These studies focus on behavior of sodium dioctylsulfosuccinate (SDOSS) surfactant molecules in styrene/n-butyl acrylate/glycidyl methacrylate (Sty/nBA/GMA) and styrene/n-butyl acrylate/methacrylic acid (Sty/nBA/MAA) blended latexes during their film formation process. Using a combination of Fourier transform infrared (FT-IR) microanalysis and FT-Raman techniques, not only stratification of SDOSS surfactant molecules during film formation process can be assessed but also the effect of latex particle structures and cross-linking reactions during coalescence can be determined. For Sty/nBA/GMA and Sty/nBA/MAA blended copolymer latexes, SDOSS exhibit nonuniform distributions at the film air (F−A) interface. However, for core/shell Sty/nBA-GMA and Sty/nBA-MAA blended latexes, SDOSS is distributed uniformly near the F−A interface, and its concentration levels are lower as compared to copolymer latex blends. At elevated coalescence temperatures, SDOSS migration to the F−A interface is prohibited due to cross-linking reactions between epoxy and acid groups. Microanalysis results show that SDOSS migration to the F−A interface is initiated after the majority of H2O (>95%) evaporates from the film. Furthermore, these studies show that latex particle surface morphology, particle−particle interdiffusion, and cross-linking reactions play a significant role in controlling mobility of low molecular weight species in latex films.

These studies focus on behavior of sodium dioctylsulfosuccinate (SDOSS) surfactant molecules in styrerie/n-butyl acrylate (Sty/n-BA) copolymers and blended latexes. Using a combination of IR and Raman spectroscopic and microanalytical techniques, not only stratification of SDOSS surfactant molecules across latex film thickness can be assessed, but also the effect of latex composition on coalescence can be analyzed. For Sty/n-BA latex copolymers, SDOSS‚‚‚H 20, SDOSS‚‚‚COOH associations, and free SDOSS are formed at the film-air (F-A) interface and exhibit nonuniform distributions across the film thickness. However, for p-Sty/p-nBA latex polymer blends, SDOSS is distributed uniformly at the F-A interface, and its concentration levels are significantly lower when compared to Sty/n-BA copolymer latexes. These studies show that, while step-scan photoacoustic Fourier transform infrared (SS-PAS FT-IR) and attenuated total reflectance (ATR) FT-IR are effective depth profiling methods for latex. films, FT-IR and FT-Raman imaging techniques provide unique analytical facilities for typically nondistinguishable surface latex components.

While molecular level interactions between sulfonate groups of sodium dioctylsulfosuccinate (SDOSS) and COOH groups in styrene/n-butyl acrylate/methacrylate acid (Sty/n-BA/MAA) copolymer particles have been the subject of our earlier studies, the main focus of this work is to establish how MAA groups affixed to polymer latex particle surfaces will affect SDOSS mobility in Sty/n-BA/MAA latex films. The ultimate objective is to develop a series of model systems simulating the degree of neutralization of polymer surfaces and how it may alter polymer contractions and release of entropically attached molecules to interfacial regions. These studies show that the release of SDOSS molecules from MAA containing Sty/ n-BA particles is attributed to two factors: (1) entropic effect due to increased compatibility resulting from surfactant penetration into latex particle surfaces and (2) enhanced particle out-layer glass transition temperature (Tg). The SDOSS release is inhibited when surface neutralization levels are 0-25%, but at higher degrees of neutralization (50-100%), excessive SDOSS exudation to the film-air (F-A) interface of a film is observed. This behavior is attributed to the displacement of SDOSS molecules from MAAcontaining latex particles during film formation as a result of the conversion of potential surface energy into mechanical movement when ionic bonds are broken. Thus, the simultaneous presence of p-MAA and SDOSS at the particle surfaces make them act as polyelectrolytes, responding to chemical changes, and during film formation, ionomeric species containing SO3 -Na + -COO -Na + entities near the F-A interface are formed.

These studies show that polystyrene/poly(n-butyl acrylate) (p-Sty/p-nBA) latex blend coalescence is inherently affected by latex composition, p-Sty particle size, and the temperature difference between coalescence (T c) and glass transition (T g) temperatures. Sodium dioctylsulfosuccinate (SDOSS) surfactant molecules are expelled to the film−air (F−A) interface when T c > T g of the p-Sty phase. Quantitative attenuated total reflectance Fourier transform infrared (ATR FT-IR) analysis shows that SDOSS−H2O concentration levels near the F−A interface diminish for larger p-Sty latex particle sizes and the magnitude of the SDOSS−COOH interactions near the F−A interface exhibits similar trends. Furthermore, the amount of SDOSS expelled to the F−A interface is directly proportional to the p-Sty phase surface area. These studies also show that SDOSS hydrophilic ends are preferentially parallel to the F−A interface, while hydrophobic ends are preferentially perpendicular.

The driving forces, kill and recovery mechanisms for the end-Permian mass extinction (EPME), the largest Phanerozoic biological crisis, are under debate. Sedimentary records of mercury enrichment and mercury isotopes have suggested the impact of volcanism on the EPME, yet the causes of mercury enrichment and isotope variations remain controversial. Here, we model mercury isotope variations across the EPME to quantitatively assess the effects of volcanism, terrestrial erosion and photic zone euxinia (PZE, toxic, sulfide-rich conditions). Our numerical model shows that while large-scale volcanism remains the main driver of widespread mercury enrichment, the negative shifts of Δ199Hg isotope signature across the EPME cannot be fully explained by volcanism or terrestrial erosion as proposed before, but require additional fractionation by marine mercury photoreduction under enhanced PZE conditions. Thus our model provides further evidence for widespread and prolonged PZE as a key kill mechanism for both the EPME and the impeded recovery afterward.