is often made into polyester, which is one of the main raw materials for clothing and carpets [22•, 23]. Therefore, the team believed that the main reason for the difference may be that infants crawl on carpets, chew, and suck on fabrics frequently,thus, they are more likely to be exposed to PET microplastics than adults. Moreover, the detection of microplastics in breast milk suggests that breast milk may be another important source of microplastics in newborns [30]. Previously, Ragusa et al. first detected PP microplastics of 5–10 µm size in the human placenta [28], while Braun et al. detected microplastics of larger particle size (50–500 µm) and higher diversity (PP, PET, and PS) in the placenta [27]. In fact, Grafmueller et al. in 2015 already demonstrated the ability of polystyrene nanoparticles to cross the placental barrier through an ex vivo human placenta perfusion model. Therefore, microplastics in infants and children may be transferred from the mother to her body through the placenta in addition to their uptake in the external environment and breast milk after birth. By contrast, an Iranian study examined and compared microplastics in the placenta of normal and intrauterine growth retardation (IUGR) pregnancies and found significantly higher levels of microplastics in the placenta of IUGR pregnancies than in the normal group. The team also measured and calculated the relationship between various indicators of the newborn fetus (weight, length, head circumference, and 1 min Apgar score) and the abundance of microplastics in the placenta [26]. They found a significant negative correlation between all indicators and the abundance of microplastics. The results of this study suggest that maternal microplastics are likely to pass through the placenta to the fetus and have toxic effects on the fetus.
Air inhalation is another important route of environmental microplastics entering the human body. Thus, the lungs are an important site for airborne microplastics accumulation. In 1998, Pauly et al. first detected the presence of microplastics in human lung tissues. Subsequent studies further detected microplastics of different sizes (1.60–5.56 µm) and categories (PP, PET, and PS) with different contents (31 and 39 microplastics) in human lung tissues [2, 3]. Given that the lungs are an organ for gas exchange with the outside, they are easily affected by the surrounding environment and people’s lifestyles [91, 92•]. Jiang et al. showed a higher abundance of microplastics in sputum and nasal lavage fluid of office staff than that of couriers. Moreover, sputum and nasal lavage fluid of office staff measured more PVC (used in the production of building materials and furniture), while couriers were detected with higher concentrations of PE (used in the production of masks) and PA (courier packaging) in the case of the COVID-19 pandemic.
A recent study first confirmed the presence of microplastics, including PP, PET, and PS, in the human blood [24]. This study provides strong evidence that microplastics can be transferred to the human body through blood circulation. The discovery of microplastics in human blood clots indicates that the impact of microplastics exposure on human health should not be underestimated. The study showed that microplastics detected in blood clots were larger, which may be caused by the aggregation of small particles in the body and the formation of large particles [31, 32]. Abbasi et al. also found the presence of microplastics in human saliva, skin, and hair. PP and PET were the most abundant, and hair had the most presence and saliva had the least [25]. Thomas et al. also found the presence of microplastics in the liver, spleen, and kidney. This study provides evidence for the aggregation of microplastics in peripheral organs through blood circulation [18•].
So far, the presence of different types and abundance of microplastics has been found in the human feces, colon, lung, placenta, breast milk, blood, liver, spleen, kidney, hand, and face skin in many places (Fig. 2), among which PP, PE, PVC, and PS are the most abundant, and these plastics are the types that humans are frequently exposed to in daily life. When microplastics in the environment enter the body through different pathways, they may reach peripheral organs through blood transport and other means. The particle size of microplastics detected in the placenta, breast milk, lungs, and other places is relatively small, while the particle size in the colon and feces is larger. We speculate that smaller particles are easily absorbed or transferred through the human body, while larger particles are more likely to accumulate and be expelled through the human body. In summary, the results of this part of the study show that environmental microplastics will accumulate in multiple organ tissues after entering the human body through different ways. This phenomenon not only threatens the body’s health but also causes certain effects on the newborn, which deserves extensive attention.
Potential Health Risks and Mechanisms of Microplastics Exposure
The increasing pollution of microplastics poses huge potential risks to human health. After entering the human body through the respiratory tract and digestive tract, microplastics can damage various barriers, induce oxidative stress, regulate gene expression, and eventually lead to functional impairment of corresponding organs and systems, which seriously endangers health.
Nervous System Function Impairment
Small-size microplastics can penetrate the blood–brain barrier, which leads to increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels and significantly lowered glutathione (GSH) levels. Therefore, microplastics can induce oxidative stress in mouse brain tissue, reduce acetylcholine levels, and affect learning and memory function in mice [94]. Microplastics exposure also reduce the expression of blood–brain barrier (BBB) connexin, stimulates reactive oxygen species production to induce nerve cell apoptosis, and promotes microthrombosis; these phenomena reduce the number of Purkinje cells [95], which leads to neurological dysfunction (Fig. 3A).
