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HIV-associated neurocognitive disorders (HAND) are highly prevalent in those ageing with HIV. High-income country data suggest that vascular risk factors (VRFs) may be stronger predictors of HAND than HIV-disease severity, but data from sub-Saharan Africa are lacking. We evaluated relationships of VRFs, vascular end-organ damage and HAND in individuals aged ≥ 50 in Tanzania. c-ART-treated individuals were assessed for HAND using consensus criteria. The prevalence of VRFs and end organ damage markers were measured. The independent associations of VRFs, end organ damage and HAND were examined using multivariable logistic regression. Data were available for 153 individuals (median age 56, 67.3% female). HAND was highly prevalent (66.7%, 25.5% symptomatic) despite well-managed HIV (70.5% virally suppressed). Vascular risk factors included hypertension (34%), obesity (10.5%), hypercholesterolemia (33.3%), diabetes (5.3%) and current smoking (4.6%). End organ damage prevalence ranged from 1.3% (prior myocardial infarction) to 12.5% (left ventricular hypertrophy). Measured VRFs and end organ damage were not independently associated with HAND. The only significant association was lower diastolic BP (p 0.030, OR 0.969 (0.943–0.997). Our results suggest that vascular risk factors are not major drivers of HAND in this setting. Further studies should explore alternative aetiologies such as chronic inflammation. [ABSTRACT FROM AUTHOR]

Background: A heterogeneous geographic distribution of childhood acute lymphoblastic leukemia (ALL) cases has been described, possibly, related to the presence of different environmental factors. The aim of the present study was to explore the geographical distribution of childhood ALL cases in Greater Mexico City (GMC). Methods: A population-based case-control study was conducted. Children <18 years old, newly diagnosed with ALL and residents of GMC were included. Controls were patients without leukemia recruited from second-level public hospitals, frequency-matched by sex, age, and health institution with the cases. The residence address where the patients lived during the last year before diagnosis (cases) or the interview (controls) was used for geolocation. Kulldorff's spatial scan statistic was used to detect spatial clusters (SCs). Relative risks (RR), associated p-value and number of cases included for each cluster were obtained. Results: A total of 1054 cases with ALL were analyzed. Of these, 408 (38.7%) were distributed across eight SCs detected. A relative risk of 1.61 (p<0.0001) was observed for the main cluster. Similar results were noted for the remaining seven ones. Additionally, a proximity between SCs, electrical installations and petrochemical facilities was observed. Conclusions: The identification of SCs in certain regions of GMC suggest the possible role of environmental factors in the etiology of childhood ALL. [ABSTRACT FROM AUTHOR]

Abstract Background The aetiology of bone cancers is poorly understood. This study examined geographical patterning in incidence of primary bone cancers diagnosed in 0–49 year olds in Great Britain during 1980–2005 to provide information on factors linked with disease development. We investigated putative associations with deprivation and population density. Methods Data on osteosarcoma and Ewing sarcoma were obtained from national population-based registries. Negative binomial regression was used to examine the relationship between incidence rates and the Townsend deprivation score (and its component variables) and small-area population density. Results The study analyzed 2566 osteosarcoma and 1650 Ewing sarcoma cases. For females with osteosarcoma, statistically significant decreased risk was associated with higher levels of deprivation (relative risk [RR] per unit increase in deprivation score = 0.969; 95% confidence interval [CI] 0.946–0.993). For all Ewing sarcoma combined, statistically significant decreased risk was associated with greater area-level population density and higher levels of non-car ownership (RR per person per hectare increase = 0.984; 95% CI 0.976–0.993, RR per 1% increase in non-car ownership = 0.994; 95% CI 0.991–0.998). Conclusions Higher incidence of osteosarcoma was observed for females in areas with lower deprivation levels indicating increased risk is linked to some aspect of affluent living. Higher incidence of Ewing sarcoma occurred in areas of low population density and where more people owned cars, both characteristic of rural environments. The study adds substantially to evidence associating Ewing sarcoma risk with rural environmental exposures. Putative risk factors include agricultural exposures, such as pesticides and zoonotic agents.

