Understanding the fate of plastics in the environment is of critical importance for the quantitative assessment of the biological impacts of plastic waste. Specially, there is a need to analyze in more detail the reputed longevity of plastics in the context of plastic degradation through oxidation and fragmentation reactions. Photo-oxidation of plastic debris by solar UV radiation (UVR) makes material prone to subsequent fragmentation. The fragments generated following oxidation and subsequent exposure to mechanical stresses include secondary micro- or nanoparticles, an emerging class of pollutants. The paper discusses the UV-driven photo-oxidation process, identifying relevant knowledge gaps and uncertainties. Serious gaps in knowledge exist concerning the wavelength sensitivity and the dose-response of the photo-fragmentation process. Given the heterogeneity of natural UV irradiance varying from no exposure in sediments to full UV exposure of floating, beach litter or air-borne plastics, it is argued that the rates of UV-driven degradation/fragmentation will also vary dramatically between different locations and environmental niches. Biological phenomena such as biofouling will further modulate the exposure of plastics to UV radiation, while potentially also contributing to degradation and/or fragmentation of plastics independent of solar UVR. Reductions in solar UVR in many regions, consequent to the implementation of the Montreal Protocol and its Amendments for protecting stratospheric ozone, will have consequences for global UV-driven plastic degradation in a heterogeneous manner across different geographic and environmental zones. The interacting effects of global warming, stratospheric ozone and UV radiation are projected to increase UV irradiance at the surface in localized areas, mainly because of decreased cloud cover. Given the complexity and uncertainty of future environmental conditions, this currently precludes reliable quantitative predictions of plastic persistence on a global scale.

Exposure of plants to mild chronic stress can cause induction of specific, stress‐induced morphogenic responses (SIMRs). These responses are characterized by a blockage of cell division in the main meristematic tissues, an inhibition of elongation and a redirected outgrowth of lateral organs. Key elements in the ontogenesis of this phenotype appear to be stress‐affected gradients of reactive oxygen species (ROS), antioxidants, auxin and ethylene. These gradients are present at the the organismal level, but are integrated on the cellular level, affecting cell division, cell elongation and/or cell differentiation. Our analysis of the literature indicates that stress‐induced modulation of plant growth is mediated by a plethora of molecular interactions, whereby different environmental signals can trigger similar morphogenic responses. At least some of the molecular interactions that underlie morphogenic responses appear to be interchangeable. We speculate that this complexity can be viewed in terms of a thermodynamic model, in which not the specific pathway, but the achieved metabolic state is biologically conserved.