No município de São Paulo, em 1970 foram relatados 169 casos novos de câncer de laringe, com uma taxa de incidência ajustada por idade pela população mundial de 25,5/100.000 (30-74 anos) e 299 casos em 1985, elevando a taxa para 37,6 (ambos nosexo masculino). O Tabagismo e o consumo de álcool são os fatores de risco mais bem estabelecidos para o câncer de laringe. Com relação aos fatores ocupacionais, o único carcinógeno estabelecido é a exposição à névoa de ácidos inorgânicosfortes. É proposto um estudo caso-controle de base hospitalar, para investigar e quantificar o papel da exposição ocupacional no desenvolvimento do câncer de laringe e é discutida uma nova proposta de avaliação de exposição que visa melhorar avalidade interna desse tipo de estudo / Laryngeal cancer comprises 3,1% of the new cases of cancer in men in the world, representing the tenth most common malign neoplasm for males. In São Paulo City, 169 new cases of laryngeal cancer were reported in 1970, representing 25,5/100.000 and 299 cases in 1985, increasing the rate to 37,6/100.000 (both for males, age standardized truncated rate, 30-74 years). The best established risk factors for laryngeal cancer are tobacco and alcohol. In respect to occupational factors, the only established carcinogen is exposure to strong inorganic acid mists. However, asbestos, pesticides, paints, gasoline and diesel engine emissions, dusts, among other factors are reported in the literature as occupational agents that increase the risk of laryngeal cancer. A hospital-based case-control study was conducted, in seven hospitals in São Paulo, to investigate occupational risk factors for laryngeal cancer. The study included 122 laryngeal cancers and 187 controls, selected by frequency matching on sex and age. Detailed information on smoking, alcohol consumption, and occupational history was collected. Occupational hygienists assessed the exposure to 49 agents. Odds Ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression, and were adjusted for sex, age, smoking and alcohol. Laryngeal cancer was associated with exposure to respirable free crystalline silica (OR 1,83, 95% CI 1,00 - 3,36), soot (from coal, coke, fuel oil, wood) (OR 1,78, 95% CI 1,03 - 3,03), fumes (OR 2,55, CI 95% 1,14 - 5,67) and to live animals (OR 1,80, 95% CI 1,02 - 3,19). This study showed that occupational exposures to: respirable free crystalline silica, soot (from coal, coke, fuel oil, wood), fumes and live animals are risk factors for laryngeal cancer.

by Chiu Yuk Lan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 127-133). / Abstract also in Chinese. / TABLE OF CONTENTS / ABSTRACT (ENGLISH) --- p.a / ABSTRACT (CHINESE) --- p.b / ACKNOWLEDGEMENTS --- p.iv / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Cancer in Food-service Workers --- p.1 / Chapter 1.2 --- Carcinogenicity of Cooking Fumes --- p.1 / Chapter 1.3 --- High Risk of Lung Cancer in Chinese Women --- p.2 / Chapter 1.4 --- Why do We Conduct This Study? --- p.3 / Chapter 1.5 --- Implication of This Study --- p.4 / Chapter 1.6 --- What Types of Cancer were Included in This Study? --- p.4 / Chapter 1.7 --- Aims and Hypothesis of This Study --- p.5 / Chapter 1.8. --- Outline of the Thesis --- p.5 / Chapter CHAPTER 2 --- LITERATURE REVIEW --- p.8 / Chapter 2.1. --- Occupational Epidemiological Studies --- p.8 / Chapter 2.1.1 --- Studies of occupation and cancer occurrence based on routine records --- p.8 / Chapter 2.1.2 --- Retrospective cohort studies among food service workers --- p.21 / Chapter 2.1.3 --- Case-control studies --- p.27 / Chapter 2.1.4 --- Case reports --- p.29 / Chapter 2.1.5 --- Summary --- p.29 / Chapter 2.2. --- Mutagens and Carcinogens in Cooking Fumes --- p.39 / Chapter 2.2.1 --- Mutagens and carcinogens in cooking fumes --- p.40 / Chapter 2.2.2 --- Summary --- p.42 / Chapter CHAPTER 3 --- METHODS --- p.44 / Chapter 3.1 --- Study Design --- p.44 / Chapter 3.2 --- Study Population and Subjects --- p.46 / Chapter 3.3 --- Reference Population --- p.48 / Chapter 3.4 --- Sample Size Estimation --- p.48 / Chapter 3.5 --- Data Sources and Data Collection --- p.49 / Chapter 3.6 --- Data Processing --- p.53 / Chapter 3.7 --- Data Analyses --- p.54 / Chapter 3.7.1 --- Standardised proportional mortality ratio (SPMR) --- p.54 / Chapter 3.7.2 --- Adjusted' SPMRs --- p.56 / Chapter 3.7.3 --- Mortality odds