The Mexico City Metropolitan Area (MCMA) is one of the largest cities in the world, and as with many megacities worldwide, it experiences serious air quality and pollution problems, especially with ozone and particulate matter. Ozone levels exceed the health-based standard, which is equivalent to the U.S. standard, on approximately 80% of all days, and concentrations of particulate matter 10 μm and smaller (PM10) exceed the standard on more than 40% of all days in most years. Particulate polycyclic aromatic hydrocarbons (PAHs) are a class of semi-volatile compounds that are formed during combustion and many of these compounds are known or suspected carcinogens. Recent studies on PAHs in Mexico City indicate that very high concentrations have been observed there and may pose a serious health hazard. The first part of this thesis describes results from the Megacities Initiative: Local and Regional Observations (MILAGRO) study in Mexico City in March 2006. During this field campaign, we measured PAH and aerosol active surface area (AS) concentrations at six different locations throughout the city using the Aerodyne Mobile Laboratory (AML). The different sites encompassed a mix of residential, commercial, industrial, and undeveloped land use. The goals of this research were to describe spatial and temporal patterns in PAH and AS concentrations, to gain insight into sources of PAHs, and to quantify the relationships between PAHs and other pollutants. We observed that the highest measurements were generally found at sites with dense traffic networks. Also, PAH concentrations varied considerably in space. An important implication of this result is that for risk assessment studies, a single monitoring site will not adequately represent an individual's exposure. Source identification and apportionment are essential for developing effective control strategies to improve air quality and therefore reduce the health impacts associated with fine particulate matter and PAHs. However, very few studies have separated gasoline- versus diesel-powered vehicle emissions under a variety of on-road driving conditions. The second part of this thesis focuses on distinguishing between the two types of engine emissions within the MCMA using positive matrix factorization (PMF) receptor modeling. The Aerodyne Mobile Laboratory drove throughout the MCMA in March 2006 and measured on-road concentrations of a large suite of gaseous and particulate pollutants, including carbon dioxide, carbon monoxide (CO), nitric oxide (NO), benzene (C6H6), formaldehyde (HCHO), ammonia (NH3), fine particulate matter (PM2.5), PAHs, and black carbon (BC). These pollutant species served as the input data for the receptor model. Fuel-based emission factors and annual emissions within Mexico City were then calculated from the source profiles of the PMF model and fuel sales data. We found that gasoline-powered vehicles were responsible for 90% of mobile source CO emissions and 85% of VOCs, while diesel-powered vehicles accounted for almost all of NO emissions (99.98%). Furthermore, the annual emissions estimates for CO and VOC were lower than estimated during the MCMA-2003 field campaign. The number of megacities is expected to grow dramatically in the coming decades. As one of the world's largest megacities, Mexico City serves as a model for studying air quality problems in highly populated, extremely polluted environments. The results of this work can be used by policy makers to improve air quality and reduce related health risks in Mexico City and other megacities. / Master of Science

Target shooting in the United States has become an increasingly popular sport in the last century. In addition to the large quantity of lead pellets littering range grounds and surrounding land, considerable amounts of clay target fragments cover shooting range areas as well as adjoining habitats. Polycyclic aromatic hydrocarbons (PAHs) within the target, as well as lead pellets from shotguns pose multiple threats to a variety of wildlife. To determine the effects of clay target and lead pellet ingestion on wildlife, I conducted controlled experiments on Coturnix quail exposed to clay targets in the lab, and collected wild birds and mammals exposed to lead pellets at a shooting range. The first Coturnix study determined whether quail voluntarily consumed target fragments or limestone fragments. In both fall (F=29.2, P<0.01) and spring (F=6.45, P=0.02) experiments, I found that quail consistently selected limestone fragments, but almost completely rejected clay target fragments. In the second study, quail were force-fed varying amounts of target dust