Chapter 1.This chapter investigates the direct behavioral impact of information-based regulations by examining the effect of ozone alerts on cycling trips in Sydney. Moreover, the dynamics of individuals' response is studied by examining the behavioral impact of two successive day ozone alerts on cycling demand. A common problem in estimating direct avoidance behavior is that an increase in the pollution level could be an endogenous response to alerts. While controlling for the endogenous effect of alerts and air quality, results show that cycling trips decrease by 35 percent in response to a smog alert. When alerts are issued for two successive days, however, individuals appear to neglect the second day alerts. Our findings also indicate that ozone alerts induce one and half times larger impacts on weekends compared to weekdays. These patterns suggest that the cost of cycling substitution for commuter goals is higher than leisure goals. Furthermore, the cost of intertemporally avoiding cycling is increasing over time. Chapter 2. If decisions with lasting consequences are influenced by extraneous or transient factors then welfare can be damaged. This chapter investigates the impact of outdoor temperature on high-stakes decisions (immigration adjudications) made by professional decision-makers (US immigration judges). In our preferred specification, which includes spatial, temporal and judge fixed effects, and controls for various potential confounders, a 10 F degree increase in case-day temperature reduces positive decisions by 6.55%. This is despite judgements being made indoors, `protected' by climate-control. Results are consistent with established links from temperature to mood and risk appetite and have important implications for evaluating the welfare-burden of climate change. Chapter 3. The carbon tax in the Canadian province of British Columbia is widely-regarded as a `poster child' application of market-based methods to address greenhouse gas emissions. However the implications for local air quality have been ignored. Using synthetic control and difference-in-difference methods, in this chapter we evidence a causal link from carbon tax implementation and level to increased nitrogen oxides NOx and ultra-fine particulates PM_2.5 pollution problems in Vancouver, the province's largest city. We provide evidence consistent with the mechanism working through induced switching from gasoline to diesel vehicles. The results prove highly robust to inclusion of a wide set of controls in various combinations, alternative specifications, and satisfy a set of falsification checks. The analysis points to the possibility of negative secondary effects of climate policies, contrary to the usual presumption that secondary benefits are inevitably positive.

M.Sc. / This study is an investigation of environmental impacts caused by airborne fluorides around an industrial uranium and chemical facility in South Africa, the Necsa Pelindaba site. The literature study in Chapter 2 illustrates that industrial atmospheric fluoride emissions can have negative environmental impacts, including accumulation in surface soil horizons, necrosis in leaves, and fluorosis in plants and animals. Fluorides from this site are from two sources – stacks and evaporation pans. Samples to measure fluoride concentration in air, soil and vegetation and deposition rate were taken and analysed from February to August 2007. Standard analytical methods were used for the analysis of fluorides in all samples. Evaluation of historical environmental monitoring at Pelindaba showed that stack emissions were high in the year 2002 followed by a dramatic decrease in 2003 and 2004. In 2005, there was a sharp increase in emissions, with further slight increases until August 2007. For all media and sample types taken (air concentration, deposition, soil and vegetation), samples from nearby the evaporation pans had the highest fluoride concentrations. Results from sampling sites close to the stacks were lower, but still well above off-campus background sites, and above values from Pelindaba sites distant from the stacks. Fluoride concentrations in animal bones from previous studies done at the site showed enhanced fluoride concentrations compared to control samples. The project hypothesis was that fluoride emissions from Necsa Pelindaba site do not have a negative impact on the environment. This hypothesis is proven correct to the extent that no off-site adverse impacts or concentrations were observed. Limited on-campus impacts were observed localised around the evaporation pans and to a lesser extent around the stacks. Airborne fluoride concentration values around the pans only were above the South African guideline values. Deposition values were highest around the pans. The only visible leaf damage attributable to fluoride was on a Karee tree ~50 m from the edge of the pan. Soil fluoride concentrations from the current study were within the range of natural fluoride concentrations in soil. Despite evidence of local deposition, there was no evidence of fluoride accumulation in surface or subsurface soils. No impacts were observed elsewhere around the site or off-site. Based on the results of this work, fluoride emissions from the stacks do not pose a threat to the environment, provided that efficiency of the gas scrubbing equipment is maintained at current levels. Emissions from the pans pose a minor localised problem that nevertheless requires investigation and mitigation.

