79 research outputs found

    Hematologic malignancies in South Africa 2000-2006: analysis of data reported to the National Cancer Registry.

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    Little is known about the incidence patterns of hematologic malignancies in Sub-Saharan Africa, including South Africa. We estimated incidence rates of pathology-confirmed adult cases of leukemia, myeloma and related diseases (myeloma), Hodgkin lymphoma (HL), and non-Hodgkin lymphoma (NHL) reported to the National Cancer Registry of South Africa (NCR) between 2000 and 2006, by age, gender, and population group (Black, White, Coloured, Asian/Indian). Gender-specific age-standardized rates were calculated overall and by population group and incidence rate ratios (IRRs) were estimated using Poisson regression models. Between 2000 and 2006, there were 14662 cases of leukemia, myeloma, HL, and NHL reported to the registry. Incidence rates of reported hematologic malignancies were generally 20-50% higher among males than females. Our analyses suggested marked differences in the rates of reported hematologic malignancies by population group which were most pronounced when comparing the White versus Black population groups (IRRs ranging from 1.6 for myeloma to 3.8 for HL for males and females combined). Challenges related to diagnosis and reporting of cancers may play a role in the patterns observed by population group while the set-up of the NCR (pathology-based) could lead to some degree of under-ascertainment in all groups. This is the first country-wide report of the incidence of hematologic malignancies in South Africa. Despite challenges, it is important to analyze and report available national cancer incidence data to raise awareness of the cancer burden and to characterize patterns by demographic characteristics so as ultimately to improve the provision of cancer-related health care

    Risks for Central Nervous System Diseases among Mobile Phone Subscribers: A Danish Retrospective Cohort Study

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    The aim of this study was to investigate a possible link between cellular telephone use and risks for various diseases of the central nervous system (CNS). We conducted a large nationwide cohort study of 420 095 persons whose first cellular telephone subscription was between 1982 and 1995, who were followed through 2003 for hospital contacts for a diagnosis of a CNS disorder. Standardized hospitalization ratios (SHRs) were derived by dividing the number of hospital contacts in the cohort by the number expected in the Danish population. The SHRs were increased by 10–20% for migraine and vertigo. No associations were seen for amyotrophic lateral sclerosis, multiple sclerosis or epilepsy in women. SHRs decreased by 30–40% were observed for dementia (Alzheimer disease, vascular and other dementia), Parkinson disease and epilepsy among men. In analyses restricted to subscribers of 10 years or more, the SHRs remained similarly increased for migraine and vertigo and similarly decreased for Alzheimer disease and other dementia and epilepsy (in men); the other SHRs were close to unity. In conclusion, the excesses of migraine and vertigo observed in this first study on cellular telephones and CNS disease deserve further attention. An interplay of a healthy cohort effect and reversed causation bias due to prodromal symptoms impedes detection of a possible association with dementia and Parkinson disease. Identification of the factors that result in a healthy cohort might be of interest for elucidation of the etiology of these diseases

    Africa’s oesophageal cancer corridor: geographic variations in incidence correlate with certain micronutrient deficiencies

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    Background The aetiology of Africa’s easterly-lying corridor of squamous cell oesophageal cancer is poorly understood. Micronutrient deficiencies have been implicated in this cancer in other areas of the world, but their role in Africa is unclear. Without prospective cohorts, timely insights can instead be gained through ecological studies. Methods Across Africa we assessed associations between a country’s oesophageal cancer incidence rate and food balance sheet-derived estimates of mean national dietary supplies of 7 nutrients: calcium (Ca), copper (Cu), iron (Fe), iodine (I), magnesium (Mg), selenium (Se) and zinc (Zn). We included 32 countries which had estimates of dietary nutrient supplies and of better-quality GLOBCAN 2012 cancer incidence rates. Bayesian hierarchical Poisson lognormal models were used to estimate incidence rate ratios for oesophageal cancer associated with each nutrient, adjusted for age, gender, energy intake, phytate, smoking and alcohol consumption, as well as their 95% posterior credible intervals (CI). Adult dietary deficiencies were quantified using an estimated average requirements (EAR) cut-point approach. Results Adjusted incidence rate ratios for oesophageal cancer associated with a doubling of mean nutrient supply were: for Fe 0.49 (95% CI: 0.29–0.82); Mg 0.58 (0.31–1.08); Se 0.40 (0.18–0.90); and Zn 0.29 (0.11–0.74). There were no associations with Ca, Cu and I. Mean national nutrient supplies exceeded adult EARs for Mg and Fe in most countries. For Se, mean supplies were less than EARs (both sexes) in 7 of the 10 highest oesophageal cancer ranking countries, compared to 23% of remaining countries. For Zn, mean supplies were less than the male EARs in 8 of these 10 highest ranking countries compared to in 36% of other countries

