Open access peer-reviewed chapter

The Toxicity of Plastics

Written By

Edda E. Guareschi

Submitted: 28 June 2023 Reviewed: 29 June 2023 Published: 25 July 2023

DOI: 10.5772/intechopen.1002272

From the Edited Volume

Trace Metals in the Environment

Daisy Joseph

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Abstract

According to more than 200 scholarly publications, plastic pollution has been emerging as a major environmental concern in recent decades, and has been posing a relevant threat to ecosystems and global health. While the focus has primarily been on the physical, chemical and biological impacts of primary and secondary plastics, also for their ability to cross biological barriers within the human body, an additional hazard is represented by their association to heavy metals, used as additives. Metals are, in fact, added to plastics for their stabilizing actions. The examples of metal toxicity here reported are Antimony (Sb), Arsenic (As), Barium (Ba), Beryllium (Be), Cadmium (Cd), Chromium (Cr), Cobalt (Co), Copper (Cu), Iron (Fe), Lead (Pb), Manganese (Mn), Nickel (Ni), Selenium (Se), Vanadium (V) and Zinc (Zn). This chapter explores the toxicity of metals associated with plastic pollution in the environment, illustrating their potential consequences for the global ecological system, with prevalent focus on human health. The interdisciplinary approach, which includes environmental science, chemistry and toxicology, aims to enhance the understanding of this complex issue and highlight the urgent need for efficient mitigation strategies.

Keywords

  • environment
  • heavy metals
  • human health
  • nanoplastics
  • plastic pollution

1. Introduction

Plastics are synthetic organic polymers that are produced by the polymerization of monomers extracted from oil or gas [e.g., Polyvinylchloride (PVC)]. Additives are added to plastics to achieve desirable commercial properties, for example mechanical resistance. Examples of additives are antioxidants, flame retardants and ultraviolet (UV) stabilizers [1], which include heavy metals, that is, chemical elements characterized by atomic number > 20, density > 5 g cm−3 and toxicity at low concentrations [2, 3, 4, 5, 6]. Plastics are classified as primary, when they are manufactured products, or secondary, when they result from the breakdown and degradation of the manufactured products. Beside the shapes of whole manufactured objects, the shapes of plastics include fibers, beads (also known as “nurdles”), pellets, foam, agglomerates, films and irregular fragments. The size of plastics varies from bigger than 50 cm (megaplastics) to nanoplastics, that is, smaller than 0.1 μm, passing through macroplastics (between 5 and 50 cm), mesoplastics (between 0.5 and 5 cm) and microplastics (smaller than 5 mm). The mass production of plastics began in the 1940s, and until 2017 an estimated 9 billion tons of plastic had been produced [7], with 710 million metric tons of plastic waste expected to enter the natural environment by 2040 [8]. As of 2015, only 9% of the plastic waste was recycled, 12% was incinerated and 79% went to landfills or were spread out in the environment [7]. The aim of this chapter was to characterize the pollution caused by plastics and their toxicity on the human organism, with a special focus on metal additives.

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2. Environmental impact of plastic pollution

In the environment, plastics are degraded by physical, chemical and biological agents, such as abrasion, thermal action, oxidization of the polymer matrix by UV radiation (photodegradation), hydrolysis and biodegradation, that is, the degradation of starch into the products made of the so-called biodegradable plastics. Plastic debris is then transported and dispersed in aquatic environments [9], sediment [10], soil [11] and air [12]. Notably, the aging of plastics increases their ability to sorb chemicals and leads to free radical formation by the dissociation of the C-H bonds [13]. Once fragmented, plastics and their associated additives can be incorporated by living organisms (biota), including plants [14], and exert their toxic effects through cumulative exposure [15]. The uptake by biota occurs through cracks at the emerging sites of new lateral roots in plants, from where plastics move up the xylem and reach the edible part, or by inhalation, ingestion and skin contact [16, 17]. In humans, who are estimated to ingest 0.10–5 g of plastics every week and inhale 26–130 airborne plastics every day, plastics can either be retained by tissues and organs, or cross epithelia (e.g., respiratory) [18] and the underlying endothelia of capillary vessels [19], reaching the pulmonary and/or the systemic blood circulation [20]. The consequence is bioaccumulation of plastics, with higher values in occupational exposures. Finally, a link between Coronavirus disease 2019 (COVID-19) and plastic particles is being investigated, both in terms of pollution increase (e.g., disposable face masks) [21] and of the potential role of airborne particles as viral carriers [22].

