RESUMO
Integrated Assessment Models (IAMs) have become critical tools for assessing the costs and benefits of policies to reduce greenhouse gas emissions. Three models currently inform the social cost of carbon dioxide (SCCO2, the net present value of damages from one additional ton of CO2) used by the US federal government, several states, and Canada. Here we present a new open-source implementation of one of these models (PAGE09) in the Julia programming language using a modular modeling framework (Mimi). Mimi-PAGE was coded using best coding practices (such as multiple code reviews by different individuals during development, automated testing of newly-committed code, and provision of documentation and usage notes) and is publicly available in a GitHub repository for community inspection and use under an open source license. In this paper we describe the Julia implementation of PAGE09, show that output from Mimi-PAGE matches that of the original model, and perform comparisons of the run time between the two implementations.
RESUMO
BACKGROUND: Bis-(2-ethylhexyl) tetrabromophthalate (TBPH) is widely used as a replacement for polybrominated diphenyl ethers (PBDEs) in commercial flame retardant mixtures such as Firemaster 550. It is also used in a commercial mixture called DP 45. Mono-(2-ethyhexyl) tetrabromophthalate (TBMEHP) is a potentially toxic metabolite. OBJECTIVES: We used in vitro and rodent in vivo models to evaluate human exposure and the potential metabolism and toxicity of TBPH. METHODS: Dust collected from homes, offices, and cars was measured for TBPH by gas chromatography followed by mass spectrometry. Pregnant rats were gavaged with TBMEHP (200 or 500 mg/kg) or corn oil on gestational days 18 and 19, and dams and fetuses were evaluated histologically for toxicity. We also assessed TBMEHP for deiodinase inhibition using rat liver microsomes and for peroxisome proliferator-activated receptor (PPAR) α and γ activation using murine FAO cells and NIH 3T3 L1 cells. RESULTS: TBPH concentrations in dust from office buildings (median, 410 ng/g) were higher than in main living areas in homes (median, 150 ng/g). TBPH was metabolized by purified porcine esterases to TBMEHP. Two days of TBMEHP exposure in the rat produced maternal hypothyroidism with markedly decreased serum T3 (3,3´,5-triiodo-l-thyronine), maternal hepatotoxicity, and increased multinucleated germ cells (MNGs) in fetal testes without antiandrogenic effects. In vitro, TBMEHP inhibited deiodinase activity, induced adipocyte differentiation in NIH 3T3 L1 cells, and activated PPARα- and PPARγ-mediated gene transcription in NIH 3T3 L1 cells and FAO cells, respectively. CONCLUSIONS: TBPH a) is present in dust from indoor environments (implying human exposure) and b) can be metabolized by porcine esterases to TBMEHP, which c) elicited maternal thyrotoxic and hepatotoxic effects and d) induced MNGs in the fetal testes in a rat model. In mouse NIH 3T3 L1 preadipocyte cells, TBMEHP inhibited rat hepatic microsome deiodinase activity and was an agonist for PPARs in murine FAO and NIH 3T3 L1 cells.