on a weekly basis to simulate sporadic exposure to clay target dust. In both summer (F=1.63, P=0.23) and winter (F=0.34, P=0.8) trials, male quail did not have significant weight loss. Female quail had insignificant weight losses in summer trials (F=1.63, P=0.23) but experienced weight gains in winter trials (F=3.53, P=0.04). In the third and final Coturnix study, varying amounts of target dust were incorporated into daily feed rations to simulate frequent exposure to clay target dust. Male quail experienced weight loss in both summer (F=16.13, P<0.01) and winter (F=8.47, P<0.01) trials. Female quail also suffered weight loss in both summer (F=15.62, P<0.01) and winter (F=17.50, P<0.01) trials. Weight loss likely resulted from inadequate nutrition as opposed to target poisoning. However, because there were no biochemical analyses performed to test for PAH presence, no definite conclusions can be made. The second study focused on lead contamination in Passeriformes, perching birds, and small mammals. Seventeen of 20 birds (85%) (Passerine spp) captured at the shooting range had elevated lead levels (F=5.21, P<0.028), when compared to birds (n=20) at the control site. Nine of 26 (35%) white-footed mice (Peromyscous leucopus), trapped at the shooting range had elevated liver (F=9.78, P=0.0029) and kidney (F=22.49, P<0.01) lead levels. These results indicate that Passerine species as well as Peromyscous species around shooting ranges inadvertently consume lead, either as lead pellets, mistaking them for grit or dietary items, or through environmental sources such as water, soil, and vegetation. / Master of Science

In 1997, a phytoremediation program began at a creosote-contaminated former railroad tie yard in Oneida, Tennessee with the planting of over 1000 hybrid poplar trees onsite. Creosote, a mixture of hazardous chemicals composed of 85% polycyclic aromatic hydrocarbons (PAH) had entered the site soil and ground water. After planting, a seasonal ground water testing program began that monitored the progress of remediation by measuring the concentration of the 10 predominant PAHs in the contaminant plume: naphthalene, acenaphthylene, acenaphthene, fluorene, phenanthrene, anthracene, fluoranthene, pyrene, chrysene, and benzo(b)fluoranthene. The concentrations of these compounds steadily decreased over time, but the role the trees played in the remediation was unclear. In order to gain a clearer understanding of the role the trees played in contaminant remediation, chemical analysis of tree tissue began. It was not known whether the trees were taking up PAH contaminants or their metabolites or if the rhizosphere zone created by the trees simply enhanced the ability of the site microflora to degrade the PAH. The objectives of this research were to (1) develop a suitable method for the chemical analysis of tree tissue collected from a field site, (2) determine if there were any chemicals not usually found in poplar trees that occurred in the trees growing over contamination, (3) determine if bud, bark, and twig tissue differed in their ability to predict ground water contamination, and (4) determine if a spatial correlation existed between the aromatic compounds in the tree tissue and the ground water total PAH plume. Two types of tree tissue/ground water comparisons were performed: spatial distribution of isoeugenol concentration in tree tissue with spatial distribution of total PAH in ground water over the area of interest; and the spatial distribution of the quantity of aromatic compounds in tree tissue with the spatial distribution of total PAH concentration in ground water. Due to unit discrepancies between the quantities of interest, all comparisons were made on a percentile basis. Initial tree sampling revealed that several compounds not usually present in poplar trees occurred only in those trees growing over contamination. In the first part of this study, the concentration of one of these chemicals, the substituted phenol isoeugenol, was compared with the concentration of total PAH in ground water from samples collected from February-March 2002. The bark tissue percentiles fell within 20 percentiles of ground water total PAH concentrations in 60% of the study area. The twig tissue showed slightly better agreement, with 67% of the study area differing from ground water by twenty percentiles or less. The second comparison took place over three sampling events: March 2001, July 2001, and February-March 2002. The number of unique aromatic compounds in bark, bud, and twig tissue was compared with the total PAH concentration in ground water. Twig tissue aromatic compound content was the most accurate predictor of ground water contamination among the tissue types. After excluding those chemicals likely to be interferences from consideration, twig tissue aromatic content agreed with ground water total PAH concentration to within 20 percentiles over 2/3 or more of the study area during each sampling event, suggesting the potential uptake of PAHs or their microbial metabolites as a mechanism of phytoremediation at the site. / Master of Science