Background Epidemiological studies from Europe and North America have provided evidence that exposure to air pollution can aggravate symptoms in asthmatic patients. Methods Daily number of AEDv, air pollution levels (PM10, PM2.5, SO2, NO2 and CO) and meteorological variables was obtained from Jubail Industrial City, Saudi Arabia, for the period of 2007–11. Data were analyzed using a time-series approach. Relative risks (RRs) were estimated using Poisson regression. Results The associations between AEDv and PM10, PM2.5, SO2 and NO2 remained positive and statistically significant after mutual adjustment in the multi-pollutant model. The RR of AEDv increased by 5.4, 4.4, 3.4 and 2.2% per an inter-quartile range increase in SO2 (2.0 ppb), PM2.5 (36 μg/m3), NO2 (7.6 ppb) and PM10 (140 μg/m3), respectively. No significant associations between AEDv and CO were found. Conclusions Current levels of ambient air pollution are associated with AEDv in this industrial setting in the Middle East. Greater awareness of environmental health protection and the implementation of effective measures to improve the quality of air in such settings would be beneficial to public health. [ABSTRACT FROM AUTHOR]

Objective: To analyze trends in external mortality in Hungary between 1995 and 2014 by sex. Methods: Data on the numbers of deaths due to external causes were obtained from the published nationwide population register. Negative binomial regression was applied to investigate the yearly trends in external-cause mortality rates. Cyclic trends were investigated using the Walter-Elwood method. Results: Suicide and accidents accounted for approximately 84% of the all-external-cause of deaths in Hungary. Annual suicide, unintentional falls and traffic accidents mortality declined significantly (p-value for annual trend: p < 0.001) from 30.5 (95% CI: 29.5–31.5) to 15.8 (15.1–16.5), from 31.2 (30.2–32.2) to 12.2 (11.7–12.8) and from 17.2 (16.4–18) to 5.4 (5–5.8) per 100 000 persons per year, respectively, during the study period. A significant declining trend in annual mortality was also found for assault, cold/heating-related accidents and accidents caused by electric current. However, the declining trend for drowning-related accidents was significant only for males. Significant winter-peak seasonality was found in the mortality rates from accidental falls, cold/heat-related accidents, other accidents caused by submersion/obstruction and other causes. Seasonal trends with a peak from June to July were observed in death rates from suicide/self-harm, accidental drowning/submersion and accidents caused by electric current. A significant seasonal variation with a peak in September was revealed in the mortality due to traffic accidents. Conclusions: This Hungarian study suggests that there was a significant seasonal effect on almost all kinds of deaths from external causes between 1995 and 2014. Environmental effects are involved in the aetiology of suicide and accidents. [ABSTRACT FROM AUTHOR]

Abstract: Mitochondrial disease associated with the pathogenic m.3243A>G variant is a common, clinically heterogeneous, neurogenetic disorder. Using multiple linear regression and linear mixed modelling, we evaluated which commonly assayed tissue (blood N = 231, urine N = 235, skeletal muscle N = 77) represents the m.3243A>G mutation load and mitochondrial DNA (mtDNA) copy number most strongly associated with disease burden and progression. m.3243A>G levels are correlated in blood, muscle and urine (R2 = 0.61–0.73). Blood heteroplasmy declines by ~2.3%/year; we have extended previously published methodology to adjust for age. In urine, males have higher mtDNA copy number and ~20% higher m.3243A>G mutation load; we present formulas to adjust for this. Blood is the most highly correlated mutation measure for disease burden and progression in m.3243A>G‐harbouring individuals; increasing age and heteroplasmy contribute (R2 = 0.27, P < 0.001). In muscle, heteroplasmy, age and mtDNA copy number explain a higher proportion of variability in disease burden (R2 = 0.40, P < 0.001), although activity level and disease severity are likely to affect copy number. Whilst our data indicate that age‐corrected blood m.3243A>G heteroplasmy is the most convenient and reliable measure for routine clinical assessment, additional factors such as mtDNA copy number may also influence disease severity. [ABSTRACT FROM AUTHOR]

Background: The aetiology of neuroblastic tumours is unclear with both genetic and environmental factors implicated. The possibility that an infectious agent may be involved has been suggested. 'Temporal clustering' occurs if cases display an irregular temporal distribution and may indicate the involvement of an agent that exhibits epidemicity. We tested for the presence and nature of temporal clustering using population-based data from northern England. Methods: We extracted all cases of neuroblastic tumours diagnosed in children and young adults aged 0-24 years during 1968-2011 from the Northern Region Young Persons' Malignant Disease Registry. This is a population-based registry, covering a population of approximately 900,000 young persons, and includes all cases resident in northern England at the time of diagnosis. Tests for temporal clustering were applied using a modified version of the Potthoff-Whittinghill method. Estimates of extra-Poisson variation (β̂) and standard errors (SEs) were obtained. Results: 227 cases of neuroblastic tumours were diagnosed during the study period. All the analyses between fortnights and between months found significant extra-Poisson variation, with β̂ =0.846 (SE = 0.310, P = 0.004) for the analysis between fortnights within months. Restricting the analyses to the 76 cases diagnosed at ages less than 18 months showed significant extra-Poisson variation between fortnights within months (β̂ =1.532, SE = 0.866, P = 0.038), but not between months. In contrast, analyses of cases aged 18 months to 24 years showed significant extra-Poisson variation between quarters within years, as well as over shorter timescales. Conclusions: Transient environmental agents may be involved in the aetiology of neuroblastic tumours. The initiating factor might be a geographically-widespread agent that occurs in 'mini-epidemics'. [ABSTRACT FROM AUTHOR]