Over the past decade there has been a substantial increase in evidence suggesting an increased risk of adverse pregnancy outcomes from ambient air pollution exposure. However, there is yet to be enough convincing evidence to confirm a causal link between specific air pollutants and adverse pregnancy outcomes. The objective of this project was to address the paucity of evidence from the UK on the risk from air pollution in pregnancy. The research aim was to investigate the effects of ambient air pollution on adverse pregnancy outcomes using retrospective birth outcome data from the ‘North West Perinatal Survey Unit’ (NWPSU) during the period 2004 to 2008.In addition, primarily to determine the most appropriate exposure estimation method, a prospective comparison study (n=85) was performed to compare personal measurements of nitrogen oxides (NOx) and specifically nitrogen dioxide (NO₂) with commonly used exposure estimation techniques. This study informed two further studies which quantified the effects from air pollution in pregnancy using a large retrospective cohort from the NWPSU. The first, investigated the effects of maternal residential proximity to major roads on low birthweight (LBW), small for gestational age (SGA) and preterm birth (PTB). The second, investigated the effects of NOx, NO₂, carbon monoxide (CO) and particulate matter (PM₂.₅ and PM₁₀) based on estimates from a novel spatio-temporal air pollution model and stationary monitor sites on SGA, PTB and mean birth weight change. Linear and logistic regression models were used to quantify the risk of adverse pregnancy outcomes from living in close proximity to a major road and to specific ambient pollutants. Odds ratio (OR) associations and mean birth weight change were calculated for each of the pollutants with exposure averaged over the entire pregnancy and for specific pregnancy periods to establish critical windows of exposure. Models were adjusted for maternal age, ethnicity, parity, socio-economic status, birth season, body mass index and smoking. No statistically significant associations were found between living <200m from a major road and adverse pregnancy outcomes. Based on the spatio-temporal modelled air pollution estimates, an increased risk of SGA was found in later pregnancy with NO₂ (OR=1.14, 95%CI= 1.00-1.30), CO (OR=1.21, 1.02-1.42), PM₂.₅ (OR=1.10, 1.00-1.21) and PM₁₀ (OR=1.12, 1.00-1.25). This study provides additional evidence that women exposed to high air pollution concentrations in pregnancy are at an increased risk of an SGA birth, but not for PTB. However, there was no evidence of an effect on SGA for exposures below the current legal air quality limits.

No description available.

No description available.