ratio (MOR) --- p.58 / Chapter 3.8. --- Exploring if Smoking could be a Confounding Factor --- p.62 / Chapter CHAPTER 4 --- RESULTS --- p.64 / Chapter 4.1 --- Characteristics of the Food-service Workers --- p.64 / Chapter 4.2 --- Cancer Mortality Patterns of Food-service Workers --- p.69 / Chapter 4.3 --- Adjusted SPMRs --- p.72 / Chapter 4.4 --- Mortality Odds Ratios (MORs) --- p.76 / Chapter 4.5 --- Mortality Odds Ratios Using Multiply Reference Diseases --- p.77 / Chapter 4.6. --- Comparing SPMRs with MORs --- p.82 / Chapter 4.7. --- Internal Comparison --- p.83 / Chapter 4.8 --- Summary of Results --- p.90 / Chapter 4.9. --- Survey on Smoking and Drinking Prevalence among Current Food-service Workers --- p.92 / Chapter 4.9.1 --- Smoking habit --- p.92 / Chapter 4.9.2 --- Drinking habit --- p.94 / Chapter CHAPTER 5 --- DISCUSSION OF FINDINGS --- p.95 / Chapter 5.1 --- Outcomes for This Study --- p.95 / Chapter 5.1.2 --- Cancer risks for the kitchen workers --- p.96 / Chapter 5.1.3 --- Cancer risks for the outside kitchen workers --- p.102 / Chapter 5.2 --- Limitations of the Methods Adopted in the Present study --- p.107 / Chapter 5.2.1 --- Standardised proportional mortality ratio (SPMR) --- p.107 / Chapter 5.2.2 --- Morality odds ratio (MOR) --- p.109 / Chapter 5.3 --- Bias and Control --- p.111 / Chapter 5.3.1 --- Selection bias --- p.111 / Chapter 5.3.2 --- Information bias --- p.113 / Chapter 5.3.3 --- Confounding --- p.116 / Chapter 5.4 --- Implications from the Results of the Present Study --- p.117 / Chapter 5.5 --- Conclusion --- p.119 / APPENDIX --- p.121 / Appendix 1 --- p.121 / Appendix 2 --- p.123 / Appendix 3 --- p.124 / Appendix 4 --- p.125 / REFERENCES --- p.127

Chan Siu-chung Andrew. / "December 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 120-136). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

No município de São Paulo, em 1970 foram relatados 169 casos novos de câncer de laringe, com uma taxa de incidência ajustada por idade pela população mundial de 25,5/100.000 (30-74 anos) e 299 casos em 1985, elevando a taxa para 37,6 (ambos nosexo masculino). O Tabagismo e o consumo de álcool são os fatores de risco mais bem estabelecidos para o câncer de laringe. Com relação aos fatores ocupacionais, o único carcinógeno estabelecido é a exposição à névoa de ácidos inorgânicosfortes. É proposto um estudo caso-controle de base hospitalar, para investigar e quantificar o papel da exposição ocupacional no desenvolvimento do câncer de laringe e é discutida uma nova proposta de avaliação de exposição que visa melhorar avalidade interna desse tipo de estudo / Laryngeal cancer comprises 3,1% of the new cases of cancer in men in the world, representing the tenth most common malign neoplasm for males. In São Paulo City, 169 new cases of laryngeal cancer were reported in 1970, representing 25,5/100.000 and 299 cases in 1985, increasing the rate to 37,6/100.000 (both for males, age standardized truncated rate, 30-74 years). The best established risk factors for laryngeal cancer are tobacco and alcohol. In respect to occupational factors, the only established carcinogen is exposure to strong inorganic acid mists. However, asbestos, pesticides, paints, gasoline and diesel engine emissions, dusts, among other factors are reported in the literature as occupational agents that increase the risk of laryngeal cancer. A hospital-based case-control study was conducted, in seven hospitals in São Paulo, to investigate occupational risk factors for laryngeal cancer. The study included 122 laryngeal cancers and 187 controls, selected by frequency matching on sex and age. Detailed information on smoking, alcohol consumption, and occupational history was collected. Occupational hygienists assessed the exposure to 49 agents. Odds Ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression, and were adjusted for sex, age, smoking and alcohol. Laryngeal cancer was associated with exposure to respirable free crystalline silica (OR 1,83, 95% CI 1,00 - 3,36), soot (from coal, coke, fuel oil, wood) (OR 1,78, 95% CI 1,03 - 3,03), fumes (OR 2,55, CI 95% 1,14 - 5,67) and to live animals (OR 1,80, 95% CI 1,02 - 3,19). This study showed that occupational exposures to: respirable free crystalline silica, soot (from coal, coke, fuel oil, wood), fumes and live animals are risk factors for laryngeal cancer.