Previous studies have found marked increases in melanoma incidence. The increase among young people in northern England was especially apparent among females. However, overall 5-year survival has greatly improved. The present study aimed to determine whether socioeconomic factors may be involved in both etiology and survival. All 224 cases of malignant melanoma diagnosed in patients aged 10-24 years during 1968-2003 were extracted from a specialist population-based regional registry. Negative binomial regression was used to examine the relationship between incidence and area-based measures of socioeconomic deprivation and small-area population density. Cox regression was used to analyze the relationship between survival and deprivation and population density. There was significantly decreased risk associated with living in areas of higher unemployment (relative risk per 1% increase in unemployment=0.93; 95% confidence interval (CI) 0.90-0.96, P<0.001). Survival was better in less deprived areas (hazard ratio (HR) per tertile of household overcrowding=1.52; 95% CI 1.05-2.20; P=0.026), but this effect was reduced in the period 1986-2003 (HR=0.61; 95% CI 0.40-0.92; P=0.018). This study found that increased risk of melanoma was linked with some aspects of greater affluence. In contrast, worse survival was associated with living in a more deprived area. [ABSTRACT FROM AUTHOR]

Background and study aims: Adenoma detection is a key objective of colonoscopy, particularly in the context of colorectal cancer screening. The aim of this observational study was to identify the technical colonoscopy factors associated with adenoma detection. Patients and methods: The study analyzed data from the English Bowel Cancer Screening Programme. The indication for all colonoscopies was a positive fecal occult blood test. The relationships between the following colonoscopy factors and adenoma detection (one or more adenomas, advanced adenomas, right-sided adenomas, and total number of adenomas) were examined in multivariable analyses: bowel preparation quality, cecal intubation, withdrawal time, rectal retroversion, colonoscopist experience, antispasmodic use, sedation use, and start time of procedure. The following patient factors were controlled for: age, sex, body mass index, smoking, alcohol, deprivation, and geographical location. Results: A total of 31088 colonoscopies were analyzed. The following technical factors increased the relative risk of adenoma detection (P<0.001 in multivariable analysis unless otherwise stated): cecal intubation, increased withdrawal time, higher quality bowel preparation, intravenous antispasmodic use, earlier procedure start time within a session (P=0.018), and greater colonoscopist experience. Detection of advanced and right-sided adenomas also increased with these factors. Adenoma detection did not differ between sedated and unsedated colonoscopy (P= 0.143). Conclusion: This study demonstrated important associations between colonoscopy practice and adenoma detection. Use of intravenous antispasmodic was associated with increased adenoma detection. The effect of the start time of colonoscopy suggests that endoscopist fatigue may have a deleterious impact on adenoma detection. [ABSTRACT FROM AUTHOR]

Background: Artificial fluoridation of drinking water to improve dental health has long been a topic of controversy. Opponents of this public health measure have cited the possibility of bone cancer induction. The study objective was to examine whether increased risk of primary bone cancer was associated with living in areas with higher concentrations of fluoride in drinking water.Methods: Case data on osteosarcoma and Ewing sarcoma, diagnosed at ages 0-49 years in Great Britain (GB) (defined here as England, Scotland and Wales) during the period 1980-2005, were obtained from population-based cancer registries. Data on fluoride levels in drinking water in England and Wales were accessed through regional water companies and the Drinking Water Inspectorate. Scottish Water provided data for Scotland. Negative binomial regression was used to examine the relationship between incidence rates and level of fluoride in drinking water at small area level.Results: The study analysed 2566 osteosarcoma and 1650 Ewing sarcoma cases. There was no evidence of an association between osteosarcoma risk and fluoride in drinking water [relative risk (RR) per one part per million increase in the level of fluoride = 1·001; 90% confidence interval (CI) 0·871, 1·151] and similarly there was no association for Ewing sarcoma (RR = 0·929; 90% CI 0·773, 1·115).Conclusions: The findings from this study provide no evidence that higher levels of fluoride (whether natural or artificial) in drinking water in GB lead to greater risk of either osteosarcoma or Ewing sarcoma. [ABSTRACT FROM AUTHOR]

