ABSTRACT
OBJECTIVE: Environmental and occupational agents are causes of cancer and disease worldwide while their control and the reduction of the associated disease burden remains complex. MATERIALS AND METHODS: This paper summarizes the current status of the burden of environmental and occupational causes of disease in the Americas based on presentations from a panel on environment, occupation and other environmental risk factors for cancer in the Americas, delivered in Panama, at the international conference Promoting Health Equity and Transnational Collaborations for the Prevention and Control of Cancer in the Americas. RESULTS: Three case studies are presented to illustrate the impact of specific environmental and occupational agents and the challenge of control. CONCLUSIONS: There are still fully avoidable exposures to carcinogens, as well documented in the case of asbestos in Brazil. Thus, there are abundant targets for intervention to reduce cancer in the Americas.
OBJETIVO: Los agentes ambientales y ocupacionales son causas de cáncer y enfermedades en todo el mundo, mientras que su control y reducción de la carga de enfermedad asociada siguen siendo puntos complejos. MATERIAL Y MÉTODOS: Este documento resume el estado actual de la carga de las causas ambientales y ocupacionales de las enfermedades en las Américas a partir de las presentaciones de un panel sobre medio ambiente, ocupación y otros factores de riesgo ambientales para el cáncer en las Américas, realizado en Panamá, en la conferencia internacional Promoviendo la Equidad en Salud y las Colaboraciones Transnacionales para la Prevención y el Control del Cáncer en las Américas. RESULTADOS: Se presentan tres estudios de caso para ilustrar el impacto de agentes ambientales y ocupacionales específicos y el desafío del control. CONCLUSIONES: Todavía hay exposiciones totalmente evitables a los carcinógenos, como está bien documentado en el caso del asbesto en Brasil. Hay abundantes puntos estratégicos de intervención para reducir el cáncer en las Américas.
Subject(s)
Disease/etiology , Environmental Pollutants/toxicity , Occupational Diseases/etiology , Occupational Exposure/adverse effects , Air Pollution, Indoor/adverse effects , Americas , Asbestos/toxicity , Brazil , Carcinogens/toxicity , Epidemiology , Humans , Mortality, Premature , Neoplasms/etiology , Neoplasms/prevention & control , Occupational Diseases/prevention & control , Panama , Petroleum Pollution/adverse effects , Risk Factors , Sex DistributionABSTRACT
Abstract: Objective: Environmental and occupational agents are causes of cancer and disease worldwide while their control and the reduction of the associated disease burden remains complex. Materials and methods: This paper summarizes the current status of the burden of environmental and occupational causes of disease in the Americas based on presentations from a panel on environment, occupation and other environmental risk factors for cancer in the Americas, delivered in Panama, at the international conference Promoting Health Equity and Transnational Collaborations for the Prevention and Control of Cancer in the Americas. Results: Three case studies are presented to illustrate the impact of specific environmental and occupational agents and the challenge of control. Conclusions: There are still fully avoidable exposures to carcinogens, as well documented in the case of asbestos in Brazil. Thus, there are abundant targets for intervention to reduce cancer in the Americas.
Resumen: Objetivo: Los agentes ambientales y ocupacionales son causas de cáncer y enfermedades en todo el mundo, mientras que su control y reducción de la carga de enfermedad asociada siguen siendo puntos complejos. Material y métodos: Este documento resume el estado actual de la carga de las causas ambientales y ocupacionales de las enfermedades en las Américas a partir de las presentaciones de un panel sobre medio ambiente, ocupación y otros factores de riesgo ambientales para el cáncer en las Américas, realizado en Panamá, en la conferencia internacional Promoviendo la Equidad en Salud y las Colaboraciones Transnacionales para la Prevención y el Control del Cáncer en las Américas. Resultados: Se presentan tres estudios de caso para ilustrar el impacto de agentes ambientales y ocupacionales específicos y el desafío del control. Conclusiones: Todavía hay exposiciones totalmente evitables a los carcinógenos, como está bien documentado en el caso del asbesto en Brasil. Hay abundantes puntos estratégicos de intervención para reducir el cáncer en las Américas.