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3. The toxicity of plastics

In nonhuman organisms, e.g., mice, polystyrene particles can modify the gastrointestinal microbiome and cause hepatic lipid disorder [23], or can be retained in the hippocampal brain region of embryos, increasing the risk of neurodevelopmental defects [24]. The number of oocytes and the sperm velocity in oysters decrease with the exposition to polystyrene particles, while other marine organisms, such as crabs, clams and worms, slow down their feeding activity [25]. In fish (Daphnia magna), nanoplastics can accumulate in brain tissues, causing behavioral disorders [26]. Hitherto, the physiology of more than 200 nonhuman species has shown some form of disruption when exposed to plastic particles [27]. In humans, plastic particles smaller than 20 μm in size can penetrate biological membranes, such as the blood-brain barrier, the placenta and the gut epithelium [28], and accumulate in tissues, while nanoplastics can penetrate within cells through multiple mechanisms, e.g., phagocytosis [29]. The plastics uptake, estimated as 0.1–5.0 g/week by ingestion and 26–130 particles/day by inhalation [17, 30, 31], is influenced by distinct factors, including but not limited to surface charge, hydrophobicity and the presence of a protein corona [1]. Other influencing factors are comorbidities and socioeconomic, through the increase in the permeability of the gastrointestinal epithelia in inflammatory bowel diseases (e.g., Chron, Ulcerative Colitis), diet, excessive alcohol intake, occupational exposure (e.g., synthetic textile mill workers) and the use of low-quality cosmetics with added microbeads [32].

The human health risks associated with plastic particles and their metal additives have not been completely characterized; however, multiple and diversified correlations are under continuous investigation. Examples are oxidative stress and cytotoxicity, chronic inflammation (e.g., foreign body reaction, bronchitis and interstitial pneumonitis) [17], metabolic alterations favoring obesity [16], disruption of the immune system with diabetes mellitus mediated by insulin resistance [33], beside the scarce response to infections (COVID-19 in highly polluted areas) [34], neurotoxicity due to nanoplastics crossing the blood-brain barrier and affecting neurotransmission [35], gastrointestinal dysbiosis linked to the disruption of epithelial permeability [36, 37], occlusion of capillaries, whose diameter is typically 5–8 μm [38], toxicity of the endocrine system by estrogenic activity with early puberty, breast and prostate cancer [39], decreased reproductive function supported by the crossing of the placental barrier by nanoplastics smaller than 240 nm, which can promote preeclampsia, fetal anomalies and birth defects [40], carcinogenesis [41] through chronic inflammation and DNA damage, with the altering of gene expression, induction of angiogenesis and mitogenesis favoring the formation and progression of malignant cells, transport of chemicals [e.g., bisphenol A, heavy metals] [42, 43] and microorganisms (e.g., Vibrio spp.) [44].