Background: Previous studies have indicated that type 1 diabetes may have an infectious origin. The presence of temporal clustering—an irregular temporal distribution of cases—would provide additional evidence that occurrence may be linked with an agent that displays epidemicity. We tested for the presence and form of temporal clustering using population-based data from northeast England. Materials and Methods: The study analysed data on children aged 0–14 years diagnosed with type 1 diabetes during the period 1990–2007 and resident in a defined geographical region of northeast England (Northumberland, Newcastle upon Tyne, and North Tyneside). Tests for temporal clustering by time of diagnosis were applied using a modified version of the Potthoff-Whittinghill method. Results: The study analysed 468 cases of children diagnosed with type 1 diabetes. There was highly statistically significant evidence of temporal clustering over periods of a few months and over longer time intervals (p<0.001). The clustering within years did not show a consistent seasonal pattern. Conclusions: The study adds to the growing body of literature that supports the involvement of infectious agents in the aetiology of type 1 diabetes in children. Specifically it suggests that the precipitating agent or agents involved might be an infection that occurs in “mini-epidemics”. [ABSTRACT FROM AUTHOR]

Infection with human papillomavirus is an established risk factor for cervical carcinoma. However, the role of other environmental factors is less well established. To further investigate whether other agents may be involved, the authors have analyzed seasonal variation in cervical cancer with respect to month of birth and separately month of diagnosis. All 85 cases diagnosed in 15-24-yr-olds during the period 1968-2005 were extracted from the specialist population-based Northern Region Young Persons' Malignant Disease Registry. The chi-square heterogeneity test was used to assess overall nonuniform variation in month of birth and separately month of diagnosis. Poisson regression analysis was used to fit sinusoidal (harmonic) models to the data using month of birth and month of diagnosis in separate models. Based on month of birth, there was statistically significant heterogeneity ( p == .03) and a significant sinusoidal pattern, with an incidence peak involving births in the autumn months ( p == .03). Based on month of diagnosis, there was marginally significant heterogeneity ( p == .06). The evidence of seasonal variation around time of birth for cervical carcinoma is highly novel and suggests possible early etiological involvement of environmental factors. (Author correspondence: ) [ABSTRACT FROM AUTHOR]

Objectives The UK National Health Service Bowel Cancer Screening Programme (BCSP) is based on a strategy of biennial faecal occult blood (FOB) testing. Positive results are classified as 'abnormal' or 'weak positive' based on the number of positive windows per kit or need for repeat testing. Colonoscopy is offered to both groups. We evaluate the relationship between FOB test positivity and clinical outcome in the BCSP. Setting The South of Tyne and Tees (UK) Bowel Cancer Screening Centres. Methods Data were collected prospectively on all individuals who were offered FOB testing and colonoscopy between February 2007 and February 2009. Univariable and multivariable analyses were performed to investigate the relationship between FOB test positivity and clinical outcome. Results Following FOB testing, 1524 individuals underwent colonoscopy, 1259 (83%) after a 'weak positive' and 265 (17%) an 'abnormal' result. Cancer was detected in 180 (11.8%) and adenomas in 758 (49.7%). Individuals with an 'abnormal' result were more likely to have cancer or be 'high risk' for the development of future adenomas (110/265, 41.5%) than those with 'weak positive' results, (236/1259, 18.7%, P < 0.0001). Those with Dukes stage B, C or D cancers or cancers proximal to the splenic flexure were more likely to have an 'abnormal' result. Conclusions The majority of colonoscopies were performed following 'weak positive' FOB results. Those with an 'abnormal' result were more likely to be diagnosed with cancer. The high yield of pathology in both the 'abnormal' and 'weak positive' groups justifies the need for colonoscopy in both. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented regarding the study which examines the relationship between birth weight and risk of childhood acute leukemia (CAL) among young people born from 1961-2002.