The preparation of 2-(3-chloro-l-naphthylmethyl)bromobenzene was achieved by the cross-condensation reaction of 3-chloro-l-naphthylmagnesium bromide and 2-bromobenzyl bromide, as well as by the reaction of this Grignard reagent with 2-bromobenzaldehyde, followed by reduction of the resulting carbinol with lithium aluminum hydride and aluminum chloride. It was found that 2-bromophenyl-1-(3-chloronaphthyl)carbinol thermally decomposed into the corresponding methylene compound and ketone. A study of the thermally induced reaction of the carbinol was made, and the products were quantitatively analyzed by means of gas chromatography. It was concluded that the anomalous products of the reaction of an aryl Grignard reagent with a benzaldehyde were actually p~duced by the thennal disproportionation of the resulting carbinols during the distillation step. The keto-acid, 2-(3-chloro-l-naphthylmethyl)- 2’-carboxybenzophenone was prepared by the inverseaddition of the Grignard reagent of 2-(3-chloro-l-naphthylmethyl)bromobenzene to phthalic anhydride. Cyclization of this keto-acid with an acetic and hydrobromic acid mixture gave 6-chloro-7-(2-carboxyphenyl)benz[a]anthracene. Methyl ester derivatives were prepared from both this acid and the precursor keto-acid. The cyclodehydration of either 2-(3-chloro-l-naphthylmethyl)-2'-carboxybenzophenone or 6-chloro-7-(2-carboxyphenyl)benz[a]anthracene with polyphosphoric acid gave 14-chlorodibenzo[hi,l]chrysen-9-one.· Treatment of this ketone with lithium aluminum hydride and aluminum chloride gave the reduction derivative, 14-chloro-9H-dibenzo[hi,l]chrysene. The unequivocal synthesis of dibenzo[hi,l]- chrysen-9-one was achieved by the dehalogenation of 14-chlorodibenzo[hi,l]chrysen-9-one with 10% palladiumcharcoal catalyst and hydrazine. The dehalogenated product was shown to be identical to the compound produced from the cyclodehydration of 7-(2-carboxyphenyl)benz[a]anthracene. The ketone, 2-(3-chloro-l-naphthylmethyl)benzophenone was prepared by the inverse-addition of the Grignard reagent of 2-(3-chloro-l-naphthylmethyl)- bromobenzene to benzoyl chloride. It was found that a small amount (16%) of 6-chloro-7-phenylbenz[a]-anthracene was formed during the distillation of the precursor ketone. The cyclodehydration of this ketone failed when various standard cyclizing media were employed, and the reason for this is discussed. Cyclization attempts with polyphosphoric acid or alumina gave dibenzo[a,l]pyrene as the only identifiable product. This unusual reaction obviously involves a rearrangement. A study was made and a mechanism for this reaction was postulated which is consistent with the experimental observations. The ketone, 2-(3-cyano-l-naphthylmethyl)benzophenone was prepared by the reaction of the corresponding chloro ketone with cuprous cyanide in N-methylpyrrolidone. 6-Cyano-7-phenylbenz[a]- anthracene was also produced in small quantity in this reaction as a consequence of the presence of the corresponding chloro compound in the ketone prior to reaction. Naphtho[3, 2, l-fg]naphthacen-9-one was prepared by the treatment of 6-cyano-7-phenylbenz[a]anthracene with a hydrobromic and acetic acid mixture at 180°, and also by the treatment of the precursor cyano ketone with polyphosphoric acid. The novel use of polyphosphoric acid in cyano group hydrolysis is discussed. Phenalo[2, 3, 4, 5-defg]naphthacene-4, 8-quinone was prepared by the treatment of 6-cyano-7-(2-carboxyphenyl)benz[a]anthracene with a hydrobromic and acetic acid mixture at 180°. An attempted procedure for the. preparation of this quinone involved the oxidation of 7-(2,6-dimethylphenyl)benz[a]anthracene to the corresponding diacid with aqueous sodium dichromate. Unfortunately this new method of oxidation failed in this case. The partial resolution of 7-(2-carboxyphenyl)-benz[a]anthracene was achieved with the use of brucine. Only one optically active isomer was obtained, and this was racemized by treatment with boiling ethanol. An empirical rule used to quantitatively determine the resistance of optically active biphenyls to racemization was applied to this acid, and the experimental observations were supported. During the course of this investigation, sixteen new compounds were prepared and were all properly characterized, except 6-cyano-7-(2-carboxyphenyl)- benz[a]anthracene, which did not give acceptable analytical data. The reason for this is discussed. Infrared and ultraviolet spectra of all new compounds were recorded. Infrared spectral observations were made which gave further support to the assigned structures of the isomeric compounds naphtho[3,2,l-fg]- naphthacen-9-one and dibenzo[hi,l]chrysen-9-one. / Doctor of Philosophy