Song, Qingkun. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 144-157). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

by Kai-Hang Choi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 217-232). / Abstract also in Chinese. / ABSTRACT --- p.i / ACKNOWLEDGMENT --- p.iv / TABLE OF CONTENTS --- p.v / LIST OF FIGURES --- p.viii / LIST OF TABLES --- p.xiii / Chapter CHAPTER I --- INTRODUCTION --- p.1 / Chapter 1.1 --- Background --- p.1 / Chapter 1.2 --- Role of GIS in Health Studies --- p.4 / Chapter 1.3 --- Research Objectives --- p.5 / Chapter 1.4 --- Organization of the Thesis --- p.6 / Chapter CHAPTER II --- LITERATURE REVIEW --- p.8 / Chapter 2.1 --- Introduction --- p.8 / Chapter 2.2 --- Human cancer --- p.8 / Chapter 2.3 --- Environment and Cancer --- p.10 / Chapter 2.4 --- Cancer Etiology and Epidemiology --- p.13 / Chapter 2.5 --- Observational Cancer Epidemiology --- p.15 / Chapter 2.6 --- Geography of Cancer --- p.17 / Chapter 2.7 --- Geographical Epidemiology of Cancer --- p.19 / Chapter 2.7.1 --- Geographical Variation in Cancer Occurrence --- p.21 / Chapter 2.7.1.1 --- Cancer Mapping --- p.24 / Chapter 2.7.1.2 --- Spatial Autocorrelation --- p.26 / Chapter 2.7.2 --- Identifying Causal Association --- p.29 / Chapter 2.7.3 --- Environmental Factors of Cancer --- p.31 / Chapter 2.8 --- Geographical Information Systems --- p.40 / Chapter 2.9 --- GIS and Health --- p.41 / Chapter 2.9.1 --- GIS Applications in Health Planning --- p.42 / Chapter 2.9.2 --- GIS Applications in Health Research --- p.43 / Chapter 2.10 --- Cancer Studies with GIS --- p.45 / Chapter 2.11 --- Conclusion --- p.47 / Chapter CHAPTER III --- THE STUDY AREA AND RESEARCH METHODOLOGY --- p.49 / Chapter 3.1 --- Introduction --- p.49 / Chapter 3.2 --- Disease Transition in Hong Kong --- p.49 / Chapter 3.3 --- Cancer in Contemporary Hong Kong --- p.52 / Chapter 3.3.1 --- Trends of Cancer Mortality and Incidence --- p.52 / Chapter 3.3.2 --- The Common Types of Cancer --- p.55 / Chapter 3.3.3 --- Geographical Variation of Cancer in Hong Kong --- p.58 / Chapter 3.4 --- The Research --- p.61 / Chapter 3.4.1 --- Cartographic Analysis --- p.62 / Chapter 3.4.2 --- Statistical Analyses --- p.63 / Chapter 3.4.3 --- Cancer Variables --- p.67 / Chapter 3.4.4 --- Environmental Variables --- p.70 / Chapter 3.5 --- Conclusion --- p.71 / Chapter CHAPTER IV --- DATABASE CONSTRUCTION --- p.73 / Chapter 4.1 --- Introduction --- p.73 / Chapter 4.2 --- Data Collection --- p.73 / Chapter 4.2.1 --- Base Maps --- p.73 / Chapter 4.2.2 --- Cancer Data --- p.74 / Chapter 4.2.3 --- Socio-demographic Data --- p.75 / Chapter 4.2.4 --- Air Pollution --- p.76 / Chapter 4.2.5 --- ELF EMFs --- p.77 / Chapter 4.3 --- Data Input --- p.77 / Chapter 4.3.1 --- Spatial Data --- p.77 / Chapter 4.3.1.1 --- Base Maps --- p.78 / Chapter 4.3.1.2 --- Point Data --- p.78 / Chapter 4.3.1.3 --- Line Data --- p.79 / Chapter 4.3.2 --- Attribute Data --- p.79 / Chapter 4.4 --- Data Editing and Conversions --- p.80 / Chapter 4.4.1 --- Spatial Data --- p.80 / Chapter 4.4.1.1 --- Standard Coverage Editing Procedures --- p.80 / Chapter 4.4.1.2 --- Specific Coverage Editing Procedures --- p.81 / Chapter 4.4.2 --- Attribute Data --- p.83 / Chapter 4.4.2.1 --- Cancer