published_or_final_version / Public Health / Master / Master of Public Health

published_or_final_version / Public Health / Master / Master of Public Health

published_or_final_version / Public Health / Master / Master of Public Health

Objective: To present a systematic review of existing literature that investigates biological plausibility of prenatal hazardous air pollutants’ (HAPs) exposure, in the etiology of autism spectrum disorder (ASD) and related outcomes. Method: Electronic databases Pubmed, Biomed Central and National Database for Autism Research, and grey literature pertaining to air pollution association with ASD and related outcomes were searched using specific keywords. The search included 190 HAPs as defined by The Clean Air Act Amendments of 1990 [U.S.Environmental Protection Agency (EPA) 1994] including air pollutants CO, SO2, NOx, O3 and Particulate Matter (PM). Studies selected for systematic review were assessed on quality and causality. Result: Total of 628 articles from electronic search and 16 articles from grey literature were retrieved. 12 studies that cleared the inclusion and exclusion criteria were systematically reviewed using the PRISMA checklist. Outcomes considered included ASD, Attention Deficit Hyperactivity Disorder, social behavior, social interaction, child behavior, communication, cognitive development, attention problems, mental and psychomotor development, and social competence. Studies were from two countries, United States of America and Spain. Study design was case control and cohort study. Follow up duration for cases ranged from in-utero to less than 9 years. Exposure was measured in ambient air using predictive models and cord blood. Although there were discrepancies in the studies, related to strength of association, analysis and covariates adjusted, the association between air pollution and ASD related outcomes could not be dismissed. Most studies lacked information on blinding when quality was assessed and lacked consistency when assessed on causality, while scored well on temporality and biological plausibility. Discussion: Evidence suggests HAPs are capable of transplacentally affecting cognitive function, especially traffic related pollutants. Study design, sample size, response rate, exposure misclassification, failing to adjusting covariates related to lifestyle, nutrition and other chemical exposures have influenced the estimates and the strength of association. Shortcomings of this review are the English language restriction and single reviewer on study selection process and assessments. Immuno-toxic, neuro-toxic and endocrine disrupting properties of these HAPs necessitates comprehensive prospective studies especially in Hong Kong with the rising prevalence of ASD and ever high reported air pollution indexes. Conclusion: Repeated studies were carried out on the same cohorts and studies were concentrated in U.S.A. On account of a lack of consistency, it is difficult to confirm whether air pollution is a plausible candidate for prenatal exposure in ASD. (Abstract of 391 words) / published_or_final_version / Public Health / Master / Master of Public Health

Objective To investigate whether traffic pollutants have any effect on human cognitive functions and behavior by performing a systematic review on existing research studies. Methods Research articles were identified through four databases – CINAHL Plus, Academic Search Premier and MEDLINE via EBSCOhost and Pubmed using the online electronic resources of the libraries of the Hong Kong University. A total of 119 articles from Pubmed and 86 articles from EBSCOhost were identified, and 72 and 64 studies after limits were applied. The studies used a variety of measures to assess the effects of traffic-related air pollution and cognitive functions and behaviors in both children and adults. Results There were 19 articles in total in the systematic review – 13 on children (aged from 1- 17 years) and six on adults (aged from 26 - 83.5 years). Data were employed from nine different countries. Although there were some discrepancies in the results, there was evidence of the effects of traffic-related air pollution on the brain. Conclusions The causal relationship between traffic-related air pollution and cognitive decline cannot be clearly determined. The systematic review however, generated evidence to support the hypothesis that traffic-related air pollution may affect cognitive development in children, increase risks of behavioral disorders in both children and adults, and increase the rate of cognitive decline in older adults. As a result, this systematic review suggests that the research findings have important implications in the development of public health policy and practice. / published_or_final_version / Public Health / Master / Master of Public Health