Poly(arylene ether phosphine oxide)s (PEPO) are a recently identified subset of an important macromolecular series which includes industrially important high performance thermoplastics, such as the polysulfones, e.g. UDEL@ and polyether ketones, e.g. PEEK@, PEKK@, etc. The PEPO materials show an elevated glass transition temperature, high thermal and oxidative stability, improved solubility, and increased flame resistance. It has been demonstrated that a variety of metal salts including metals such as iron, zinc, cobalt, and copper, can be complexed at a molecular level with the phosphoryl group in films of these polymers producing novel transparent metal/polymer "composites". A procedure for obtaining homogeneous films from solutions of the metal halide complexed polymers has been developed. FTIR experiments as well as Tl phosphorus (31 P) NMR measurements were conducted to demonstrate the existance of metal complexation in the solid state. The effect of the chemical composition of the chain, type of metal salt, molar concentration of the metal salt, and heating cycle were investigated and found to influence properties of the films such as solubility, glass transition temperature, thermal stability, and storage mexiulus. Additionally, linear poly(arylene ether phosphine oxide)s were reduced to different extents to the corresponding phosphine containing polymers. Properties such as intrinsic One of these phosphine polymers was subsequently used in the generation of a rhodium catalyst for the hydroformylation of octene-l. The utilization of polymer-supported catalysts has important advantages such as catalyst recovery and the ease of separation of the product. The catalyst activity of the polymeric rhodium complex was studied as a function of reaction time as well as ligand to rhodium ratio. For a phosphorus/rhodium ratio of two these heterogeneous catalysts suffer in tenns of reaction rate in relation to their homogeneous counterparts. However, at phosphorus/rhodium ratios of approximately eight the reaction is almost quantitative after three hours, and the selectivity is greatly improved over that of monomeric homogeneous catalysts for the same P/Rh ratio. / Master of Science

The prenatal period of development is uniquely susceptible to lasting harmful health effects from exposure to environmental toxicants. Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants which have a wide variety of associated health effects, including impaired neurodevelopment when exposure occurs in-utero. While a handful of mechanisms have been implicated in PAH neurodevelopmental toxicity, none fully resolve the intricate biological processes that contribute to these outcomes. Mitochondria are increasingly being studied as sensitive targets of many environmental toxicants including PAHs. Despite the known mitochondrial sensitivity to PAHs, and the role of mitochondrial functions in neurodevelopment, little research has been done to evaluate mitochondrial dysfunction as mechanism of PAH neurodevelopmental toxicity. The work of this dissertation seeks to investigate a number of questions on this topic using a wide variety of techniques. We study exposure sources of individual PAHs, the relationship between prenatal PAH exposure constituents and mitochondrial functional outcomes and mitochondrial DNA copy number (mtDNAcn) in multiple biospecimens, including windows of exposure. We employ both epidemiological and experimental techniques, leveraging the advantages of one approach against the weakness of another to draw robust conclusions. Chapter 2 begins by comprehensively studying the demographic and behavioral variables predictive of personal PAH exposure. We combined a significant amount of personal exposure data collected using silicone wristbands with prenatal questionnaires to identify variables most predictive of both exposure to individual PAH compounds and total exposure. This work revealed complex relationships between multiple parameters in the prediction of each individual PAH. We found demographic and socioeconomic variables to be the most common predictors of exposure, followed