Rates --- p.83 / Chapter 4.4.2.2 --- Socio-economic Status --- p.85 / Chapter 4.5 --- Data Pre-processing and Manipulation --- p.86 / Chapter 4.5.1 --- Socio-economic Variables --- p.86 / Chapter 4.5.1.1 --- Interpretation of Factor Scores --- p.97 / Chapter 4.5.2 --- Compromised Traffic Index --- p.99 / Chapter 4.5.3 --- ELFEMFs --- p.104 / Chapter 4.6 --- Conclusion --- p.106 / Chapter CHAPTER V --- RESULTS AND DISCUSSIONS --- p.111 / Chapter 5.1 --- Introduction --- p.111 / Chapter 5.2 --- Geographical Analysis of Cancer Patterns --- p.111 / Chapter 5.2.1 --- Results --- p.112 / Chapter 5.2.1.1 --- Total Cancer --- p.113 / Chapter 5.2.1.2 --- Cancer of the Female Breast --- p.118 / Chapter 5.2.1.3 --- Cancer of the Cervix Uteri (Cervical Cancer) --- p.121 / Chapter 5.2.1.4 --- Cancer of the Colon and Rectum (Colorectal Cancer) --- p.124 / Chapter 5.2.1.5 --- Cancer of the Stomach (Gastric Cancer) --- p.129 / Chapter 5.2.1.6 --- Leukaemia --- p.129 / Chapter 5.2.1.7 --- Cancer of the Liver --- p.134 / Chapter 5.2.1.8 --- Cancer of the Lung --- p.143 / Chapter 5.2.1.9 --- Cancer of the Nasopharynx (NPC) --- p.149 / Chapter 5.2.1.10 --- Cancer of the Oesophagus --- p.154 / Chapter 5.3 --- Correlation among Cancer Variables --- p.160 / Chapter 5.3.1 --- Correlation among Cancer types --- p.160 / Chapter 5.3.2 --- Temporal Correlation among Cancers --- p.168 / Chapter 5.3.3 --- Correlation between Cancer Mortality and Incidence --- p.170 / Chapter 5.4 --- Correlation between Cancer and Environmental Variables --- p.172 / Chapter 5.4.1 --- Results --- p.174 / Chapter 5.5 --- Weighted Stepwise Regression Modeling --- p.182 / Chapter 5.5.1 --- Results --- p.183 / Chapter 5.5.1.1 --- Total Cancer --- p.184 / Chapter 5.5.1.2 --- Cancer of the Female Breast --- p.186 / Chapter 5.5.1.3 --- Cancer of the Cervix Uteri (Cervical Cancer) --- p.188 / Chapter 5.5.1.4 --- Cancer of the Colon and Rectum --- p.189 / Chapter 5.5.1.5 --- Cancer of the Stomach (Gastric Cancer) --- p.191 / Chapter 5.5.1.6 --- Leukaemia --- p.193 / Chapter 5.5.1.7 --- Cancer of the Liver --- p.195 / Chapter 5.5.1.8 --- Cancer of the Lung --- p.197 / Chapter 5.5.1.9 --- Cancer of the Nasopharynx (NPC) --- p.199 / Chapter 5.5.1.10 --- Cancer of the Oesophagus --- p.201 / Chapter 5.6 --- Interpretations of Results --- p.203 / Chapter CHAPTER VI --- CONCLUSION --- p.207 / Chapter 6.1 --- Summary of Findings --- p.207 / Chapter 6.1.1 --- Summary on Geographical Analysis of Cancer Patterns --- p.207 / Chapter 6.1.2 --- Summary on Statistical Analysis of Cancer Variables --- p.209 / Chapter 6.1.3 --- Summary on Associations between Cancers and Environment --- p.211 / Chapter 6.2 --- Research Limitations --- p.212 / Chapter 6.3 --- Implications for Future Studies --- p.215 / BIBLIOGRAPHY --- p.217 / APPENDICES --- p.233 / Appendix I Community Map of hong Kong --- p.234 / Appendix II List of Communities and their Components --- p.236 / Appendix III Tertiary Planning Units (TPUs) - Community Conversion Lists --- p.240 / Appendix IV BASIC Program for Calculating Moran and Geary Indices --- p.244