Background Epidemiological studies have shown that air pollution was associated with both mortality and morbidity of various diseases including cardiovascular diseases, respiratory diseases and cancers. However, the various traffic-related exposure indicators are difficult to compare due to the diversity of study areas, populations, measures of traffic exposures and confounders. Moreover, most of the studies were conducted in the western and European countries. Few studies using the traffic density as surrogate of traffic-related exposure for effects on mortality risk have been performed in Asia and none has been performed in Hong Kong. Objective This study aims to assess the association between the traffic-related exposure and the all-cause and cause-specific mortality risk in the densely populated city of Hong Kong, where traffic emission plays an important role on the ambient air quality. Methods Three traffic-related indicators were employed including: Road Density (RD) in terms of total length of roads divided by Tertiary Planning Unit (TPU) area; Traffic Density (TD) defined by road lengths times the Annual Average Daily Traffic (AADT) and divided by the TPU area; and Vehicle Density (VD) means average AADT over TPU area. Each exposure was divided into three groups according to tertiles. An ecological study was conducted first with population census and mortality data. The age-sex standardized all-cause and cause-specific mortality rate was calculated for each TPU with the whole Hong Kong death rate in 2010 as the standard. Poisson regression models were performed to estimate risks of traffic-related exposure with adjustment of the marital status, race, education, housing tenure, and median household income. After the TPU-level analyses, a cohort with 64,888 elderly subjects being followed up from 1998 to 2012 was used to assess the association with further control for the individual-level factors including age, sex, education, income, housing, and smoking. The Multilevel Cox proportional regression models were built with adjustment for both the individual level confounders and TPU-level covariates. Excess risks from both models were reported. Results Higher exposure areas were found in the northern part of Hong Kong Islands and the inner city of Kowloon peninsula. Statistically significant association between traffic-related exposure and mortality was observed. For the investigation in the general population, the all-nonaccidental cause mortality was associated with 43% (95% confidence interval 37-48%) and 50% (44-56%) excess risk for areas with the middle and high level TD exposure compared with the low level group. The association was similar with measures of RD and VD. For the cause-specific mortality, the respiratory deaths showed a higher risk when compared with the cardiovascular and cancer deaths. For the elderly subjects, the excess risk of all-nonaccidental causes relative to the low level exposure of 13% (1-26%) and 12% (0-25%) for the middle and high level exposure were smaller when compared with the risk in the general population. Conclusion There is an association between traffic-related exposure and mortality in the general and older population of Hong Kong. In future comprehensive investigations with the individual-level exposure measure are needed. Assessment on the younger population should also be studied. / published_or_final_version / Public Health / Master / Master of Philosophy

Objective Large quantities of epidemiological studies manifest that indoor and outdoor air pollutants may trigger and aggravate asthma symptoms, whose mechanism, however, has not been completely made clear yet. As shown by the result of the experiment in which in-vitro cells and animals are exposed to high-density air pollution, the triggering effect of air pollution on asthma is associated with inflammatory reaction, IgE expression and regulation pathways. However, there is a lack of evidence from population studies to support that association. This study plans to conduct continuous monitoring over indoor and outdoor air pollutants facing the asthmatic children from Beijing with a view to carry out an overall assessment of their exposure to air pollutants. Meanwhile, biomarkers which are directly reflecting airway inflammation as well as the signal molecules which are related to IgE expression and regulation are monitored. The next step is to establish an exposure-effect relationship to explore the trigger effect of air pollutants on childhood asthma. Methods 1. Questionnaires were used to collect general information (including age, drug use, indoor home decoration, passive smoking, diet during the study, indoor mildew, allergic history, history of diseases and family heredity history) in 60 asthmatic children (males, Han nationality, aged 5 to 14 years)from Beijing who were recruited into this study. 2. A comprehensive evaluation was conducted on their exposure levels of air pollutants by continuous monitoring of indoor PM2.5, black carbon, benzene, toluene, xylene and formaldehyde in their houses and collecting monitoring data with respect to PM2.5, PM10, NO2and SO2at air quality monitoring sites near their houses. Benzene, toluene and xylene were measured by two-stage thermal desorption-gas chromatography (GC), formaldehyde by AHMT spectrophotometry, mass concentration of PM2.5by gravimetric method, black carbon in PM2.5by multi-wavelength absorption spectroscopy. The concentration data of ambient outdoor air pollutants were available from the real-time air quality publishing platform of Beijing Municipal Environmental Monitoring Center. 3. Exhaled FeNO of asthmatic children were taken as biomarkers reflecting their airway inflammation. FeNO was measured by electrochemical method (off-line monitoring). 4. Trigger effect of air pollution on IgE signaling pathway of asthmatic children was investigated by determining signal molecules of two signaling pathways related to IgE expression and regulation in peripheral serum. Signal molecules were determined by ELISA. 5. Confounding factors were controlled by stratification analysis and multiple linear regression model, and a comprehensive analysis was conducted of the triggering effect of air pollution on children asthma. Results 1. During the research, as for subjects, concentrations of indoor PM2.5, BC, formaldehyde, benzene, toluene, m-, p-and o-xylenes were 55.3±29.9 μg/m3, 3.8±1.4 μg/m3,62.2±42.7 μg/m3, 13.1±15.9 μg/m3, 18.7±16.7 μg/m3, 7.9±7.9 μg/m3and 3.1±5.0 μg/m3, respectively. The7-day weighted average concentrations of outdoor PM2.5, PM10, SO2and NO2were 101.3±87.6μg/m3, 152.8±88.4μg/m3, 48.6±39.8 μg/m3and 63.1±27.7μg/m3, respectively. There was a significant correlation between 7-day weighted average concentrations of indoor and outdoor PM2.5 simultaneously (r=0.697, P<0.001), with a indoor/outdoor PM2.5concentration ratio (I/O ratio) of 0.86±0.39 (P25-P75ranging from 0.62 to 1.01). 2. After adjusting for such influencing factors as age, types of asthma, and season, analysis of all subjects found that FeNO was significantly positively correlated with either benzene in indoor air, or PM2.5, SO2and NO2 in ambient outdoor air. Separate analysis of subjects untreated with inhaled corticosteroids (ICSs) found that FeNO was significantly positively correlated with PM2.5, SO2and NO2 in ambient outdoor air, while this correlation was not significant in the ICS-treated group. 3. In serum, there was a significantly positive correlation between signal molecules in the two regulatory pathways of IgE expression. After adjusting for such influencing factors as age, types of asthma, and passive smoking. No effect of air pollutants on level of signaling molecule was observed in this study. Conclusion Monitoring results of indoor and outdoor air pollutants show that, at a high level of exposure to air pollutants, exposure of asthmatic children to indoor and outdoor air pollutants may cause or aggravate the airway inflammation. Administration of ICSs can control or attenuate the airway inflammation caused by air pollutants in asthmatic children, while the level of signaling molecule in the regulatory pathway of IgE expression in serum may not be an ideal marker for reflecting the trigger effect of air pollution on children asthma. / published_or_final_version / Public Health / Master / Master of Public Health

