Assessing the Risks that Microand Nanoplastics Pose to Human Health
Leaching of Toxic Chemicals from Plastics
As discussed previously, plastics can contain complex mixtures of additives to enhance their physical properties, which can leach from the polymer into the surrounding milieu. Leaching will occur primarily at the surface of the plastic particle, with the possibility of constant diffusion of chemicals from the core of the particle to the surface. Thus, leaching from plastic particles could present a longterm source of chemicals into tissues and body fluids, despite the fact that many of these chemicals are not persistent and have short half lives in the body (Engler 2012). Plastics additives of concern to human health include phthalates, bisphenol A, brominated flame retardants, triclosan, bisphenone and organotins.
The potential migration of polymer constituents and additives into food and drinks is considered to be a major route of exposure of the human population and as might be expected is subject to extensive legislation. The measurement of migration levels is typically estimated from measurements using different solvents to simulate the receiving environment (e.g. foodstuffs), or can be estimated using partitioning models that consider aspects including the desportion rates from the polymers, dimensions of the polymer framework and dimensions of the diffusing molecules (Helmroth et al. 2002). The European Food Standards Agency has a total migration limit of 10 mg/dm2 for additives within plastics intended for packaging use, with a more stringent migration limit of 0.01 mg/kg for certain chemicals of concern (Commission Directive 2007/19/CE that modifies Directive 2002/72/CE). This means that for an average 60 kg adult who consumes 3 kg of foods and liquids per day, exposures to individual substances from food packaging could be up to 250 μg/kg body weight per day (Muncke 2011).
Bisphenol a and Human Health
There is very little information on the leaching of additives into biological tissues directly, but one chemical monomer that has received considerable attention in relation to its human health effects is bisphenol A (Fig. 13.2). Bisphenol A (BPA) was first synthesised in the 1930s as a synthetic estrogen (Dodds and Lawson 1936) and is now a high-production volume chemical used as a monomer in the production of polycarbonate plastic and in the epoxy resins lining food and beverage cans. There are numerous studies showing that BPA can migrate out of polycarbonate (reviewed
Fig. 13.2 Bisphenol A
in Guart et al. 2013) and contaminate foodstuffs and drinks, and oral ingestion is considered the major route of exposure of the human population (Calafat et al 2008). Additional routes of exposure are predicted from the inhalation of household dusts and dermal uptake from printed materials (Ehrlich et al. 2014). BPA undoubtedly enters the human body, with studies showing exposure of >95 % of populations in USA, Europe and Asia (Galloway et al. 2010; Vandenberg et al. 2010).
Bisphenol A exerts its biological activity predominantly through interaction with steroid hormone receptors, showing both estrogenic and antiandrogenic activity and suppressing aromatase activity (Bonefeld-Jørgensen et al. 2007, Lee et al 2003). Additional receptor-mediated effects reported in various model systems include binding to the orphan estrogen-related receptor ERRα (Okada et al. 2008), thyroid hormone disruption (Moriyama et al. 2002), altered pancreatic beta cell function (Ropero et al. 2008) and obesity promoting effects (Newbold et al. 2008). There is growing evidence from epidemiological and laboratory studies that exposure to BPA at levels found in the general population, around 0.2–20 ng/ml (values given for urinary BPA), is associated with adverse human health effects, including the onset of obesity and cardiovascular disease (Lang et al. 2008; Melzer et al. 2010, 2012; Cipelli et al. 2013) and with numerous reproductive and developmental outcomes. These include increases in abnormal penile/urethra development in males, an increase in hormonally-mediated cancers including breast and prostate cancers, neurobehavioural disorders including autism and early sexual maturation in females (reviewed by vom Saal et al. 2007; Hengstler et al. 2011; Rochester 2013).
Whether the release of BPA from ingested microor nanoplastics directly into the body contributes to human exposure remains unknown. The current tolerable daily intake is 0.05 mg/kg/day (EFSA 2006) and compared with this, the median exposure of the general adult population globally has been estimated from human biomonitoring or urinary BPA to be 0.01–0.12 μg/kg/day (EFSA 2015). The concentrations of BPA in plasma are higher than would be predicted only from this level of exposure to BPA through food and drink (Mielke and Gundert-Remy 2009), and it is therefore plausible that other routes of exposure could occur, e.g. from ingestion of plastic particles containing BPA, which subsequently leaches into tissues. BPA can certainly be absorbed across body surfaces other than the gut. Gayrard et al. (2013) showed that BPA can be absorbed with relatively high efficiency sublingually, an effect likely enhanced by its low molecular weight and moderate water solubility, allowing it to penetrate the sublingual membrane.
There are no studies in humans of the transfer of BPA from plastic directly into tissues, but the potential for BPA to leach from ingested polycarbonate into aquatic species was explored by Koelmans et al. (2014) who used biodynamic modeling to calculate the relative contribution of plastic ingestion to total exposure to chemicals residing in the ingested plastic. They estimated plastic:lipid exchange coefficients for a range of plastic particle sizes for two species, fish and sediment-dwelling worms. They proposed that a continuous ingestion of plastic containing 100 mg/kg BPA would lead to a very low steady-state concentration of 0.044 ng/kg BPA in fish and 60 μg/kg (normalized to lipid) in worms. Whilst this represents a substantial exposure pathway, the risk of exposure through this route was considered low in comparison with other pathways of exposure, based on the reported abundance of microplastics.