Background: There is a paucity of recent epidemiological data on bone cancers. The aim of this study was to describe incidence and survival patterns for bone cancers diagnosed during 1981 - 2002. Methods: Cases aged 0 - 39 years (236 osteosarcomas, 166 Ewing sarcomas and 73 chondrosarcomas) were analysed using Poisson and Cox regressions. Results: Incidence rates (per million persons per year) for osteosarcoma were 2.5 at age 0 - 14 years; 4.5 at age 15 - 29 years and 1.0 at age 30 - 39 years. Similarly, for Ewing sarcoma the incidence rates were 2.2; 2.9; 0.4 and for chondrosarcoma rates were 0.1; 1.2; 1.8 respectively. Incidence of osteosarcoma increased at an average annual rate of 2.5% (95% CI 0.4 - 4.7; P = 0.02), but there was no change in incidence of Ewing sarcoma or chondrosarcoma. There was a marginally statistically significant improvement in survival for Ewing sarcoma (hazard ratio (HR) per annum = 0.97; 95% CI 0.94 - 1.00; P = 0.06), although patients aged 15 - 39 years (n = 93) had worse overall survival than those aged 0 - 14 (n = 73; HR = 1.46; 95% CI 0.98 - 2.17; P = 0.06). There was no significant improvement in osteosarcoma survival (HR per annum = 0.98; 95% CI 0.95 - 1.01; P = 0.18). Conclusions: Reasons for poorer survival in Ewing sarcoma patients aged 15 - 39 years and failure to significantly improve survival for osteosarcoma patients requires further investigation. [ABSTRACT FROM AUTHOR]

Background: The aetiology of type 1 diabetes in children is uncertain. A number of recent studies have suggested an infectious aetiology. It has been postulated that an infectious agent may be involved. Support for this hypothesis may be provided by a finding of space-time clustering. The aims of this study were: (i) to determine whether there was space-time clustering in cases of childhood diabetes from north-east England; and to test for differences in space-time clustering: (ii) due to age at diagnosis; (iii) between the sexes and (iv) between levels of residential population density. Methods: We studied incidence of type 1 diabetes diagnosed in children aged 0-14 years and diagnosed during the period 1990-2007. All cases were resident in a defined geographical region of north-east England (Northumberland, Newcastle upon Tyne and North Tyneside). We applied a second-order procedure based on K-functions to test for global clustering. Locations were residential addresses at time of diagnosis. Tests were repeated using nearest neighbour thresholds to allow for variable population density, providing the primary result for each analysis. Differences between sexes and between levels of population density were assessed. Results: We analysed 457 cases of type 1 diabetes. Overall, there was marginally significant evidence of global space-time clustering (P = 0.089). There was statistically significant clustering amongst pairs of cases that contained at least one female (P = 0.017), but not amongst pairs of cases that contained at least one male (P = 0.190). Furthermore, there was significant clustering amongst pairs of cases that contained at least one from a more densely populated area (P = 0.044), but not amongst pairs of cases that contained at least one from a less densely populated area (P = 0.226). Conclusion: Although the analyses have only found marginally significant evidence of global spacetime clustering for cases of type 1 diabetes diagnosed in north-east England, there were two notable findings. First, there was evidence of clustering amongst females and secondly clustering was confined to cases from more densely populated areas. These findings are consistent with a possible aetiological involvement of an infectious agent. [ABSTRACT FROM AUTHOR]

Background: This study examined sex-specific patterns and temporal trends in the incidence of solid tumours in the Northern Region of England from 1968 to 2005. This updates earlier analyses from the region where sex was not considered in depth. Sex-specific analyses were carried out to determine whether sex differences might provide clues to aetiology. Methods: Details of 3576 cases, aged 0-24 years, were obtained from a specialist population-based cancer registry. There were 1843 males (886 aged 0-14 years and 957 aged 15-24 years) and 1733 females (791 aged 0-14 years and 942 aged 15-24 years). Age-standardized incidence rates (per million population) were calculated. Linear regression was used to analyze temporal trends in incidence and annual percentage changes were estimated. Analyses were stratified by sex and by age-group. Results: There were marked differences in incidence patterns and trends between males and females and also between age-groups. For males central nervous system (CNS) tumours formed the largest proportion of under- 15 cases and germ cell tumours was the largest group in the 15-24's, whilst for females CNS tumours dominated in the under-15's and carcinomas in the older group. For 0-14 year olds there were male-specific increases in the incidence of rhabdomyosarcoma (2.4% per annum; 95% CI: 0.2%-4.5%) and non-melanotic skin cancer (9.6%; 95% CI: 0.0%-19.2%) and female-specific increases for sympathetic nervous system tumours (2.2%; 95% CI: 0.4%-3.9%), gonadal germ cell tumours (8.6%; 95% CI: 4.3%-12.9%) and non-gonadal germ cell tumours (5.4%; 95% CI: 2.8%-7.9%). For 15-24 year olds, there were male-specific increases in gonadal germ cell tumours (1.9%; 95% CI: 0.3%-3.4%), non-gonadal germ cell tumours (4.4%; 95% CI: 1.1%-7.7%) and non-melanotic skin cancer (4.7%; 95% CI: 0.5%-8.9%) and female-specific increases for osteosarcoma (3.5%; 95% CI: 0.5%-6.5%), thyroid cancer (2.8%; 95% CI: 0.1%-5.6%) and melanoma (4.6%; 95% CI: 2.2%-7.1%). Conclusion: This study has highlighted notable differences between the sexes in incidence patterns and trends for solid tumours. Some of these sex-specific differences could have been obscured if males and females had been analysed together. Furthermore, they suggest aetiological differences or differential susceptibility to environmental factors between males and females. [ABSTRACT FROM AUTHOR]