Pulmonary Inflammatory Response and Functional Impairment
Studies have found that microplastics that enter the body through respiration after exposure can enter the deep alveoli. Long-term exposure to microplastics in the air may lead to lung damage, altered lung morphology, protective lung barrier damage, inflammatory response, and functional damage [96]. The results of lung examination of workers exposed to high concentrations of microplastic factories showed that the incidence of chronic interstitial pneumonia among workers was significantly increased [97], and it was accompanied by pulmonary hair glass nodule phenomenon [6, 7]. Microplastics that enter the human body through the respiratory tract will enter the respiratory epithelial cells through various ways. This condition will induce phosphorylation and related protein expression reduction through oxidative stress, which destroys the tight connection between lung cells. Ultimately, lung barrier function damage occurs [98].
Microplastics disruption of protective lung barrier function increases the risk of lung disease and easily induces inflammatory responses and functional impairment. Previous results have shown that cellular inflammatory infiltration induced pneumonia in the lungs of mice exposed to high concentrations of microplastics, macrophage aggregation in bronchi and alveoli, and increased mucus production with asthma symptoms [99]. At the same time, microplastics can induce the formation of reactive oxygen species, cause cytotoxic and inflammatory effects, and trigger the corresponding apoptotic pathway by inducing the expression of pro-inflammatory cytokines and proapoptotic proteins [100]; ultimately, the normal function of the lungs is affected (Fig. 3B).
Hepatic Fibrosis and Metabolic Disorders
The liver, as the largest gland in the human body, has extremely complex functions and plays an important role in maintaining the body’s health. The liver is the most active metabolic organ of the body. It is involved in the synthesis, transformation, and decomposition of proteins, lipids, sugars, and other substances. When the microplastics invade the liver through blood circulation, it will cause impaired liver function, induce the damage and release of DNA in the nucleus and mitochondria, activate the corresponding pathway, promote the expression of pro-inflammatory cytokines, and enhance liver fibrosis [101, 102] (Fig. 3C).
The aggregation of microplastics in liver tissues can inhibit the accumulation of fatty acids, fatty acid methyl esters, and fatty acid ethyl esters in the liver. This condition destroys the normal lipid metabolism, which causes hepatic steatosis [103, 104]. In addition to the abnormal lipid metabolism, some studies have reported that exposure to microplastics in the environment can affect the fatty acid metabolism, amino acid metabolism, and carbon metabolism in the zebrafish liver. Therefore, microplastics exposure can induce hepatic glucose and lipid metabolism disorders [102]. At the same time, microplastics can absorb more toxic and harmful substances than their large surface area, such as heavy metal cadmium [105•]). Microplastics have been reported to induce liver iron death caused by heavy metal poisoning [106].
Ecological Imbalance and Metabolic Disorder of Intestinal Flora
The intestine, including the large and small intestines, is an important part of digestion and absorption, and it is also immune competent (lymph nodes). Microplastics that enter the body through feeding and respiration can gather in the intestine, larger microplastics can be excreted with metabolites, and smaller microplastics can enter the system and tissues through the active uptake and phagocytosis of intestinal epithelial cells. The microplastics in the gut can lead to intestinal microbial community imbalance, intestinal barrier dysfunction, and metabolic disorders.
Gut flora can regulate intestinal peristalsis and digestive juice secretion and participate in the nutrient digestion and absorption of the body and is the health guard of the body [107]. Intake of high concentrations of microplastics can affect the balance of intestinal flora. It can change the species and number of intestinal microorganisms, which results in altered bacterial abundance and flora diversity due to the imbalance of intestinal flora [108, 109]. This condition causes the release of some toxic bacterial products, which causes inflammation. As a result, the immune system is affected, which leads to the body’s increased susceptibility to pathological infections or chronic diseases, as well as intestinal nutrient metabolism disorders [110]. After exposure to microplastics by feeding methods, the abundance of Staphylococcus in the gut increases significantly, while the abundance of Parabacteroides is significantly decreased. This variation changes the special physiological function that the gut is supposed to have, which potentially leads to related diseases. Microplastics exposure also reduce mouse intestinal mucus secretion, induces oxidative stress, causes epithelial cell apoptosis, increases intestinal permeability, and leads to intestinal barrier damage [111, 112] (Fig. 3D).
Significant Impairment of Renal Function
The kidney is one of the important target organs of microplastics aggregation. Its exposure can cause significant damage to kidney function in mice [113, 114]. The main mechanism is through the induced oxidative stress [115], which causes an inflammatory response and tissue damage. When microplastics enter the body and are absorbed by kidney cells, they can lead to mitochondrial ROS production and the expression of associated proteins [116]. Meanwhile, they can increase the expression of genes related to ER oxidative stress and inflammatory response in kidney cells. Regulation of related signaling pathways through gene expression affects renal cell ER stress, cellular inflammation, and autophagy pathways, which leads to kidney injury [51, 117] (Fig. 3E).
