Artículos científicos

URI permanente para esta colecciónhttp://10.0.96.45:4000/handle/11056/14755

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Causas y prevención del cáncer ocupacional
(Colegio de Médicos y Cirujanos, Costa Rica, 2009-04-28) Partanen, Timo; Monge, Patricia; Wesseling, Catharina
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.
Manganese exposure and working memory-related brain activity in smallholder farmworkers in Costa Rica: Results from a pilot study
(Academic Press Inc., 2019-04-06) Rojas Valverde, Daniel; Gutierrez Vargas, Randall; Fuhrimann, Samuel; Menezes Filho, José; Mora, Ana Maria; Palzes, Vanessa; Sagiv, Sharon; Baker, Joseph; Winkler, Mirko; Staudacher, Philipp; Reiss, Allan; Eskenazi, Brenda
Main sources of manganese (Mn) in the general population are diet and drinking water. Mn is also found in ethylene bisdithiocarbamate (EBDC) fungicides used in agriculture or emitted into the air by ferromanganese plants and welding fumes, which can be additional environmental and occupational sources of exposure. High occupational Mn exposure has been linked with motor, behavioral, and cognitive impairment, but its effects on neural function remain poorly understood. We conducted a functional neuroimaging study in a sample of 48 farmworkers in Zarcero County, Costa Rica, an agricultural region where EBDC fungicides are sprayed. We measured Mn concentrations in farmworkers’ toenails (n = 40 farmworkers) and hair (n = 33 farmworkers), and recorded brain activity in the dorsolateral prefrontal cortex during a letter-retrieval working memory task using functional near-infrared spectroscopy (fNIRS). We estimated exposure-outcome associations using multivariable linear egression models adjusted for age and education level. Geometric mean (geometric standard deviation) toenail and hair Mn concentrations were 0.40 μg/g (3.52) and 0.24 μg/g (3.54), respectively. We did not find strong evidence that Mn concentrations were associated with working memory-related brain activity in this sample of farmworkers; we also found null associations between working memory task accuracy and brain activity. However, our small sample size may have limited our ability to detect small effect sizes with statistical precision. Our study demonstrates that fNIRS can be a useful and feasible tool in environmental epidemiology for examining the effects of toxicants, like Mn, on neural function. This may prove to be important for elucidating neuropathological pathways that underlie previously reported ssociations of elevated Mn exposure with neurotoxic effects.
Parental age and the risk of childhood acute myeloid leukemia: results from the Childhood Leukemia International Consortium
(Elsevier Ltd, 2019-04) Panagopoulou, Paraskevi; Auvinen, Anssi; Spector, Logan; Roman, Eve; Pombo-de-Oliveira, Maria; Scheurer, Michael; Mora, Ana Maria; Doody, David; Kane, Eleanor; Ntzani, Evangelia; Martínez Rodríguez, Elenita
Parental age has been associated with several childhood cancers, albeit the evidence is still inconsistent. To examine the associations of parental age at birth with acute myeloid leukemia (AML) among children aged 0–14 years using individual-level data from the Childhood Leukemia International Consortium (CLIC) and non-CLIC studies. We analyzed data of 3182 incident AML cases and 8377 controls from 17 studies [seven registry-based case-control (RCC) studies and ten questionnaire-based case-control (QCC) studies]. AML risk in association with parental age was calculated using multiple logistic regression, meta-analyses, and pooled-effect estimates. Models were stratified by age at diagnosis (infants < 1 year-old vs. children 1–14 years-old) and by study design, using five-year parental age increments and controlling for sex, ethnicity, birthweight, prematurity, multiple gestation, birth order, maternal smoking and education, age at diagnosis (cases aged 1–14 years), and recruitment time period. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) derived from RCC, but not from the QCC, studies showed a higher AML risk for infants of mothers ≥40-year-old (OR = 6.87; 95% CI: 2.12–22.25). There were no associations observed between any other maternal or paternal age group and AML risk for children older than one year. An increased risk of infant AML with advanced maternal age was found using data from RCC, but not from QCC studies; no parental age-AML associations were observed for older children.

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