Aim: There is much debate as to whether the prevalence rates of cryptorchidism and hypospadias are increasing. To address this issue we investigated the birth prevalence of cryptorchidism and hypospadias in the northern region of England during the period 1993-2000. Methods: Cases of cryptorchidism and hypospadias were identified from northern region hospital episodes statistics (HES). Trends in birth prevalence, based on the number of male live births, were assessed using linear regression. Results: Prevalence was 7.6 per 1000 male live births for cryptorchidism and 3.1 per 1000 male live births for hypospadias. The orchidopexy rates for 0-4 year olds and 5-14 year olds were 1.8 and 0.8 per 1000 male population, respectively. The rates for hypospadias repair for 0-4 year olds and 5-14 year olds were 0.6 and 0.1 per 1000 male population, respectively. There was a statistically significant decreasing temporal trend for the corrective procedure in cryptorchidism of 0.1 per 1000 male population aged under 5 years per annum (95% confidence interval: -0.01 to -0.05, p<0.00), but no temporal change for the corrective procedure in hypospadias (p=0.60. Conclusion: HES data were of high quality for the study period. There was no significant change in the prevalence of surgically corrected hypospadias. However, there was an apparent decline in the prevalence of surgically corrected cryptorchidism that may reflect a decrease in the prevalence of the condition or may be due to a decrease in the rate of surgical intervention. [ABSTRACT FROM AUTHOR]

This review considers recent studies regarding the role of environmental factors in the etiology of childhood leukemia and lymphoma. Potential environmental risk factors identified for childhood leukemia include exposure to magnetic fields of more than 0.4 micro Tessla, exposure to pesticides, solvents, benzene and other hydrocarbons, maternal alcohol consumption (but only for certain genotypes), contaminated drinking water, infections, and high birth weight. The finding of space-time clustering and seasonal variation also supports a role for infections. There is little evidence linking childhood leukemia with lifetime exposure to ionizing radiation although fetal exposures to X-rays are associated with increased risk. Breast-feeding, consumption of fresh fruit and vegetables and having allergies all appear to be protective. Burkitt lymphoma (BL) is confined to areas of the world where malaria is endemic, with the additional involvement of the Epstein-Barr virus (EBV) as a co-factor. Environmental risk factors suggested for other types of non-Hodgkin lymphoma (NHL) include exposure to ionizing radiation (both lifetime and antenatal), pesticides, and, in utero exposure to cigarette smoke, benzene and nitrogen dioxide (via the mother). Hodgkin lymphoma (HL) is especially associated with higher levels of socioeconomic deprivation, but breast-feeding seems to confer lower risk. This is consistent with an infection or immune-response mediated etiology for HL. [ABSTRACT FROM AUTHOR]

The nearest neighbour analysis method has been developed to determine whether a disease case may be regarded as being unusually close to other neighbouring cases of the same disease. Using this method, each disease case is classified as spatially 'clustered' or 'nonclustered'. The method is also used to provide a test for global clustering. 'Clusters' are constructed by amalgamating geographically neighbouring clustered cases into one contiguous 'cluster area'. This paper describes a method for studying differences between clustered and non-clustered cases, in terms of case 'attributes'. These attributes may be person related, such as age and sex, or area based, such as geographical isolation. The area-based variables are subject to geographical correlation. The comparison of clustered and non-clustered cases may reveal similarities or differences, which may, in turn, give clues to disease aetiology. A method for studying 'linkage' or similarities in attributes between cases that occur in the same clusters is also described. The methods are illustrated by application to incidence data for leukaemias and lymphomas. [ABSTRACT FROM AUTHOR]