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The process of urbanization entails social improvements with the consequential better quality-of-life for urban residents. However, in many low-income and some middle-income countries, urbanization conveys inequality and exclusion, creating cities and dwellings characterized by poverty, overcrowded conditions, poor housing, severe pollution, and absence of basic services such as water and sanitation. Slums in large cities often have an absence of schools, transportation, health centers, recreational facilities, and other such amenities. Additionally, the persistence of certain conditions, such as poverty, ethnic heterogeneity, and high population turnover, contributes to a lowered ability of individuals and communities to control crime, vandalism, and violence. The social vulnerability in health is not a "natural" or predefined condition but occurs because of the unequal social context that surrounds the daily life of the disadvantaged, and often, socially excluded groups. Social exclusion of individuals and groups is a major threat to development, whether to the community social cohesion and economic prosperity or to the individual self-realization through lack of recognition and acceptance, powerlessness, economic vulnerability, ill health, diminished life experiences, and limited life prospects. In contrast, social inclusion is seen to be vital to the material, psychosocial, and political aspects of empowerment that underpin social well-being and equitable health. Successful experiences of cooperation and networking between slum-based organizations, grassroots groups, local and international NGOs, and city government are important mechanisms that can be replicated in urban settings of different low- and middle-income countries. With increasing urbanization, it is imperative to design health programs for the urban poor that take full advantage of the social resources and resourcefulness of their own communities.

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Las neoplasias ocupacionales son altamente prevenibles. Esta comunicación resume los datos de los riesgos cancerígenos ocupacionales, destacando grupos importantes de trabajadores y la prevención. La Agencia Internacional para la Investigación del Cáncer, IARC, ha identificado en el Grupo 1, causa cáncer en humanos, 29 agentes que pueden presentarse en el lugar de trabajo, 26 en el Grupo 2 A, probablemente cancerígeno, y 113 en el Grupo 2B, posiblemente cancerígeno. Los agentes frecuentes en Centroamérica incluyen la radiación solar, Grupo 1, y la radiación ultravioleta, 2A, las emisiones diesel, 2A, los hidrocarburos poliaromáticos, 1-3, el humo de tabaco ambiental, 1, los compuestos de cromo hexavalente, 1, y el benceno, 1. En cuanto a los cánceres de mujeres, estudios de cáncer de mama y ovarios sugieren asociaciones con agentes ocupacionales. Los datos en la economía informal son pocos. Peligros cancerígenos para agricultores y peones agrícolas contemplan la exposición a radiación ultravioleta solar, virus, zoonosis, polvos, aflatoxinas, emisiones de diesel, solventes y plaguicidas. Agentes cancerígenos potenciales presentes en el Sector Salud incluyen: óxido de etileno, formaldehído, humo de tabaco ambiental, tricloroetileno, tetracloroetileno, benceno, asbesto, drogas, hormonas, antibióticos, plaguicidas, virus y desechos y gases cancerígenos. Algunas exposiciones durante el desarrollo y la infancia someten a los niños a riesgos cancerígenos. Prevenir los riesgos para la salud en el lugar de trabajo es responsabilidad del empleador. Se debe actuar con precaución en respuesta a la limitada evidencia plausible y creíble, sobre un peligro probable, y establecer comisiones mixtas de salud y seguridad en lugares de trabajo.

Occupational cancers are highly preventable. This communication summarizes the data on occupational carcinogenic hazards, highlighting important worker groups and prevention. The International Agency for Research on Cancer (IARC) has classified 29 agents that may occur atwork in Group 1 (carcinogenic in humans); 26 in Group 2A (probably carcinogenic); and 113 in Group 2B (possibly carcinogenic). Frequent occupational carcinogens in Central America include solar (Group 1) and ultraviolet (2A) radiation, diesel emissions (2A), polyaromatichydrocarbons (1-3), environmental tobacco smoke (1), hexavalent chromium compounds (1) andbenzene (1). Regarding women, studies on breast and ovarian cancer suggest associations with occupational exposures. The data on carcinogenic risks in the informal economy are scanty. Carcinogenic agents that may be present occur in agriculture include solar radiation, aflatoxins, diesel emissions, viruses, dusts, solvents and pesticides. Carcinogenic agents in the health sector include ethylene oxide; formaldehyde; environmental tobacco smoke; tri- and tetrachloroethylene; benzene; asbestos; carcinogenic drugs, hormones, antibiotics, pesticides, viruses and waste materials; and carcinogenic gases. Environmental exposures during development and infancy may cause childhood cancer. Prevention of health risks at the workplace is the responsibility ofthe employer. The principle of precaution, due to sparse, plausible and credible evidence about probable danger and the establishment of safety and health committees are recommended.