Thesis (MTech (Environmental Health)--Cape Peninsula University of Technology, 2007 / The widespread use of lead (Pb) and especially Pb from vehicular emissions arising from lead additives in petrol has resulted in high levels of this metal found in various soil samples taken along the road verges of Cape Town CBD. The accumulation of lead was investigated in roadside surface soil by collecting soil samples at various sites along the three major highways (N7, N2, N1), approximately three metres from the road verges and at a depth of approximately 5 cm for a period of 12 months. After digestion with 55"70 nitric acid the Pb concentrations were determined by using an Inductively Coupled Plasma Atomic Emission Spectrophotometer (ICP-AES). Results have shown the Pb concentrations in the soil at busy intersections to be higher than at other areas along the roadsides. Lead concentrations found in the roadside soils of the N1 ranged between 200 and 2000 mg/kg and these were of the highest concentrations found compared to the other two highways and were even higher than found in other studies. The roadside soils on the N1 highway, with the most traffic, according to car count data obtained, seemed more contaminated than the other two highways. It was also investigated whether earthworms (Eisenia fetida) accumulated Pb after being exposed to the contaminated soil from the sampling sites. The earthworms in the highly contaminated soil accumulated on average much higher concentrations of Pb than the earthworms in the lower Pb contaminated soil. A potential biomarker (cell membrane integrity) was applied to determine whether the earthworms experienced toxic stress as a result of the exposure to lead contaminated soil. Behavioural and morphological changes in the earthworms were also observed. The Trypan blue exclusion assay was used to measure the effect of lead exposure on the membrane stability of the coelomocytes in the coelomic fluid of earthworms. In the highest exposure groups per highway, a significant decrease in percentage viable cells were seen (N7, 36 ± 0.07%; N2 48 ± 0.09%; N1, 34 ± 0.08%). The fact that clear statistically significant responses were seen after the five week exposure period in the highest, as well as lowest exposure groups indicate that these responses could serve as an early warning system of lead exposure. The percentage cell viability (biomarker) used in this study have been useful in identifying toxic stress in earthworms caused by lead in roadside soils. The additional information obtained by using biomarkers could not be obtained by chemical analysis of soil and earthworms alone.

