Browse by: "2019"

This paper calculates new measures of human capital. Contrary to the existing literature, they are based on realistic rates of return to education, which are allowed to vary substantially across countries and to some extent over time. The new measures perform well in regression analysis explaining productivity across OECD countries and over time. In OECD samples, coefficient estimates are broadly consistent with the private returns underlying the construction of the new measures of human capital. In a wider sample of countries, most estimates imply additional positive social returns.

The paper discusses the implications of the low-carbon transition for workers and the relevant lessons-learnt in previous industrial restructuring experiences. The evidence suggests that, while climate policies are likely to have a modest impact on aggregate employment, workers in certain regions and industries can be more severely affected. The transition may also have gender-differentiated impacts: men represent the largest share of the workforce of most negatively affected industries (e.g. coal-mining) while the growth of the renewable power generation sector, which exhibits a relatively more gender-balanced workforce, suggests that female employment may increase in the traditionally male-dominated energy sector. Lessons from the case-studies underline that a suite of polices is necessary to manage the structural adjustment process, including structural reforms and skills policies. Importantly, the low-carbon transition differentiates itself from previous restructuring experiences because of its policy-driven nature and the possibility to finance structural adjustment measures through carbon-pricing revenues.

Interference with endogenous developmental processes that are regulated by the aryl hydrocarbon receptor (AHR), through sustained exogenous activation, causes molecular, structural, and functional cardiac abnormalities in avian, mammalian and piscine embryos; this cardiotoxicity ultimately leads to severe oedema and embryo death in birds and fish and some strains of rat. There have been numerous proposed mechanisms of action for this toxicity profile, many of which include the dysregulation of vascular endothelial growth factor (VEGF). This AOP describes the indirect suppression of VEGF expression through the sequestration of the aryl hydrocarbon receptor nuclear translocator (ARNT) by AHR. ARNT is common dimerization partner for both AHR and hypoxia inducible factor alpha (HIF-1α), which stimulates angiogenesis through the transcriptional regulation of VEGF. The suppression of VEGF thereby reduces cardiomyocyte and endothelial cell proliferation, altering cardiovascular morphology and reducing cardiac output, which ultimately leads to congestive heart failure and death.

Hepatic uroporphyria is a disorder where the disturbance of heme biosynthesis results in accumulation and excretion of uroporphyrin, heptacarboxyl- and hexacarboxyl porphyrin: collectively referred to as highly carboxylated porphyrins (HCPs). The disorder is due to a homozygous mutation in uroporphyrinogen decarboxylase (UROD), an enzyme involved in the heme biosynthesis pathway, or may be chemically induced, which involves the inhibition of UROD. This AOP describes the linkages leading to chemically induced porphyria through the activation of the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor. AHR activation leads to the induction of cytochrome P450 1A2, a phase I metabolising enzyme, which in turn results in excessive oxidation of uroporphyrinogen. This oxidation produces a UROD inhibitor, preventing the conversion of uroporphyrinogen to coprouroporphyrinogen and increasing the synthesis of the UROD inhibitor in a positive feedback loop. The accumulation of uroporphyrinogen leads to its preferential oxidation and accumulation of HCP in various organs (Uroporphyria).

The present AOP describes antagonistic chemical binding to the peroxisome proliferator-activated receptor α (PPARα), resulting in preferential binding a co-repressor to the overall PPARα signalling complex causing a chain of events that includes: antagonism of PPARα nuclear signalling, decreased transcriptional expression of PPARα-regulated genes that support energy metabolism, inhibited metabolic energy production (decreased fatty acid beta oxidation and ketogenesis), and increase in catabolism of muscle protein, culminating with starvation-like weight loss. The AOP is likely to be synergised during fasting, starvation or malnutrition events. The adverse outcome of this AOP is body-weight loss, which within the context of dynamic energy budget theory, decreases energy allocations to organismal maturation and reproduction and has been demonstrated to negatively affect ecological fitness.

This AOP details the linkage between activation of the aryl hydrocarbon receptor (AhR) and early life stage mortality in oviparous vertebrates. It can be initiated mostly by dioxin-like compounds, which are able to bind to the AhR causing heterodimerisation with the aryl hydrocarbon nuclear translocator (ARNT) and interaction with dioxin-responsive elements on the DNA causing an up-regulation in dioxin responsive genes. One dioxin-responsive gene is cyclooxygenase 2 (COX-2), which has roles in development of the cardiovascular system. Up-regulation in expression of COX-2 causes alteration in cardiovascular development and function resulting in reduced heart pumping efficiency, reduced blood flow, and eventual cardiac collapse and death. Comparable apical manifestations of activation of the AhR have been recorded across freshwater and marine teleost and non-teleost fishes, as well as birds. Despite conservation in the AOP across taxa, great differences in sensitivity to perturbation exist both among and within taxonomic groups.