    European Code against Cancer 4th edition: Ultraviolet radiation and cancer

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    Ultraviolet radiation (UVR) is part of the electromagnetic spectrum emitted naturally from the sun or from artificial sources such as tanning devices. Acute skin reactions induced by UVR exposure are erythema (skin reddening), or sunburn, and the acquisition of a suntan triggered by UVR-induced DNA damage. UVR exposure is the main cause of skin cancer, including cutaneous malignant melanoma, basal-cell carcinoma, and squamous-cell carcinoma. Skin cancer is the most common cancer in fair-skinned populations, and its incidence has increased steeply over recent decades. According to estimates for 2012, about 100,000 new cases of cutaneous melanoma and about 22,000 deaths from it occurred in Europe. The main mechanisms by which UVR causes cancer are well understood. Exposure during childhood appears to be particularly harmful. Exposure to UVR is a risk factor modifiable by individuals' behaviour. Excessive exposure from natural sources can be avoided by seeking shade when the sun is strongest, by wearing appropriate clothing, and by appropriately applying sunscreens if direct sunlight is unavoidable. Exposure from artificial sources can be completely avoided by not using sunbeds. Beneficial effects of sun or UVR exposure, such as for vitamin D production, can be fully achieved while still avoiding too much sun exposure and the use of sunbeds. Taking all the scientific evidence together, the recommendation of the 4th edition of the European Code Against Cancer for ultraviolet radiation is: "Avoid too much sun, especially for children. Use sun protection. Do not use sunbeds."

    A three-dimensional point process model for the spatial distribution of disease occurrence in relation to an exposure source

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    We study methods for how to include the spatial distribution of tumours when investigating the relation between brain tumours and the exposure from radio frequency electromagnetic fields caused by mobile phone use. Our suggested point process model is adapted from studies investigating spatial aggregation of a disease around a source of potential hazard in environmental epidemiology, where now the source is the preferred ear of each phone user. In this context, the spatial distribution is a distribution over a sample of patients rather than over multiple disease cases within one geographical area. We show how the distance relation between tumour and phone can be modelled nonparametrically and, with various parametric functions, how covariates can be included in the model and how to test for the effect of distance. To illustrate the models, we apply them to a subset of the data from the Interphone Study, a large multinational case-control study on the association between brain tumours and mobile phone use