Subject(s)
Humans , Disease/etiology , Occupational Exposure/adverse effects , Environmental Pollutants/toxicity , Occupational Diseases/etiology , Panama , Asbestos/toxicity , Americas , Brazil , Carcinogens/toxicity , Petroleum Pollution/adverse effects , Epidemiology , Risk Factors , Air Pollution, Indoor/adverse effects , Sex DistributionABSTRACT
BACKGROUND: An inverse association between selenium status and incidence of different neoplasias including gastric cancer has been reported. This pilot study aimed to determine and compare selenium status in two Colombian populations with different gastric cancer risks: a high-risk area in the volcanic region of the Andes Mountains and a low-risk area on the Pacific coast. METHODS: Eighty nine adult males were recruited in the outpatient clinics of two public hospitals (44 and 45 from high- and low-risk areas, respectively) and provided a blood sample. Seventy one (79.8%) participants underwent upper gastrointestinal endoscopy. Plasma selenium was assayed using a fluorometric method, selenoprotein-P by ELISA, and glutathione peroxidase activity by a spectrophometric method. Histological diagnosis and Helicobacter pylori infection were evaluated in gastric biopsy samples. Unpaired samples t-test and linear regression analyses were used for statistical analyses. RESULTS: Although none of the subjects in either of the two geographic areas was selenium deficient, the level of plasma selenium was significantly lower in men from the high-risk area compared with those from the low-risk area. Levels of selenoprotein-P and glutathione peroxidase activity were similar between groups after adjustment for confounders. Selenium measurements were not associated with histopathological diagnosis. CONCLUSIONS: The high incidence of gastric cancer in the Andean region of Colombia is unlikely to be explained by selenium deficiency. We cannot exclude, however, that suboptimal selenium levels may exist in the gastric mucosa of subjects in the high-risk area. Therefore, the benefit of selenium supplementation in gastric cancer prevention cannot be dismissed.
Subject(s)
Selenium/blood , Selenoprotein P/blood , Stomach Neoplasms/epidemiology , Adult , Colombia/epidemiology , Diet , Humans , Male , Middle Aged , Pilot Projects , Risk Factors , Stomach Neoplasms/bloodABSTRACT
It has been proposed that eradication of Helicobacter pylori infection is a sound strategy for gastric cancer prevention. Several factors including smoking have been associated to treatment failure rates. This study aimed to evaluate the smoking effect on the efficacy of H. pylori therapy, as well as on the histological parameters in the gastric mucosa from subjects from a high gastric cancer risk area. Two-hundred-sixty-four Colombian subjects with gastric precancerous lesions who participated in a chemoprevention trial, received anti-H. pylori treatment at baseline and had data recorded on cigarette use, were included in this study. A detailed histopathological assessment of the gastric mucosa was performed in biopsies taken before any intervention. H. pylori eradication was assessed in gastric biopsies at 36 months post-treatment. The overall eradication rate was 52.3%; rates of 41.3% and 57.1% were observed for active-smokers and non-smokers, respectively. Multivariate logistic regression analysis showed that smokers had a 2-fold higher probability of failure in Helicobacter pylori eradication than non-smokers (OR: 2.0; 95% CI: 1.01-3.95). At baseline, active-smokers had a higher score of intestinal metaplasia compared to non-smokers. In the corpus mucosa, active-smokers showed lower scores of H. pylori density, total inflammation, neutrophil infiltration, and mucus depletion than non-smokers. In the antrum, no significant differences were observed between active-smokers and non-smokers. In summary, in patients who smoked, H. pylori treatment was less effective. Smoking cessation may benefit H. pylori eradication rates.
Subject(s)
Gastric Mucosa/microbiology , Gastritis, Atrophic/drug therapy , Helicobacter Infections/drug therapy , Helicobacter pylori , Smoking/adverse effects , Amoxicillin/therapeutic use , Anti-Infective Agents/therapeutic use , Bismuth/therapeutic use , Colombia , Drug Therapy, Combination , Female , Follow-Up Studies , Gastric Mucosa/pathology , Gastritis, Atrophic/microbiology , Gastritis, Atrophic/pathology , Humans , Male , Metaplasia , Metronidazole/therapeutic use , Organometallic Compounds/therapeutic use , Precancerous Conditions/drug therapy , Precancerous Conditions/microbiology , Regression Analysis , Salicylates/therapeutic use , Treatment FailureABSTRACT
It has been proposed that eradication of Helicobacter pylori infection is a sound strategy for gastric cancer prevention. Several factors including smoking have been associated to treatment failure rates. This study aimed to evaluate the smoking effect on the efficacy of H. pylori therapy, as well as on the histological parameters in the gastric mucosa from subjects from a high gastric cancer risk area. Two-hundred-sixty-four Colombian subjects with gastric precancerous lesions who participated in a chemoprevention trial, received anti- H. pylori treatment at baseline and had data recorded on cigarette use, were included in this study. A detailed histopathological assessment of the gastric mucosa was performed in biopsies taken before any intervention. H. pylori eradication was assessed in gastric biopsies at 36 months post-treatment. The overall eradication rate was 52.3%; rates of 41.3% and 57.1% were observed for active-smokers and non-smokers, respectively. Multivariate logistic regression analysis showed that smokers had a 2-fold higher probability of failure in Helicobacter pylori eradication than non-smokers (OR: 2.0; 95% CI: 1.01-3.95). At baseline, activesmokers had a higher score of intestinal metaplasia compared to non-smokers. In the corpus mucosa, active-smokers showed lower scores of H. pylori density, total inflammation, neutrophil infiltration, and mucus depletion than non-smokers. In the antrum, no significant differences were observed between active-smokers and non-smokers. In summary, in patients who smoked, H. pylori treatment was less effective. Smoking cessation may benefit H. pylori eradication rates.