Many heavy metals are used as plastic additives [4] and pose the threat of a vast array of toxic effects on biota [45, 46]. Specifically, Antimony (Sb) oxide is used as a fire-retardant, while trisulfide is a component of pigments. Since the exposure levels of the general human population are low, toxic respiratory and cardiovascular effects originate by occupational exposure or treatment of the parasitic infections by Schistosoma spp. and Leishmania spp. [47]. The toxicity of Arsenic (As) is linked to the impairment of cellular respiration, with severe gastroenteritis as the most common acute symptom, and anemia and neuropathy in the chronic course [48]. Barium, used in a variety of industries (e.g., mining) and as a rodenticide, leads to severe hypokalemia through a complex transcellular mechanism and can progress to respiratory paralysis and cardiac arrhythmia [49]. Beryllium (Be) can cause acute pneumonitis by inhalation, although a chronic pulmonary granulomatous disease (berylliosis) is much more common, and is caused by a hypersensitivity reaction in occupational exposures [50]. Pneumonitis is also caused by Cadmium (Cd) exposure, with renal damage and cancer [51], a known toxic effect of Chromium (Cr), as well, through several molecular actions, including DNA double-strand breaks and heavy DNA adducts difficult to repair [52]. Cobalt (Co), on the other hand, holds a biologically necessary role as a cofactor of cyanocobalamin (vitamin B12), and overexposure can follow excessive nutritional supplementation. Other routes of chronic toxicity include occupational exposure or the presence of orthopedic implants (e.g., hip prostheses). The main toxic effect of Cobalt is represented by pulmonary interstitial fibrosis and cardiomyopathy [53].

Another essential element in the human physiological homeostasis is Copper (Cu), which acts as a catalytic cofactor in the redox chemistry of many proteins. The ingestion of more than 1 g of Copper, commonly used in farming as a pesticide, is toxic, with gastrointestinal, neurological and hematological adverse effects induced by oxidative stress, DNA damage and reduced cell proliferation [54]. Iron (Fe), Manganese (Mn), Nickel (Ni), Selenium (Se) and Zinc (Zn) are also essential micronutrients for humans, although overloads can result in acute or chronic toxicity. The Iron balance, which maintains the total content of the human body between 3.5 g and 5 g, relies on elaborate regulatory metabolic processes aimed to minimize the systemic effects of cell death, due to the generation of free radicals. The most common diseases linked to acute or chronic iron poisoning are gastrointestinal, cardiovascular and neurodegenerative [55]. The central nervous system is the main target of Manganese (Mn) toxicity. In fact, Manganese crosses the blood-brain barrier, the cerebrospinal fluid barrier and the olfactory nerve microstructures, accumulates in specific brain regions and causes a progressive disorder of the extrapyramidal system, known as manganism [56]. Even though the functional role of Nickel in higher organisms, such as humans, is currently being researched, it has been recognized as an essential nutrient for some plants and nonhuman species. The most known adverse effect of exposure to Nickel is contact dermatitis, a type of allergy, although prolonged exposure can result in pulmonary fibrosis and kidney diseases through mitochondrial damage [57]. The acute intoxication by Selenium (Se), a component of blueing agents, is very rare and presents with nausea and abdominal symptoms, such as vomiting, diarrhea and pain, which can progress to fatal cardiac arrythmias [58] through dehydration and related electrolyte imbalances. Chronic intoxication is much more common, usually due to environmental exposure (e.g., drinking water), and induces neurotoxicity through multiple mechanisms of molecular concentration, uptake and activity [59]. Gastrointestinal and neurological symptoms also occur with an extremely high intake of Zinc (Zn), otherwise considered to be relatively nontoxic [60]. Finally, Lead (Pb) and Vanadium (V), added to plastics for their stabilizing, hardening and pigment properties, hold no evident biological role, and exert their toxic actions through neuropsychiatric symptoms, anemia [61], hepatocyte degeneration and renal failure by glomerulonephritis [62].

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4. Current analytical techniques for the detection of plastic particles and additives

The identification of plastic particles carrying metal additives in different substrates, such as water, soil and air, follows sampling with filters, mesh and sieves, which can be selective, bulk or volume-reduced depending on the research purposes, then preprocessing and extraction. After sampling, pretreatment methods commonly used include filtration, screening and density separation. Digestion by acid, alkaline or enzyme-based substances is primarily used for the pretreatment of biological samples, such as human blood [20], placenta [40] and colon [36]. Visual methods by microscopy [scanning electron (SEM), transmission electron (TEM), with the possibility of a specific configuration for nanosizes, fluorescence microscopy with stimulated emission depletion (STED)], spectrometry methods [Raman, Fourier transform infrared spectroscopy-attenuated total reflection (FTIR ATR), X-ray photoelectron spectroscopy (XPS), atomic force microscopy-infrared spectroscopy (AFM-IR, nanoIR energy-dispersive X-ray spectroscopy)] and thermal analysis by pyrolysis gas chromatography/mass spectrometry (Pyr-GC/MS) complete the identification and the quantification, including the chemical/elemental analysis [63, 64, 65, 66, 67]. The characterization of nanoplastics was unavailable until very recently [68], but has been actively researched with encouraging results, in spite of relevant challenges and limitations, such as low or no crystallinity and the ubiquitous distribution of the incorporated elements (C, H, N, O) [69, 70].