There is increasing evidence indicating that exposure to air pollutants may be associated with the onset of several respiratory diseases such as allergic airway disease and chronic obstructive pulmonary disorder (COPD). Many lung diseases demonstrate an outgrowth of pathogenic bacteria belonging to the Proteobacteria phylum, and the incidence of occurrence of these diseases is higher in heavily polluted regions. Within the human body, the lungs are among the first to be exposed to the harmful effects of inhaled pollutants and microbes. Research in the past few decades have expounded on the air-pollution-induced local and systemic inflammatory responses, but the involvement of the lung microbial communities has not yet been well-characterized. Lungs were historically considered to be sterile, but recent advances have demonstrated that the lower respiratory tract is replete with a wide variety of microorganisms - both in health and disease. Recent studies show that these lung microbes may play a significant role in modulating the immune environment by inducing IgA and mucus production. Air pollutants have previously been shown to alter intestinal bacterial populations that increase susceptibility to inflammatory diseases; however, to date, the effects of traffic-generated air pollutants on the resident microbial communities on the lungs have not been explored. The microbiome is influenced by several factors, including diet and environmental exposures. A large percentage of the Western world population consumes a high-fat (HF) diet which has resulted in the epidemic of obesity. Consumption of an HF diet has been shown to alter the intestinal microflora and increase baseline inflammation. We aimed to understand whether diet might also contribute to the alteration of the commensal lung microbiome, either alone or related to exposure. Thus, we investigated the hypothesis that exposure to air pollutants can alter the commensal lung microbiota, thereby promoting alterations in the lung's immune and inflammatory responses; in addition to determining whether these outcomes are exacerbated by a high fat-diet. We performed two studies with exposures to different components of air pollutant mixtures on C57Bl/6 mice placed on either a control (LF) diet or a high-fat (HF) diet. Our first exposure study was performed on C57Bl/6 mice with a mixture of gasoline and diesel engine emissions (ME: 30 µg PM/m3 gasoline engine emissions + 70 µg PM/m3 diesel engine emissions) or filtered air (FA) for 6h/d, 7 d/wk for 30 days. The ME study investigated the alterations in immunoglobulin A (IgA), IgG and IgM, and lung microbiota abundance and diversity. Our results revealed ME exposures alongside the HF diet causes a decrease in IgA and IgG when compared to FA controls, thereby decreasing airway barrier protection. This was accompanied by the expansion of bacteria within the Proteobacteria phylum and a decrease in the overall bacterial diversity and richness in the exposed vs. control groups. In our second study, we exposed C57Bl/6 mice to only the diesel exhaust particle component (35µg DEP, suspended in 35µl 0.9% sterile saline) or sterile saline only (control) twice a week for 30 days. We investigated immunoglobulin profiles by ELISA that revealed a significant increase in IgA and IgG in response to DEP. We also observed an increase in inflammatory tumor necrosis factor (TNF) - α, Interleukin (IL) -10, Toll-like receptors (TLR) - 2,4, nuclear factor kappa B (NF-κB) histologically and by RT-qPCR. Mucus production and collagen deposition within the lungs were also significantly elevated with DEP exposures. Microbial abundance determined quantitatively from the bronchoalveolar lavage fluid (BALF) by qPCR revealed an expansion of bacteria belonging to the Proteobacteria phylum in the DEP exposed groups on the HF diet. We also observed an increase in reactive oxygen and nitrogen species (ROS-RNS) products (nitrates), within the groups that revealed an expansion of Proteobacteria. These observations are most likely due to the unique metabolic capabilities of Proteobacteria to proliferate in inflammatory environments with excess nitrates. We assessed if treatments with probiotics could attenuate the DEP-induced inflammation by supplementing a separate group of study animals on the HF diet with 0.3 g/day of Winclove Ecologic® Barrier probiotics in their drinking water throughout the study. With probiotic treatments, we observed a significant decrease in ROS-RNS that was accompanied by complete elimination of Proteobacteria suggesting that in the absence of nitrates, the expansion of Proteobacteria is curbed effectively. We also observed a decrease in proinflammatory TNF-α and collagen deposition with probiotic treatments, and an increase in IgA levels within the BALF, suggesting that probiotics aid in balancing proinflammatory responses and enhance beneficial immune responses to efficiently mediate the DEP-induced inflammation. Both studies showed that air pollutants alter the immune defenses and contribute to lung microbial alterations with an expansion of Proteobacteria. The immunoglobulin profiles discordant between the two studies can be explained by the route and/or duration and composition of air pollutant exposure. Collectively these studies suggest that exposure to air pollutants alter immune responses and/or increase the availability of inflammatory by-products within the lungs that can enable the selective outgrowth of pathogenic bacteria. The observed detrimental outcomes are further exacerbated when coupled with the consumption of an HF diet. Importantly, these results may shed light on the missing link between air pollution-induced inflammation and bacterial expansion and also point to therapeutic alternatives to curb bacterial outgrowth in lung disease exacerbations observed in patient populations living and/or working in heavily polluted regions.

No description available.

published_or_final_version / Urban Planning and Environmental Management / Doctoral / Doctor of Philosophy

Yau Yat Man. / Bibliography: leaves 124-129 / Thesis (M.Phil.) -- Chinese University of Hong Kong, 1983

Graduation date: 2005