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OBJECTIVES: Parental exposure to pesticides and the risk of leukemia in offspring were examined in a population-based case-control study in Costa Rica. METHODS: All cases of childhood leukemia (N=334), in 1995-2000, were identified at the Cancer Registry and the Children's Hospital. Population controls (N=579) were drawn from the National Birth Registry. Interviews of parents were conducted using conventional and icon-based calendar forms. An exposure model was constructed for 25 pesticides in five time periods. RESULTS: Mothers' exposures to any pesticides during the year before conception and during the first and second trimesters were associated with the risk [odds ratio (OR) 2.4, 95% confidence interval (95% CI) 1.0-5.9; OR 22, 95% CI 2.8-171.5; OR 4.5, 95% CI 1.4-14.7, respectively] and during anytime (OR 2.2, 95% CI 1.0-4.8). An association was found for fathers' exposures to any pesticides during the second trimester (OR 1.5, 95% CI 1.0-2.3). An increased risk with respect to organophosphates was found for mothers during the first trimester (OR 3.5, 95% CI 1.0-12.2) and for fathers during the year before conception and the first trimester (OR 1.5, 95% CI 1.0-2.2 and OR 1.6, 95% CI 1.0-2.6, respectively), and benzimidazoles during the first, second, and third trimesters of pregnancy (OR 2.2, 95% CI 1.0-4.4; OR 2.2, 95% CI 1.0-5.0; OR 2.2, 95% CI 1.0-5.2, respectively). There was a suggestion of an exposure-response gradient for fathers as regards picloram, benomyl, and paraquat. Age at diagnosis was positively associated with fathers' exposures and inversely associated with mothers' exposures. CONCLUSIONS: The results suggest that parental exposure to certain pesticides may increase the risk of leukemia in offspring.

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In epidemiology, it is necessary that exposure indicators have good validity in order to obtain valid results when measuring the risks associated with occupational exposure to environmental noxious agents. However, ensuring the validity of past exposure data is no easy task. Because there are no environmental hygiene measures or representative levels of bioindicators signaling past exposure, self-reports have been used as a source of indirect exposure data. Unfortunately, data on specific agents are commonly poor and need to be complemented with data on the determinants of exposure. The validity of self-reports improves when certain techniques, such as control lists and icons, are employed, and the quality of individual exposure data improves when secondary data on exposure and its conditioning or determining factors are incorporated. Exposure can be determined by means of exposure matrices, assessment by experts, and exposure models, and by using a combination of primary and secondary data on exposure and its conditioning factors. Matrices contain pooled data and can thus lead to errors in classifying individual exposure and to biased risk estimates. Assessment by experts is probably the method with the highest validity, but it can become expensive when studies are large. It is also feasible to use a formal model for assessing perceivable exposures, complemented with expert assessments whenever the results of the model appear to deviate from reality.

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La validez de los indicadores de exposición es una condición necesaria en epidemiología si se han de obtener resultados válidos en la medición de los riesgos asociados con la exposición a agentes nocivos en el entorno laboral. Sin embargo, llevar a cabo la validación de estos indicadores de exposiciones pasadas no es tarea fácil. Debido a la falta de mediciones de referencia en el ámbito de la higiene industrial y de concentraciones representativas de bioindicadores que reflejen las exposiciones pasadas, el método de los autoinformes se ha utilizado para recoger datos de exposición indirectos. No obstante, los datos acerca de agentes nocivos específicos son a menudo deficientes y deben completarse con otros sobre los factores condicionantes de la exposición. La validez de los autoinformes mejora cuando se utilizan listas de verificación e iconos ilustrativos, mientras que la calidad de la información sobre las exposiciones personales mejora cuando se incorporan datos secundarios acerca de las exposiciones y de los factores que las condicionan o determinan. La exposición se puede determinar mediante matrices de exposición, evaluación por expertos y modelos de exposición, integrando datos primarios y secundarios acerca de las exposiciones y sus factores condicionantes. Las matrices contienen datos agrupados y, por consiguiente, pueden llevar a errores a la hora de clasificar las exposiciones individuales e introducir sesgos en la estimación de los riesgos. La evaluación por expertos es probablemente el método con el índice de validez más alto, pero puede entrañar costos muy altos en el caso de estudios de cierta magnitud. Otra posibilidad con buenas perspectivas es la de utilizar un modelo formal para evaluar las exposiciones patentes y mejorarlo mediante la evaluación por expertos en situaciones en las cuales los resultados del modelo parezcan alejarse de la realidad.