Approximately 3 billion people in developing countries rely on solid fuels for their cooking, heating and lighting needs (Smith 2000). Household air pollution (HAP) from the incomplete combustion of these fuels constitutes the fourth leading risk factor for death and morbidity worldwide, and the number one risk factor for disease burden in some developing nations, including Ghana (Lim et al. 2013; Institute for Health Metrics and Evaluation 2016). While research shows biomass fuel combustion presents a significant global health and environmental burden, no regional, national or global policies have been enacted to reduce fine particulate matter (PM2.5) and black carbon (BC) emissions from cooking with biomass fuels. More data on personal exposures to particulate matter and BC from cooking with biomass are needed across geographic areas to assess whether exposure is mediated by (cultural) cooking customs, practices and behaviors. These data are critical in informing improved cookstove design as well as policies aimed at reducing harmful emissions and exposures from biomass smoke. The overall objective of this proposal is to examine personal exposures to cooking and non-cooking sources of HAP, characterize the elemental composition of the fine particulate matter across two common biomass fuels (charcoal and wood), and assess acute respiratory symptoms in pregnant women cooking with biomass fuels in rural Ghana. Through aerosol monitoring of PM2.5, our goal is to identify and apportion sources of personal exposures borne by cooks in rural Ghana, in order to inform mitigation policies and intervention design to alleviate health burden associated with cooking with biomass fuels. Specifically, in Aim 1 we propose to measure personal exposures and kitchen air concentrations of PM2.5 and BC across cooking locations, (i.e. enclosed, semi-enclosed, outdoor) and assess cooking characteristics (e.g. fuel, kitchen type, ethnicity) as possible determinants of exposure. In Aim 2, we will characterize the elemental composition of personal and kitchen air samples across fuel and kitchen types. These two aims will allow us to assess cooking and non-cooking sources of personal HAP exposure based on air monitoring data, composition of the filters, and survey-based cooking characteristics/demographics. In Aim 3, we propose to characterize the prevalence of adult respiratory symptoms in 1183 pregnant women in the region, and assess associations between personal exposure, measured by personal carbon monoxide (CO), and other cooking and non-cooking determinants of personal exposure, including fuel type, years cooked, kerosene lamp, mosquito coils, and charcoal production.

Background There have been many multicity studies assessing health effects of the population’s exposure to PM10. They assume that there is homogeneous exposure to PM10 and the monitoring locations are representative of the population’s exposure. In a densely urban environment, like Hong Kong, street canyons are common and could alter PM10 exposure. The horizontal and vertical dispersion of PM10 in the urban environment is complex due to the interactions of street geometric, metrological and pollution source conditions. The airGIS/OSPM is a box and plume mathematical model which was designed to model this complex dispersion of PM10. Objectives This study aims to utilize the airGIS/OSPM to assess how the health impact is affected by the misclassifications of within city air pollution exposure. This helps assessing the feasibility of using the airGIS/OSPM in health studies. Methods The airGIS/OSPM was used for an urban area of Hong Kong, in the north west of Kowloon Peninsular for a period from 1998 to spring 2011. PM10 concentration’s were estimated at field measurement points, an EPD roadside monitoring site, and subjects in a subset of the elderly healthcare center cohort and for all building addresses in the modeled area. The airGIS/OSPM was validated by conducting a PM10 measurement campaign over the winter of 2010 to 2011. Also validation was conducted using the measurements of the Mong Kok EPD roadside monitoring station. A pilot study using the time stratified case-crossover analysis was conducted to explore the effects of using the airGIS/OSPM to express the subjects’ short-term outdoor residential exposure to PM10 on all cause mortality. AirGIS/OSPM PM10 estimates were compared with ambient concentrations obtained from the EPD monitoring network. The population mean exposure was calculated using the airGIS/OSPM estimated PM10 concentration at all building address points from 2007 to 2009 at the ground level and at middle building height level. The airGIS/OSPM estimate was used to identify spatial variation of PM10 within the study area. Results The airGIS/OSPM estimated well the measured PM10 concentration from the field measurement campaign and the EPD Mong Kok station. The airGIS/OSPM estimate and the ambient measure for EHC subject exposure both found an odds ratio for all cause mortality there was no difference from unity between case and control times. The airGIS/OSPM derived mean PM10 concentration at the middle height of each building was 54.8μg/m3 while that at the all EPD was 54.4μg/m3. At ground level the airGIS/OSPM PM10 estimate was 58.35μg/m3 while that at the EPD was 54.41μg/m3. Conclusion The misclassification of PM10 was negligible at the middle of buildings, but for people regularly working in ground level microenvironments are often exposed to PM10 concentrations that are higher than those measured at EPD monitors. It is feasible to use the airGIS/OSPM model to estimate PM10 exposure. The small spatial variation in exposure means the airGIS/OSPM may not be appropriate in assessing the short-term PM10 exposure, but due to the larger effect size it might be important in long-term exposure assessment. / published_or_final_version / Community Medicine / Master / Master of Philosophy