Yeung Sze-wan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references. / Abstracts in English and Chinese. / ACKNOWLEDGEMENT --- p.i / ABSTRACT --- p.ii / ABBREVIATIONS --- p.vii / TABLE OF CONTENTS --- p.ix / Chapter CHAPTER 1 --- INTRODUCTION --- p.1-1 / Chapter 1.1 --- Anatomy of the Cervix --- p.1-1 / Chapter 1.2 --- Histology --- p.1-1 / Chapter 1.2.1 --- Squamous Epithelium --- p.1-1 / Chapter 1.2.2 --- The Endocervical Epithelium --- p.1-3 / Chapter 1.2.3 --- The Squamo-columnar Junction --- p.1-4 / Chapter 1.2.3.1 --- The Embryology --- p.1-4 / Chapter 1.2.3.2 --- Definition --- p.1-4 / Chapter 1.3 --- Human Papillomaviruses (HPVs) --- p.1-6 / Chapter 1.3.1 --- Structure of the Viruses --- p.1-6 / Chapter 1.3.2 --- The Nomenclature --- p.1-7 / Chapter 1.3.3 --- HPVs Genomic Structure and Properties of Gene Products --- p.1-7 / Chapter 1.3.4 --- Target Tissues --- p.1-8 / Chapter 1.3.5 --- Role of HPVs in the Carcinogenesis of Lesions --- p.1-9 / Chapter 1.3.6 --- Risk Groups of HPVs --- p.1-10 / Chapter 1.4 --- Pathology --- p.1-11 / Chapter 1.4.1 --- Macroscopic Features --- p.1-11 / Chapter 1.4.2 --- Symptoms and Diagnosis --- p.1-12 / Chapter 1.4.3 --- Histopathology --- p.1-13 / Chapter 1.4.3.1 --- Histopathological Grading of Cervical Intraepithelial Neoplasia --- p.1-19 / Chapter 1.4.3.2 --- Staging of Cervical Cancer --- p.1-24 / Chapter 1.5 --- Epidemiology of Cervical Intraepithelial Neoplasia and Cervical Cancer --- p.1-27 / Chapter 1.5.1 --- Descriptive Epidemiology --- p.1-28 / Chapter 1.5.2 --- Risk Factors --- p.1-30 / Chapter 1.6 --- Human Papillomavirus Type 16 --- p.1-42 / Chapter 1.6.1 --- Role of HPV16 in CIN and Cervical Carcinoma --- p.1-42 / Chapter 1.6.2 --- Viral Load of HPV 16 in CIN --- p.1-43 / Chapter 1.6.3 --- HPV 16 Viral Load as a Screening Tool --- p.1-46 / Chapter 1.7 --- Quantitation of HPV 16 --- p.1-48 / Chapter 1.7.1 --- Methods in Viral Quantification --- p.1-48 / Chapter 1.7.2 --- Selection of Methodology --- p.1-51 / Chapter 1.7.3 --- Correlation of HPV 16 Viral Loading with Severity of Cervical Lesions --- p.1-54 / Chapter CHAPTER 2 --- AIMS OF STUDY --- p.2-1 / Chapter CHAPTER 3 --- MATERIALS AND METHODS --- p.3-1 / Chapter 3.1 --- Materials --- p.3-1 / Chapter 3.1.1 --- Patients and Specimens --- p.3-1 / Chapter 3.2 --- Methods --- p.3-3 / Chapter 3.2.1 --- DNA Extraction --- p.3-3 / Chapter 3.2.2 --- Polymerase Chain Reaction --- p.3-7 / Chapter 3.2.3 --- Gel Electrophoresis --- p.3-8 / Chapter 3.2.4 --- Real-time Quantitation Polymerase Chain Reaction --- p.3-11 / Chapter 3.2.5 --- Statistical Analysis --- p.3-15 / Chapter CHAPTER 4 --- RESULTS --- p.4-1 / Chapter 4.1 --- Grading of Cervical Smears --- p.4-1 / Chapter 4.2 --- Incidence of HPV 16 Detected in Cervical Smears --- p.4-2 / Chapter 4.2.1 --- Detection of HPV 16 in Women for Routine Pap Smear --- p.4-2 / Chapter 4.2.2 --- Detection of HPV 16 in Women for Colposcopic Examination --- p.4-5 / Chapter 4.3 --- Quantification of HPV 16 by Real-time PCR --- p.4-5 / Chapter 4.3.1 --- Range of Detection --- p.4-10 / Chapter 4.3.2 --- Standard Curve --- p.4-12 / Chapter 4.3.3 --- Reproducibility of Quantitative Real-time PCR --- p.4-17 / Chapter 4.3.4 --- Sensitivity of Quantitative Real-time PCR --- p.4-17 / Chapter 4.3.5 --- Detection and Quantification of HPV 16 E6/7 Genes in HPV16 Positive Cervical Scrapes --- p.4-21 / Chapter 