In epidemiology, it is necessary that exposure indicators have good validity in order to obtain valid results when measuring the risks associated with occupational exposure to environmental noxious agents. However, ensuring the validity of past exposure data is no easy task. Because there are no environmental hygiene measures or representative levels of bioindicators signaling past exposure, self-reports have been used as a source of indirect exposure data. Unfortunately, data on specific agents are commonly poor and need to be complemented with data on the determinants of exposure. The validity of self-reports improves when certain techniques, such as control lists and icons, are employed, and the quality of individual exposure data improves when secondary data on exposure and its conditioning or determining factors are incorporated. Exposure can be determined by means of exposure matrices, assessment by experts, and exposure models, and by using a combination of primary and secondary data on exposure and its conditioning factors. Matrices contain pooled data and can thus lead to errors in classifying individual exposure and to biased risk estimates. Assessment by experts is probably the method with the highest validity, but it can become expensive when studies are large. It is also feasible to use a formal model for whenever the results of the model appear to deviate from reality

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We describe a model for the retrospective assessment of parental exposure to 26 pesticides, selected by toxicity-based prioritization, in a population-based case-control study of childhood leukaemia in Costa Rica (301 cases, 582 controls). The model was applied to a subset of 227 parents who had been employed or self-employed in agriculture or livestock breeding. It combines external data on pesticide use for 14 crops, 21 calendar years and 14 regions, and individual interview data on determinants (task and technology, personal protective equipment, field reentry, storing of pesticides, personal hygiene) of exposure. Recall was enhanced by use of checklists of pesticides in the interview. An external database provided information on the application rate (proxy for intensity of potential exposure) for each pesticide. The calendar time was individually converted to five time windows (year before conception, first, second and third trimester, and first year of the child). Time-windowed individual data on determinants of exposure and their expert-based general weights and their category-specific hazard values jointly provided an individual determinant score. This score was multiplied by the application rate to obtain an individual index of exposure intensity during application. Finally, average exposure intensity during entire time windows was estimated by incorporating in the model the individual time fraction of exposure during application. Estimates of exposure intensities were proxies assumed to be proportional to dermal exposure intensity, which represents the major pathway of occupational exposure to pesticides. A simulated sensitivity analysis resulted in a correlation coefficient of 0.91 between two sets of 10 000 values of individual exposure indices, based on two different but realistic sets expert-assigned weights. Lack of measurement data on concurrent exposures in comparable circumstances precluded direct validation of the model.

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Multiple exposures and rapidly changing use patterns are obstacles for adequate recall of pesticide exposures in epidemiologic studies. We present a simple stepwise approach for prioritization of pesticides as part of the exposure assessment strategy in an ongoing case-control study on pesticides and childhood leukemia in Costa Rica. Pesticide imports between 1977 and 2000, approximately the pertinent exposure period, were surrogates for use data. In the first phase, 323 active ingredients were identified, of which 219 were eliminated based on low usage and absence or negative results in a preliminary search in three major toxicity databases. In the second phase, the remaining 104 pesticides underwent scoring for their toxicodynamic potential (TDP) with regard to carcinogenicity, mutagenicity, and teratogenicity, weighted in this order. Bioavailability was assessed when TDP was multiplied by a weight for persistence and bioaccumulation, producing the intrinsic toxic potential (ITP). ITP was multiplied by an index of quantity (QI) of pesticide used in the exposure period, resulting in a weighted toxic potential (WTP). The top 25 positions in each of the four rankings (TDP, ITP, QI, and WTP) yielded together 64 highest-priority pesticides. This prioritization process has to be complemented with a further breakdown into crop-, time-, and biocide-specific shortlists to achieve a recall tool suitable for developing countries. Different parameters for prioritization assure inclusion of all relevant pesticides with regard to toxicity and bioavailability. The method contributes to cancer epidemiology in developing countries with access to basic use data and the Internet. The method is adaptable to other health outcomes.