Since 2020, plastic particles have been identified in several human biological matrices, tissues and organs [71]. In fact, they were detected in cell cultures of human gastric adenocarcinoma [72], in colectomy specimens (331 particles per individual, or 28.1 +/− 15.4 particles per gram of tissue) [36], placenta, both on the maternal and fetal sides (with sizes smaller than 10 μm) [20], stool (a median of 20 microplastics, 50 to 500 μm in size per 10 g or 10.19 micrograms/gram (mcg/g) in another study) [73, 74, 75], lung tissue (with size smaller than 16.8 μm) [18], whole blood (with mean of the sum concentrations 1.6 μg total plastic particles/ml blood sample and size limited to 700 nm) and urine (4–15 μm size) [76]. A direct evidence of human health risk linked to the incorporation of plastic particles has not been demonstrated [77]; however, it is highly likely that chronic exposure to both the physical particles and the associated additives, including metals, will eventually cause widespread diseases, even on account of the expected global increase in plastic production related to the increase in global population.

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5. Plastic pollution mitigating strategies

Strategies are urgently needed to mitigate the impact of plastics on the environment and, as a consequence, on the global health. The prevention and the reduction of plastic pollution can be achieved by supporting research toward sustainable plastic removal methods, by implementing policies and regulatory measures and by promoting recycling and waste management practices, although not free from potential contamination hazard [78]. Plastic waste might be removed physically or by physicochemical and biological methods [3], converted into hydrogen [79], recycled [80] or biodegraded by microorganisms like bacteria, algae and fungi [81, 82, 83]. The toxicity of plastics, as particles and as carriers of toxic chemicals and microorganisms, will soon embody an urgent concern, and as such should be addressed [84]. Future research on the effect of plastics particles and their additives on the human health should consider retrospective or prospective observational population studies based on samples of biological matrices, such as bronchoalveolar fluid lavages and tissues obtained from biopsies and autopsies. Methods and methodologies need standardization, and a unified quantitative analytical technique needs to be established. Furthermore, the collaboration of various institutional sectors, such as academia, industry, regulators, environmental associations and policy, is critical. Until the complex issue of plastics pollution will be efficiently dealt with, thresholds of acceptable exposure for humans need to be determined and publicized, for example, as concentrations of milligrams per gram (mg/g) of body weight.

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6. Key points

  • The global plastic pollution has been continuously increasing in the recent decades, and it has become a serious health concern for the whole Earth ecosystem.

  • Plastic particles exert their toxicity physically and by carrying, absorbing and releasing toxic chemicals and microorganisms.

  • Heavy metals, here exemplified by arsenic, cadmium, lead, and several more, are commonly used as additives to plastics.

  • The chronic exposure to plastic particles, and their associated additives including metals, holds the potential to cause widespread diseases.

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Acknowledgments

The author wishes to thank the Royal Society of Western Australia (RSWA) in Perth (WA, Australia), the Harry Butler Institute, Dr. Paola A. Magni and James Mettam at Murdoch University (Murdoch, WA, Australia) and Prof. Ian R. Dadour with Source Certain (Wangara, WA, Australia) for the intellectual support in the achievement of this short overview.

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Conflict of interest

The author declares no conflict of interest.

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Written By

Edda E. Guareschi

Submitted: 28 June 2023 Reviewed: 29 June 2023 Published: 25 July 2023