    Mobile Phones and Multiple Sclerosis – A Nationwide Cohort Study in Denmark

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    We investigated the risk of, prognosis of and symptoms of multiple sclerosis (MS) among all Danish residents who owned a mobile phone subscription before 1996. Using the Danish Multiple Sclerosis Registry and Civil Registration System, study subjects were followed up for MS through 2004. Poisson models were used to calculate incidence rate ratios (IRR, age range: 18–64 years) and mortality rate ratios (MRR, age range: 18+) and to compare presenting symptoms among subscribers and all non-subscribers. A total of 405 971 subscription holders accrued four million years of follow up, with men accounting for 86% of the observation time. Among subscription holding men, the IRR of MS was close to unity, overall as well as 13+ years after first subscription (IRR 1.02, 95% CI: 0.48–2.16). Among women, the IRR was 3.43 (95% CI: 0.86–13.72) 13+ years after first subscription, however, based on only two cases. Presenting symptoms of MS differed between subscribers and non-subscribers (p = 0.03), with slightly increased risk of diplopia in both genders (IRR: 1.38, 95% CI: 1.02–1.86), an increased risk of fatigue among women (IRR: 3.02, 95% CI: 1.45–6.28), and of optic neuritis among men (IRR: 1.38, 95% CI: 1.03–1.86). Overall the MRR was close to one (MRR: 0.91, 95%CI 0.70–1.19) among MS-patients with a subscription and although we observed some increased MRR estimates among women, these were based on small numbers. In conclusion, we found little evidence for a pronounced association between mobile phone use and risk of MS or mortality rate among MS patients. Symptoms of MS differed between subscribers and nonsubscribers for symptoms previously suggested to be associated with mobile phone use. This deserves further attention, as does the increased long-term risk of MS among female subscribers, although small numbers and lack of consistency between genders prevent causal interpretation

    Exposure to Polycyclic Aromatic Hydrocarbons Among Never Smokers in Golestan Province, Iran, an Area of High Incidence of Esophageal Cancer – a Cross-Sectional Study with Repeated Measurement of Urinary 1-OHPG in Two Seasons

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    Studies have suggested a possible role of polycyclic aromatic hydrocarbons (PAHs) in the etiology of esophageal cancer in Golestan Province, Iran, where incidence of this cancer is very high. In order to investigate the patterns of non-smoking related exposure to PAHs in Golestan, we conducted a cross-sectional study collecting questionnaire data, genotyping polymorphisms related to PAH metabolism, and measuring levels of 1-hydroxypyrene glucuronide (1-OHPG), a PAH metabolite, in urine samples collected in two seasons from the same group of 111 randomly selected never-smoking women. Beta-coefficients for correlations between 1-OHPG as dependent variable and other variables were calculated using linear regression models. The creatinine-adjusted 1-OHPG levels in both winter and summer samples were approximately 110 μmol/molCr (P for seasonal difference = 0.40). In winter, red meat intake (β = 0.208; P = 0.03), processed meat intake (β = 0.218; P = 0.02), and GSTT1-02 polymorphism (“null” genotype: β = 0.228; P = 0.02) showed associations with 1-OHPG levels, while CYP1B1-07 polymorphism (GG versus AA + GA genotypes: β = –0.256; P = 0.008) showed an inverse association. In summer, making bread at home (> weekly versus never: β = 0.203; P = 0.04), second-hand smoke (exposure to ≥3 cigarettes versus no exposure: β = 0.254; P = 0.01), and GSTM1-02 “null” genotype (β = 0.198; P = 0.04) showed associations with 1-OHPG levels, but GSTP1-02 polymorphism (CT + TT versus CC: β = –0.218; P = 0.03) showed an inverse association. This study confirms high exposure of the general population in Golestan to PAHs and suggests that certain foods, cooking methods, and genetic polymorphisms increase exposure to PAHs

    Developing a company-specific job exposure matrix for the Asbest Chrysotile Cohort Study

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    OBJECTIVES: Exposure assessment for retrospective industrial cohorts are often hampered by limited availability of historical measurements. This study describes the development of company-specific job-exposure matrices (JEMs) based on measurements collected over five decades for a cohort study of 35 837 workers (Asbest Chrysotile Cohort Study) in the Russian Federation to estimate their cumulative exposure to chrysotile containing dust and fibres. METHODS: Almost 100 000 recorded stationary dust measurements were available from 1951-2001 (factories) and 1964-2001 (mine). Linear mixed models were used to extrapolate for years where measurements were not available or missing. Fibre concentrations were estimated using conversion factors based on side-by-side comparisons. Dust and fibre JEMs were developed and exposures were allocated by linking them to individual workers' detailed occupational histories. RESULTS: The cohort covered a total of 515 355 employment-years from 1930 to 2010. Of these individuals, 15% worked in jobs not considered professionally exposed to chrysotile. The median cumulative dust exposure was 26 mg/m3 years for the entire cohort and 37.2 mg/m3 years for those professionally exposed. Median cumulative fibre exposure was 16.4 fibre/cm3 years for the entire cohort and 23.4 fibre/cm3 years for those professionally exposed. Cumulative exposure was highly dependent on birth cohort and gender. Of those professionally exposed, women had higher cumulative exposures than men as they were more often employed in factories with higher exposure concentrations rather than in the mine. CONCLUSIONS: Unique company-specific JEMs were derived using a rich measurement database that overlapped with most employment-years of cohort members and will enable estimation of quantitative exposure-response