by behavior variables. This work provides the foundation to identify pathways to reduce exposure and protecting the most vulnerable populations. In chapter 3, we describe two epidemiological studies conducted in Northern Manhattan birth cohorts. The first study uses data from the Columbia Center for Children’s Environmental Health (CCCEH) Fair Start cohort. We measured mitochondrial DNA copy number (mtDNAcn) in umbilical cord tissue, a novel biospecimen with unique utility due to its ease of acquisition and homogenous cellular composition. We measured individual exposure to 63 PAH compounds using silicone wristband samplers and analyze this data using both individual models and quantile G computation to estimate the overall mixture effect. We identified three compounds associated with mtDNAcn in individual models, and a positive association between the mixture of 19 compounds and mtDNAcn. In the second study we expanded upon previous analyses in the CCCEH Mothers and Newborns cohort which had demonstrated an association between summed-total prenatal exposure to 8 carcinogenic PAHs and scores on the Bayley Scale of Infant Development-II at age 3. We used measures of mtDNAcn in umbilical cord blood to evaluate the role of mitochondrial toxicity in PAH neurodevelopment and improved upon prior studies by including adjustment for cell type composition. We utilized both traditional linear model approaches as well as quantile G computation to evaluate the mixture both as a sum-total and using newly developed mixture methods. We determined that while prenatal PAH exposure was negatively associated with umbilical cord blood mtDNAcn using mixtures methods mtDNAcn was not associated with neurodevelopment. The bidirectional effect of prenatal PAH exposure on mtDNAcn between these two studies reveals the complexity of mtDNAcn as a biomarker and the need for more direct measures of mitochondrial functions in the study of PAH neurodevelopmental toxicity. Chapter 4 seeks to complement the epidemiological research with an experimental system. Using mouse preimplantation embryos, we measured the effect of exposure to an environmentally relevant mixture of PAHs on morphological development, superoxide production, mitochondria membrane potential, and mtDNAcn. We found exposure to low levels of a PAH mixture from days 2.5-3.5 post fertilization caused a significant decrease in healthy embryo morphology and a reduction in mtDNAcn. PAH exposure increased mitochondrial membrane potential under several dosing regimens while the effect on superoxide levels was variable and potentially mediated by changes in mitochondrial mass. As a whole these results indicate mitochondrial dysfunction as a result of low-level PAH exposure during the earliest periods of development with a window of heightened susceptibility immediately prior to implantation. In chapter 5 we evaluate the relative mitochondrial potency of the 8 commonly studied carcinogenic PAHs and an environmental relevant mixture of those 8 compounds. Using human umbilical cord mesenchymal stem cells, we specifically study these effects in the context of prenatal development. Superoxide production, mitochondrial membrane potential, mitochondrial mass, cell death and mtDNAcn was quantified at 9 doses for each exposure. This data was used to fit dose response curves and determine relative potency of each exposure/outcome endpoint. We identified benzo[k]fluoranthene and chrysene among the most toxic compounds analyzed and noted differences between relative mitochondrial toxicity and carcinogenicity of these constituents emphasizing the need for continued research into the non-cancer endpoints of PAH exposure. With the intentional comparable exposures and outcomes utilized in these studies comes the opportunity to make connections and draw conclusions across chapters to arrive at four major conclusion: (1) Demographic variables, not behavior, are most predictive of exposure to many PAH compounds (2) prenatal PAH exposure affects multiple measures of mitochondrial functions, (3) there is variability in the susceptibility during early development, and (4) the developmental mitochondrial toxicity of previously studied PAH compounds does not follow the same patterns of relative potency seen in carcinogenesis. This work provides significant insight into the impact of prenatal PAH exposure on mitochondrial functions while highlighting critical areas for further research. More studies are needed to fully understand the mechanisms and long-term effects of PAH exposure on early development, as well as to identify effective interventions to mitigate these risks.

