Decomposition and Disintegration

Decomposition, disintegration or (bio)degradation have been reported to occur at time scales of years to decades (Andrady 2011). Recent laboratory studies report degradation of 1–1.75 % of low density PE mass in 30 d, for micro-organisms isolated from marine waters and with high microbial densities (Harshvardhan and Jha 2013). If surface oxidation or surface degradation is the rate-limiting step, overall degradation can be assumed to depend on the amount of surface area that is available. With ongoing degradation, the surface area per unit of volume will increase due to increased surface roughness, as well as reduced particle size. The shrinking-particle theory (e.g. Di Toro et al. 1996) accounts for this change in size and for mono-disperse spherical particles would predict:


in which Vt (m3) is the particle volume at time t, V0 (m3) is the initial particle volume, d0 (m) is the initial particle diameter (spheres) or thickness (polymer films), α is a particle shape factor (α = 3 for spheres and α = 1 for thin films) and ks is the apparent shrinking-rate constant (m3 m−2 d−1). Calibration of the model on the

~1 % PE mass loss in 30 d observed for thin films deployed by Harshvardhan and Jha (2013) (with α = 1 and assuming an initial thickness of 25.4 µm (1 mil) for their PE film), would yield a low value for ks of 4.2 × 10−9 m3 m−2 d−1. It can be assumed that loss of polymer equates to loss of chemical held by that volume of polymer. The time scales at which these decomposition processes occur, however, probably are orders of magnitude longer than the time scales of plastic-water partitioning or transfer inside the organisms' gut (see below). This implies that decomposition is not directly relevant for bioaccumulation assessment.


Bioaccumulation can be modelled using traditional approaches that use a mass balance of uptake and loss processes (e.g. Thomann et al. 1992; Hendriks et al. 2001) (Fig. 11.1). Extensions of these models to account for uptake from contaminated particles as diet components were fi provided by Sun et al. (2009) and Janssen et al. (2010). Koelmans et al. (2013a, b, 2014b) modelled bioaccumulation of hydrophobic chemicals (dCB,t/dt; µg × kg−1 d−1) from an environment containing plastic using:

Fig. 11.1 Schematic representation of processes required for plastic-inclusive bioaccumulation modeling (example for PCBs accumulation in a lugworm Arenicola marina): 1 Partitioning between plastic, sediment and water, 2 dermal uptake, 3 organic matter (food, biofilm) ingestion, 4 microplastic ingestion, 5 absorption from plastic, 6 absorption from organic matter, 7 elimination, 8 particle retention, 9 worm growth, 10 particle egestion (sediment and plastic). Same or similar process descriptions can be used for other marine/aquatic organisms. Reprinted with permission from Koelmans et al. (2013a). Copyright 2013 American Chemical Society


where the first term quantifies dermal (for fish; including gills) uptake from water. The second term quantifies uptake from the diet and exchange with plastic particles. The third term quantifies overall loss due to elimination and egestion. The first and third term can be parameterised following traditional approaches with kderm (L × kg × d−1) and kloss (d−1), first-order rate constants for dermal uptake and overall loss through elimination and egestion. In the second term, IR (g × g−1 × d−1) represents the mass of food ingested per unit of time and organism dry weight, aFOOD is the absorption efficiency from the diet, SFOOD and SPL are the mass fractions of food and plastic in ingested material, respectively (SFOOD + SPL = 1) and CFOOD is the chemical concentration in the diet. The product aFOOD × CFOOD quantifies the contaminant concentration that is transferred from food, i.e. prey, to the organism during gut passage. The plastic particles may contain a biofilm (BF), which may also carry chemicals. The biofilm would contribute to the pool of digestible organic matter and may therefore be covered either by the sediment term or by an optional additional term in Eq. 11.7, similar to the sediment ingestion term (e.g. IR × SBF × aBF × CBF). Where regular bioaccumulation models assume digestion of diet components and thus assume a certain fixed chemical absorption efficiency, Koelmans et al. (2013a, b, 2014b) assumed plastic not to degrade in the short time scale of gut passage. The transferred concentration from plastic during gut passage (CPLR,t, µg/kg) thus was modelled to be dependent on the concentrations in plastic and biota lipids, the kinetics of transfer between plastic and lipids and the GIT residence time (GRT) (see Koelmans et al. 2013a, b for detailed derivation):


in which k1G and k2G (d−1) are forward and backward first-order rate constants describing the transport between plastic and biota lipids inside the GIT. If the numerator term k1GCPLk2GCL,t in Eq. 11.8 is positive, transfer from the plastic to biota lipids occurs, whereas opposite transfer ('cleaning by plastic') occurs when the term is negative. Various authors have provided these k values at simulated gut conditions, showing about an order of magnitude enhancement of transfer rates in artificial gut fluids up to k1G = 10–12 d−1 (Teuten et al. 2007; Bakir et al. 2014). GRT is gut residence time (d), CPL and CL,t (µg/kg) are the chemical concentrations in the ingested plastic particle and the biota lipids at the moment of ingestion and MPL and ML are the mass of plastic and lipids in the organism, respectively (kg). If CW is constant in time (Eqs. 11.2 and 11.5) and CPL is estimated by Eq. 11.2, an analytical solution to Eqs. 11.7 and 11.8 is available that calculates the body burden at steady state (CSS) (Koelmans et al. 2014b):

Note, that Eq. 11.9 accounts for all uptake and loss pathways and can be used to assess the relative importance of plastic ingestion as an uptake pathway compared to other pathways such as food ingestion and dermal uptake, as well as the importance of chemical loss by plastic egestion compared to regular loss mechanisms.

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