    Latin America and the Caribbean code against cancer: Developing evidence-based recommendations to reduce the risk of cancer in Latin America and the Caribbean

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    Latin America and the Caribbean (LAC) has a population of more than 650 million inhabitants (8.5% of the world population),1 with a cancer incidence of more than 1.4 million new patients and more than 670,000 deaths in 2018. These figures will increase by 78% by 2040 to more than 2.5 million people diagnosed with cancer each year, and these patients will require medical attention, care, and support. However, many of these new cancer diagnoses can be prevented through public policies, supportive environments, and lifestyles that promote health and prevent cancer (Fig 1).2 In the LAC region, there are many organizations and institutions providing information on cancer prevention, including national cancer institutes, cancer societies and foundations, and public health agencies. Nevertheless, the information is frequently confusing, overwhelming, or even contradictory. The scientific source and credibility, as well as the primary message, differ according to the type of organization that provides the information (eg, patient organization, scientific or governmental institution).For the LAC region, a coalition of institutions and international organizations has joined forces to adapt the European Code to the cancer risks and situation in the LAC region. This involves collecting, analyzing, and evaluating the scientific evidence to support suitable cancer prevention recommendations to the LAC context. A multistakeholder participation in the project is a key approach to ensure that all players will be owners of the Code and true promoters. The coalition is composed of the Pan-American Health Organization (PAHO; also part of the WHO) and the IARC as leading international organizations; a Scientific Committee of senior researchers and distinguished leaders in cancer prevention from LAC; and an Advocacy Group representing important organizations in LAC, including the Latin American and Caribbean Society of Medical Oncology, the Network of Latin-American Cancer Institutes, the Healthy Caribbean Coalition, and the Association of Latin American Leagues Against Cancer.Fil: Cazap, Eduardo. Sociedad Latinoamericana y del Caribe de Oncología Médica; ArgentinaFil: de Almeida, Liz Maria. Instituto Nacional de Câncer Brasil Jose Alencar Gomes da Silva; BrasilFil: Arrossi, Silvina. Centro de Estudios de Estado y Sociedad; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: García, Patricia J.. Universidad Cayetano Heredia; PerúFil: Garmendia, María Luisa. Universidad de Chile; ChileFil: Gil, Enrique. South America Pan-American Health Organization; PerúFil: Hassel, Trevor. Healthy Caribbean Coalition; BarbadosFil: Mayorga, Rubén. South America Pan-American Health Organization; PerúFil: Mohar, Alejandro. Universidad Nacional Autónoma de México; MéxicoFil: Murillo, Raúl. Centro Javeriano de Oncología; ColombiaFil: Owen, Gabriel O.. Healthy Caribbean Coalition; BarbadosFil: Paonessa, Diego. Liga Argentina de Lucha contra el Cancer; ArgentinaFil: Santamaría, Julio. Centro Hemato Oncológico Panamá; PanamáFil: Tortolero Luna, Guillermo. Universidad de Puerto Rico; Puerto RicoFil: Zoss, Walter. Red de Institutos e Instituciones Nacionales de Cancer; BrasilFil: Herrero, Rolando. Agencia Internacional para la Investigación del Cáncer; FranciaFil: Luciani, Silvana. Pan-American Health Organization; Estados UnidosFil: Schüz, Joachim. Agencia Internacional para la Investigación del Cáncer; FranciaFil: Espina, Carolina. Agencia Internacional para la Investigación del Cáncer; Franci
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