No / This study aims to determine the concentration of 16 Polycyclic Aromatic Hydrocarbons (PAHs) in urban soils from Leeds in order to determine what the factors are controlling their distribution and abundances. Soil samples were collected across an area from Leeds. Gas chromatography with mass spectrometry (GC-MS) using selected ion monitoring (SIM) was used to identify and quantify PAHs in the soil samples with the aid of PAH external standards. The results showed the highest concentrations of total PAHs in sample L8 (1344 ng/g) taken from an area located near a parking site and road in Leeds and the lowest total concentration of the 16 PAHs in sample L16 (87 ng/g) taken from a private garden. The ratio of anthracene to anthracene plus phenanthrene AN/(AN + PH), fluoranthene to fluoranthene plus pyrene FLU/(PY+FLU) and benzo[a]anthracene to 228 (BaA/228) implied that the PAHs pollution originated from pyrogenic, biomass and petroleum combustion in the samples which were collected from Leeds city.

Yes / This study aims to determine the concentration of 16 Polycyclic Aromatic Hydrocarbons (PAHs) in urban soils from Leeds in order to determine what the factors are controlling their distribution and abundances. Soil samples were collected across an area from Leeds. Gas chromatography with mass spectrometry (GC-MS) using selected ion monitoring (SIM) was used to identify and quantify PAHs in the soil samples with the aid of PAH external standards. The results showed the highest concentrations of total PAHs in sample L8 (1344 ng/g) taken from an area located near a parking site and road in Leeds and the lowest total concentration of the 16 PAHs in sample L16 (87 ng/g) taken from a private garden. The ratio of anthracene to anthracene plus phenanthrene AN/(AN + PH), fluoranthene to fluoranthene plus pyrene FLU/(PY+FLU) and benzo[a]anthracene to 228 (BaA/228) implied that the PAHs pollution originated from pyrogenic, biomass and petroleum combustion in the samples which were collected from Leeds city.

Yes / Ynamide, is an understudied but attractive class of alkynes, activated by the donating ability of the nitrogen adjacent to alkynes. With the nucleophilicity on β-carbon and the electrophilicity on α-carbon of ynamides, this review summarizes the syntheses of ynamides and miscellaneous reactions - oxidation, rearrangement, cyclization, and cycloaddition to construct complicated heterocyclic rings. The synthetic methodologies were further applied into natural products synthesis, e.g. marinoquinolines A and C, aplidiopsamine A, rigidin A, and 7-azaserotonin derivative. / We thank National Science Foundation of China (NSFC) (21462004), State Key Laboratory for the Chemistry and Molecular Engineering of Medicinal Resources (CMEMR2014-A04), 2015 GXNSFBA (139032), GXNU, and Newton International Fellowship granted by Royal Society.

We investigated the modifying effects of ultraviolet (UV) light and chemical dispersant (Corexit 9500A) on crude oil toxicity in juvenile mysids (≤ 24 h) (Americamysis bahia) and larval red drum (24-72 hpf) (Sciaenops ocellatus). These results demonstrate that crude oil toxicity significantly increases with co-exposure to environmentally relevant UV levels in both species, indicating photo-induced toxicity. This toxicity was further exacerbated by the application of chemical dispersants which increased the dissolution and concentration of oil-derived polycyclic aromatic hydrocarbons (PAHs) in test solutions. To better understand the mechanisms and initiating events of this observed photo-induced toxicity, the incidence of apoptotic cell death and global transcriptomic changes were assessed in larval red drum (24-72 hpf) following co-exposure to crude oil and UV. These results showed that co-exposure to UV and low concentrations of crude oil (<1 µg/L ∑PAH50) induced apoptotic cell death in skin and eye tissue and altered transcriptomic pathways related to visual processing and dermatological disease. To link these cellular and molecular impacts of photo-induced toxicity to apical endpoints of ecological performance, sublethal impacts to growth, metabolic rate, and visually mediated behaviors were explored in larval red drum at 2 developmental stages. These results suggested that earlier life stages may be more sensitive to photo-induced toxicity and that growth and development, particularly of sensory systems, can be sensitive targets of photo-induced toxicity. Together, these studies provide novel insights into the photo-induced toxicity of crude oil in aquatic organisms and can be used to inform future ecological risk assessments.