Reproductive Capacity Impairment
The accumulation of microplastics in the reproductive organs can lead to reproductive toxicity and affect the reproductive capacity. Microplastics can induce testicular inflammation, destroy the testicular blood barrier [84], activate the NF-kB signaling pathway and the p38 MAPK signaling pathway, and induce inflammation to cause testicular sperm abnormalities. These phenomena lead to a significant decrease in sperm number and motility and a significant increase in sperm malformation rate [118, 119]. At the same time, microplastics can also induce ovarian inflammation, reduce the first pole body extrusion rate and superovulation survival rate [86], and decrease the quality of oocytes in female mice. Microplastics induce apoptosis of ovarian granulosa cell and uterine pyroptosis and fibrosis through oxidative stress [31, 35, 118,119,120], which lead to infertility in female mice (Fig. 3F).
In brief, microplastics exposure is known to cause metabolic disorders in the liver, pulmonary inflammatory response, and significant impairment of renal function and affect the nervous and reproductive systems. At the same time, they will also cause intestinal flora disorders, seriously affect immunity and digestion, and lead to great hidden dangers to the body. All these considerations remind human beings to pay attention to environmental protection, curb microplastics pollution, and protect life and health.
Summary and Outlook
The large number of microplastics detected in the aqueous environment has encouraged most of the current research to focus on the detection of the type and abundance of microplastics in the aqueous environment. However, the results of this study found that the abundance and variety of microplastics absorbed by humans through atmospheric environments may be larger than those in water and soil environments. Microplastics absorbed by the human body through the atmospheric environment also enter the body directly without any processing (e.g., drinking water may be filtered and food may be cooked) and may therefore cause a greater health risk. Microplastics in the atmosphere are smaller in size, are more penetrating when absorbed by humans, have a larger specific surface area, are more likely to adsorb toxic organic compounds and heavy metals, and can be directly and continuously exposed to humans compared with those in marine and soil environments. As a result, airborne microplastics pose a greater potential risk to human health. However, a gap still exists in the research on modeling exposure to microplastics in the “real atmosphere.” Therefore, more attention should be paid to the health risks posed by microplastics in the atmosphere. However, no standardized procedure is available for the collection and analysis of microplastics. Therefore, standardizing the collection of microplastics in the environment is still impossible. Microplastics smaller than 5 µm cannot be detected by current detection methods, but the abundance of microplastics in the air tends to increase with the decrease in particle size. Therefore, new technologies that can detect smaller particle sizes and a wider range of microplastics need to be developed.
To date, microplastics have been detected in more than 10 organs and tissues in the human body. However, a gap still exists in the detection of important parts of the body such as the heart, brain, and spinal cord. Researchers should minimize the use of plastic products during sampling and testing to reduce possible cross-contamination issues. Current studies on the health effect of microplastics exposure are still limited to high concentrations, single species, single particle size, and acute exposure conditions. The uptake and accumulation of microplastics in the real environment are a complex, long-term, chronic process. Therefore, researchers need to pay more attention to the potential health risk of microplastics exposure under real environmental conditions. The long-term lasting effects of microplastics exposure and the impact on their offspring should be comprehensively explored as well. Researchers can also draw from epidemiological and occupational studies to understand the current potential health risks regarding microplastics. The complexity of environmental conditions is that environmental pollutants can often act in concert with other pollutants to expose humans. Thus, research should focus more on the synergistic and antagonistic effects of pollutants.
This study explores the exposure of microplastics in the human body under different routes, investigates the distribution characteristics of microplastics in different parts of the human body, and summarizes the current analysis on microplastics exposure, target effector organs, and potential health risk assessment. The results show that air inhalation is the most common mode of microplastics intake in humans compared with dietary and drinking routes. Reviewing the detection of microplastics in different parts of the human body and analyzing the adverse effects of microplastics exposure on liver fibrosis and metabolic disorders, significant impairment of kidney function, inflammatory response and functional impairment of the lung, ecological imbalance and metabolic disorders of intestinal flora, reproduction, and neurological impairment can arouse public attention and encourage people to reduce the use of single-use plastic products. In conclusion, exposure to microplastics in the environment will cause many adverse effects on body health. Thus, raising people’s awareness of the crisis, urgent discussion, and practical actions are necessary to reduce microplastics pollution in the environment.
Data Availability
The data that support the findings of this study are available from the corresponding author upon reasonable request.
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We thank all the members in our lab for their great assistance with this study.
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This work was supported by the National Key Research and Development Program of China (grant numbers: 2022YFF1202900), the National Natural Science Foundation of China (grant numbers: 31771100 and 32000815), and the key technologies R & D program of Tianjin (21JCZDJC00580).
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Under the supervision of Liqun Chen and Can Wang, Ziye Yang, Zhihong Feng, and Meixue Wang conducted article search, information analysis, and article writing. Ziqi Wang sorted out the information and wrote part of the content. Mingxia Lv cooperatively collected information and compiled some table contents. Jinghao Chang supplemented and revised the details of the article. All authors read and contributed to the manuscript.
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Yang, Z., Wang, M., Feng, Z. et al. Human Microplastics Exposure and Potential Health Risks to Target Organs by Different Routes: A Review. Curr Pollution Rep 9, 468–485 (2023). https://doi.org/10.1007/s40726-023-00273-8
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DOI: https://doi.org/10.1007/s40726-023-00273-8