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An icon-calendar interview form (ICF) for a case-control study of childhood leukemias and parental exposures to pesticides is described. It includes calendar sheets, icons for life events, crops, jobs, regions, non-agricultural jobs, application techniques and personal protection, markers for durations of exposure patterns, and checklists of pesticides. The ICF collects monthly data from two years before birth until diagnosis of cancer (index children) or until either the interview date or age 15 (controls). Data ascertainment was easy in 62% of interviews, moderately easy in 32%, and difficult in 6%. Seventy-eight subjects delivered data on specific pesticides with pesticide checklists, which improved identification of pesticides. ICF performs satisfactorily for crops, tasks, and other determinants of exposure. Data on pesticides will be further improved by introducing external data use on different crops, time periods, and regions, and by exposure modeling for 27 pesticides.

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The CAREX data system converts national workforce volumes and proportions of workers exposed to workplace carcinogens into numbers of exposed in 55 industrial categories. CAREX was adapted for Costa Rica for 27 carcinogens and seven groups of pesticides. Widespread workplace carcinogens in the 1.3 million workforce of Costa Rica are solar radiation (333,000 workers), diesel engine exhaust (278,000), environmental tobacco smoke (71,000), hexavalent chromium compounds (55,000), benzene (52,000), wood dust (32,000), silica dust (27,000), lead and inorganic lead compounds (19,000), and polycyclic aromatic compounds (17,000). The most ubiquitous pesticides were paraquat and diquat (175,000), mancozeb, maneb, and zineb (49,000), chlorothalonil (38,000), benomyl (19,000), and chlorophenoxy herbicides (11,000). Among women, formaldehyde, radon, and methylene chloride overrode pesticides, chromium, wood dust, and silica dust in numbers of exposed. High-risk sectors included agriculture, construction, personal and household services, land and water transport and allied services, pottery and similar industries, woodworks, mining, forestry and logging, fishing, manufacturing of electrical machinery, and bar and restaurant personnel.

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Childhood leukaemia incidence in Costa Rica during 1981-96, among the highest in the world, was analysed by histology, gender, birth year, time period of diagnosis, age at diagnosis and region. Numbers of cases were extracted from the database of the National Cancer Registry (RNT) of Costa Rica. Person-years at risk were calculated from census data and post-census population estimates. During the follow-up, 918 cases of leukaemia in children under 15 years (510 boys, 408 girls) were reported to the RNT (41% of all childhood malignancies), with an overall age-standardised incidence rate of 56 per million person-years. Acute lymphocytic leukaemia (ALL) represented 79% and acute non-lymphocytic leukaemia (ANLL) 16% of the cases, with rates of 43 and 9 per million person-years respectively. There were downward trends in incidence of total leukaemias, ALL and ANLL and 'not otherwise specified' (NOS) combined. Incidence of ALL was highest at 1-4 years of age in boys and girls, whereas ANLL peaked in girls during the first year of life. During 1991-96, the decrease in ALL was significant (P = 0.042). A multivariable Poisson regression model identified significant excesses of ALL for boys, for age groups 1-4 and 5-9 years and for three out of seven regions. Possible reasons for the high rates in Costa Rica are discussed.

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Incidence rates of malignant central nervous system (CNS) tumours in children in Costa Rica are presented in an international perspective. For the 16-year period 1981-96, a total of 256 CNS tumours were registered in children below age 15 years by the National Tumour Registry of Costa Rica. The age-standardised incidence rate was 15.2 per million person-years, with a male-to-female ratio of 1.4. The median age-standardised incidence rates of selected registries in other Latin American countries were 19.3, in other developing countries 12.0 and in industrialised countries 29.6 per million person-years. The comparatively low incidence rates in Costa Rica were evident in all diagnostic subgroups, most notably in the youngest age group and for tumours in the brain stem. In the Central Valley, where the capital and the only specialised paediatric hospital are situated, the crude incidence rate was 18.1 [95% CI 15.1, 21.1] compared with 10.5 [95% CI 8.3, 12.8] per million person-years in the rest of the country (RR = 1.7, 95% CI 1.3, 2.3). There was no evidence of any increase over time. The data in this study cannot exclude under-diagnosis and, to a lesser degree, under-registration as a partial explanation of the low incidence rates of malignant CNS tumours in children in Costa Rica.

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