4.4 --- Comparison of HPV 16 Copy Number Detected among Three Lesion Groups --- p.4-22 / Chapter 4.5 --- Clinical Analysis --- p.4-27 / Chapter 4.6 --- HPV 16 DNA Copy Number in Lesion Groups --- p.4-28 / Chapter CHAPTER 5 --- DISCUSSION --- p.5-1 / Chapter 5.1 --- Selection of Material (Scrapes) --- p.5-1 / Chapter 5.2 --- Detection of HPV 16 in Cervical Scrapes --- p.5-3 / Chapter 5.2.1 --- Selection of HPV Type --- p.5-3 / Chapter 5.2.2 --- Techniques in Detecting HPV Viral Load --- p.5-3 / Chapter 5.2.2.1 --- Advantages of Quantitative Real-time PCR --- p.5-6 / Chapter 5.2.2.2 --- Parameters Affecting the Performance of Real-time PCR --- p.5-8 / Chapter 5.2.3 --- Selection of Detection Sites --- p.5-9 / Chapter 5.2.4 --- Standard Curve Establishment --- p.5-10 / Chapter 5.3 --- Comparison between Real-time PCR and Traditional PCR --- p.5-12 / Chapter 5.4 --- Role of HPV Viral Load in Cervical Neoplasm --- p.5-13 / Chapter 5.5 --- HPV Infection in Hong Kong Chinese Women --- p.5-17 / Chapter 5.6 --- Clinical Significance of HPV 16 Viral Load Detected in Cervical Neoplasm --- p.5-18 / Chapter 5.7 --- Future Prospect --- p.5-20 / Chapter CHAPTER 6 --- CONCLUSION --- p.6-1 / REFERENCES --- p.R-I

Background: Although rare relative to adult cancers, cancer is still the leading cause of disease-related death in children in developed countries, including Canada. Few studies have specifically examined the epidemiology and public health significance of diagnosis and treatment delays in childhood cancer. This study aimed to investigate the nature of delays in care for children and adolescents with cancer in Canada and to assess the potential impact of such delays on clinical outcomes. / Study Design: I conducted a prospective cohort study to investigate the delays of cancer symptoms reporting, diagnosis, and treatment in children between 0-19 years of age in Canada. This study used a database from Health Canada's Treatment and Outcomes component of the Canadian Childhood Cancer Surveillance and Control Program. / Methodology: Patients were identified from 17 paediatric cancer centres across Canada. Subjects included in this study were residents of Canada, aged less than 20 years, diagnosed with a malignant tumour and had information on date of first symptoms, diagnosis, treatment and outcome available. Descriptive statistics and regression techniques (linear, logistic and Cox regression) were used as appropriate. I measured the individual impact of patient and provider delays on disease severity and prognosis by using judicious control for potential confounding mechanisms and mediating factors. / Study Findings and Significance: By measuring various types of delays in Canada, I found that varying lengths of patient and referral delay, across age groups, types of cancers, and Canadian settings, are the main contributors to diagnosis, HCS and overall delay. Factors relating to the patients, the parents, healthcare and the cancer may all exert different influences on different segments of cancer care. I also found a negative association between diagnosis delay and disease severity for lymphoma and CNS tumour patients. Furthermore, I found that diagnosis and physician delay had a negative effect, while patient delay had a positive effect, on survival for patients diagnosed with CNS tumours. The information provided from this study may form the basis for new effective policies aimed at eliminating obstacles in cancer the diagnostic and care trajectories for Canadian children with cancer and for improving their prognosis.