This AOP begins with the interaction of chemicals to the picrotoxin binding site of the ionotropic GABA receptor complex causing blockage of the ion channel. As a result, decrease in inward chloride conductance occurs, followed by a reduction in postsynaptic inhibition, reflected as reduced frequency and amplitude of spontaneous inhibitory postsynaptic current or abolishment of GABA-induced firing action. Consequently, the resistance of excitatory neurons to fire is decreased, resulting in the generation of a large excitatory postsynaptic potential (EPSP) that causes voltage-gated Na⁺ to open, which results in action potentials. The depolarisation is followed by a period of hyper-polarisation mediated by Ca²⁺-dependent K⁺ channels or GABA-activated Cl⁻ influx, which becomes smaller, gradually disappears, and is replaced by a depolarisation known as “paroxysmal depolarizing shift” (PDS). A PDS is an indication of epilepsy at the cellular level and initiates the adverse outcome at the organismal level of epileptic seizure.

The thyroid hormones (TH) are essential for brain development, maturation, and function as they regulate the early key developmental processes. Normal human brain development and cognitive function relays on sufficient production of TH during the perinatal period. The function of Na⁺/I^- symporter (NIS) is critical for the physiological production of TH levels in the serum. The present AOP describes causative links between inhibition of NIS function leading to the decreased levels of TH in the blood and consequently in the brain, causing learning and memory deficit in children. Learning and memory depend upon the coordinated action of different brain regions and neurotransmitter systems creating functionally integrated neural networks. Hippocampus and cortex are the most critical brain structures involved in the process of cognitive functions. The function of NIS and its essentiality for TH synthesis is well known across species, however, quantitative information of KERs is limited.

This AOP describes one adverse outcome that may result from the inhibition of thyroperoxidase (TPO) during mammalian development. Chemical inhibition of TPO results in decreased thyroid hormone (TH) synthesis, and subsequent reduction in circulating concentrations of THs. THs are essential for normal human brain development, both prenatally and postnatally, modulating genes critical for a normal neuroanatomical development, with subsequent effects on neurophysiology, and finally neurological function. Therefore, chemicals that interfere with TH synthesis have the potential to cause TH insufficiency that may result in adverse neurodevelopmental effects in offspring. Herein, we discuss the implications of developmental TPO inhibition for hippocampal anatomy, function, and ultimately neural function. The hippocampus is known to be critically involved in cognitive, emotional, and memory function. The adverse consequences of TH insufficiency depend both on severity and developmental timing, indicating that exposure to TPO inhibitors may produce different effects at different developmental windows of exposure.

OECD countries and their regions are ageing fast. In principle, the negative impact of ageing on the growth rate of per capita gross domestic product could be offset by increases in productivity. However, for many regions, productivity growth required to maintain per capita GDP levels constant has been higher than the actual growth rates they recorded in the past years. One reason for this is that ageing also has a direct negative impact on productivity growth, with the effect being concentrated in urban areas. One possible explanation is that cities specialise in sectors, such as tradable services, where the content of tasks makes it difficult to automate stages of the production process and where business dynamism, negatively affected by demographic change, is a more solid driver of productivity growth. Finally, ageing seems to be associated with a redistribution of revenues away from workers and towards capital and firm owners.

This report analyses market-distorting factors in the shipbuilding industry with a focus on government interventions. This paper argues that government interventions in this cyclical industry do more harm than good by exacerbating and prolonging economic downturns through two channels. First, it promotes an over-ordering of vessels through lower delivery time, distorting ship buyers’ investment behaviour. Second, it may maintain unproductive capacity in the market that re-enters a new economic cycle, restarting the vicious circle of industrial excess capacity. Against the background of the global nature of this industry, these channels reinforce the case for effective international disciplines on government interventions. Overall, the mature nature of the shipbuilding industry undermines the need for an active industrial policy, beyond facilitating structural adjustment, and emphasizes the necessity for a horizontal policy approach. The work seeks to provide policy makers with a better understanding of how different factors can contribute to excess capacity.

This paper presents the results of an ex post evaluation of the impacts of a vehicle tax reform in Ireland, by carrying out a full social cost benefit analysis of a vehicle tax reform that began in Ireland in 2008 and shows that whilst successful in improving the fuel economy of new passenger cars, it may also have caused unintended effects, such as an increased proliferation of diesel vehicles in the passenger car fleet. These outcomes have mitigated the overall benefits. In addition to quantifying the scale of the various effects and outcomes, this paper clearly demonstrates the importance of broad scope policy design.