Effects of incomplete combustion on atmospheric chemistry: Black carbon climate forcing and global carbon monoxide emissions

This thesis is actually the composition of two separate studies aimed at further understanding the role of incomplete combustion products on atmospheric chemistry. The first explores the sensitivity of black carbon (BC) forcing to aerosol vertical location since BC has an increased forcing per unit mass when it is located above reflective clouds. We used a column radiative transfer model to produce globally-averaged values of normalized direct radiative forcing (NDRF) for BC over and under different types of clouds. We developed a simple column-weighting scheme based on the mass fractions of BC that are over and under clouds in measured vertical profiles. The resulting NDRF is in good agreement with global 3-D model estimates, supporting the column-weighted model as a tool for exploring uncertainties due to diversity in vertical distribution. BC above low clouds accounts for about 20% of the global burden but 50% of the forcing. We estimate maximum-minimum spread in NDRF due to modeled profiles as about 40% and uncertainty as about 25%. Models overestimate BC in the upper troposphere compared with measurements; modeled NDRF might need to be reduced by about 15%. Redistributing BC within the lowest 4 km of the atmosphere affects modeled NDRF by only about 5% and cannot account for very high forcing estimates. The second study estimated global year 2000 carbon monoxide (CO) emissions using a traditional bottom-up inventory. We applied literature-derived emission factors to a variety of fuel and technology combinations. Combining these with regional fuel use and production data we produced CO emissions estimates that were separable by sector, fuel type, technology, and region. We estimated year 2000 stationary source emissions of 685.9 Tg/yr and 885 Tg/yr if we included adopted mobile sources from EDGAR v3.2FT2000. Open/biomass burning contributed most significantly to global CO burden, while the residential sector, primarily in Asia and Africa, were the largest contributors with respect to contained combustion sources. Industry production in Asia, including brick, cement, iron and steel-making, also contributed significantly to CO emissions. Our estimates of biofuel emissions are lower than most previously published bottom-up estimates while our other fuel emissions are generally in good agreement. Our values are also universally lower than recently estimated CO emissions from models using top-down methods.

A decrease in dkk1, a Wnt inhibitor, contributes to placental and fetal lipid accumulation in an obesity-prone rat model

Placenta, as the sole transport mechanism between mother and fetus, links the maternal physical state and the immediate and life-long outcomes of the offspring. The present study examined the mechanisms behind the effect of maternal obesity on placental lipid accumulation and metabolism. Pregnant Obese Prone (OP) and Obese Resistant (OR) rat strains were fed a control diet throughout gestation. Placentas were collected on gestational d21 for analysis and frozen placental sections were analyzed for fat accumulation as well as β-Catenin and Dkk1 localization. Additionally, DKK1 was overexpressed in JEG3 trophoblast cells, followed by treatment with NEFA and Oil Red O stain quantification and mRNA analysis to determine the relationship between placental DKK1 and lipid accumulation. Maternal plasma and placental NEFA and TG were elevated in OP dams, and offspring of OP dams were smaller than OR. Placental Dkk1 mRNA content was 4-fold lower in OP placentas, and there was a significant increase in β-Catenin accumulation as well as mRNA content of fat transport and TG synthesis enzymes, including Ppar-delta, Fatp1, Fat/Cd36, Lipin1, and Lipin3. There was significant lipid accumulation within the decidual zones in OP but not OR placentas, and the thickness of the decidual and junctional zones was significantly smaller in OP than OR placentas. Overexpression of DKK1 in JEG3 cells decreased lipid accumulation and the mRNA content of PPAR-Delta, FATP1, FAT/CD36, LIPIN1, and LIPIN3. Our results indicate that Dkk1 may be regulating placental lipid metabolism through Wnt-mediated mechanisms. Additionally, recent studies have suggested that maternal obesity may also program early development of non-alcoholic fatty liver disease (NAFLD), rates of which have correlated with the increase in the obesity epidemic. In the current study, livers of OP offspring had significantly increased TG content (P<0.05) and lipid accumulation when compared to offspring of OR dams. Additionally, hepatic Dkk1 mRNA content was significantly decreased in OP livers when compared to OR (P<0.05), and treating H4IIECR rat hepatocyte cells with NEFA showed that Dkk1 mRNA was also decreased in NEFA-treated cells (P<0.05) that also had lipid accumulation. Chromatin Immunoprecipitation (ChIP) analysis of the Dkk1 promoter in fetal livers showed a pattern of histone modifications associated with decreased gene transcription in OP offspring, which agrees with our gene expression data. These results demonstrate that the hepatic Dkk1 gene is epigenetically regulated via histone modification in neonatal offspring in the current model of gestational obesity, and future studies will be needed to determine whether these changes contribute to excessive hepatic lipid accumulation in offspring of obese dams.