The Papanicolaou Smear is a screening test which detects premalignant lesions of the uterine cervix. By treating these lesions, cervical cancer can be evaded. In 1988, a cytological diagnosis which communicated a state of uncertainty in the atypicality of cervical cells was first created in the Bethesda Cytology Classification scheme. This diagnosis is now known as atypical squamous cells of undetermined significance (ASC-US) and still little is known about its natural history. / This paper analyzes the results of a longitudinal study incorporating repeated regular measurements of viral and cytological endpoints as well as lifestyle and behavioural aspects, to understand the natural history of an ASC-US Pap smear and identify determinants of ASC-US acquisition and clearance. / Overall, the median duration of ASC-US is short, and is dependent on the definition of clearance since most lesions regress to normal. The factors most predictive of ASC-US acquisition but not clearance relate to HPV infection.

Background: The causes of childhood brain tumors (CBT) are essentially unknown. Exposure to extremely low frequency magnetic fields (ELF-MF) (3-3000Hz) is an ubiquitous part of modern life. However, very few studies have investigated the possible effect of maternal occupational ELF-MF exposure on CBT and the available findings are inconsistent across studies. / Methods: We examined the role of maternal occupational exposure to ELF-MF shortly before and during pregnancy on the incidence of childhood brain tumors. A total of 548 incident cases and 760 healthy controls recruited between 1980 and 2002 from two Canadian provinces (Quebec and Ontario) were included and their mothers were interviewed. Tumors were classified as astroglial tumors, primitive neuroectodermal tumors (PNET), and other gliomas. Quantitative occupational ELF-MF exposure in microtesla units was estimated using individual exposure estimations or a job exposure matrix. We used three metrics to analyze exposure: cumulative, average, and maximum level attained. / Results: Using the average exposure metric measured before conception, an increased risk was observed for astroglial tumors (OR=1.5, and 95% CI=1.0-2.4). During the entire pregnancy period, a significantly increased risk was observed for astroglial tumors as well as for all childhood brain tumors with the average metric (OR=1.6, 95% CI=1.1-2.5 and OR=1.5; 95% CI=1.1-2.2, respectively). Based on job titles, a two-fold risk increase was observed for astroglial tumors (OR=2.3, 95% CI=0.8-6.3) and for all childhood brain tumors (OR=2.3, 95% CI=1.0-5.4) among sewing machine operators. / Conclusion: Results are suggestive of a possible association between maternal occupational ELF-MF exposure and certain brain tumors in their offspring. / Keywords: brain tumors, occupational exposures, maternal exposures, magnetic fields, childhood cancer, job exposure matrix