La erradicación del Helicobacter pylori ha sido propuesta como medida promisoria en la prevención del cáncer gástrico. Varios factores, incluyendo el tabaquismo, se asocian con la falla del tratamiento. El objetivo de este estudio fue evaluar el efecto del tabaquismo en la eficacia del tratamiento anti-H. pylori y en la histología gástrica en residentes de una zona de alto riesgo de cáncer gástrico. Este estudio incluyó 264 sujetos colombianos con lesiones gástricas preneoplásicas que participaron en un estudio de quimioprevención, recibieron tratamiento anti-H. pylori al ingreso, y proveyeron información sobre tabaquismo. Se realizó un detallado análisis histopatológico en las biopsias colectadas al ingreso. La erradicación de la infección fue evaluada en las biopsias gástricas a los 36 meses post-tratamiento. El porcentaje general de erradicación fue de 52.3%, con proporciones de 41.3% y 57.1% en fumadores activos y no fumadores, respectivamente. El análisis de regresión logística múltiple mostró que el riesgo de presentar falla al tratamiento fue doble en fumadores en comparación con los no fumadores (OR: 2.0; 95% CI: 1.01-3.95). Los fumadores presentaron un mayor índice de metaplasia intestinal comparado con los no fumadores. En la mucosa del cuerpo gástrico los fumadores mostraron menores índices de colonización por H. pylori, inflamación total, infiltración de neutrófilos y depleción de moco que los no fumadores. En el antro no se observaron diferencias significacomtivas entre ambos grupos. En conclusión, el tratamiento anti-H. pylori fue menos efectivo en sujetos fumadores. La cesación del consumo de tabaco puede beneficiar las tasas de erradicación del H. pylori.
Subject(s)
Humans , Male , Female , Bismuth/therapeutic use , Gastric Mucosa/microbiology , Gastritis, Atrophic/drug therapy , Helicobacter Infections/drug therapy , Helicobacter pylori , Organometallic Compounds/therapeutic use , Salicylates/therapeutic use , Smoking/adverse effects , Amoxicillin/therapeutic use , Anti-Infective Agents/therapeutic use , Colombia , Drug Therapy, Combination , Follow-Up Studies , Gastric Mucosa/pathology , Gastritis, Atrophic/microbiology , Gastritis, Atrophic/pathology , Metaplasia , Metronidazole/therapeutic use , Precancerous Conditions , Regression Analysis , Treatment FailureABSTRACT
PURPOSE: The aim of the study is to investigate whether a new infection caused by Helicobacter pylori in preschool children transiently or permanently affects height and weight. METHODS: A cohort of 347 children from three day care centers was followed up for a median of 494 days. Breath tests and anthropometric measurements were performed every 2 to 4 months. The lag effect of a new infection on linear growth during a period of 8 months was analyzed by using mixed-effects models. RESULTS: One hundred five children (30.3%) became infected during the follow-up period and accumulated 92 person-years of follow-up. A significant decrease in growth velocity was observed during the first 4 months after infection. There was no height catch-up in infected children, and after 8 months, an infected child had a cumulative difference of 0.24 cm (growth velocity; 95% confidence interval, 0.22-0.26) compared with an uninfected child. Newly infected children experienced a small decrease in weight at the first visit compared with uninfected children, which became nonsignificant after the second visit without catch-up. CONCLUSIONS: This study shows a significant and nontransient effect of infection caused by H. pylori on height and weight. Potential interventions that target infected preschool children are likely to prevent growth retardation.
Subject(s)
Body Height , Body Weight , Helicobacter Infections/complications , Helicobacter pylori , Child, Preschool , Cohort Studies , Colombia/epidemiology , Female , Humans , Infant , MaleABSTRACT
The 13C-urea breath test (UBT) is currently regarded as one of the most important noninvasive diagnostic methods for detecting Helicobacter pylori (H. pylori) infection in adults and children. However, for infants and young children, the standard for UBT interpretation has not been validated, and its reliability has not been established for diagnosing H. pylori infection in this group. The primary outcome data from UBT consist of mixture data, which come from subjects whose H. pylori infection classifications are unconfirmed. In this paper, we propose the finite mixture distribution method to identify a reliable UBT cut-off value in a large baseline sample in which gastric biopsy is not available to confirm the H. pylori infection in younger children. Maximum likelihood estimators of the parameters in the mixture model were obtained using an expectation maximization (EM) algorithm. The standard deviation of the cut-off point was estimated by bootstrap methods. We applied the same analytical methods to the UBT results yielded from the follow up, as well as the overall UBT results in the longitudinal cohort data. The cut-off points from those UBT data sets are similar. The advantage of the finite mixture model is that it may be used to calculate sensitivity and specificity in the absence of other diagnostic tests.
Subject(s)
Breath Tests , Helicobacter pylori/isolation & purification , Urea/analysis , Carbon Isotopes , Child, Preschool , Cohort Studies , Colombia , Humans , Infant , Likelihood Functions , ROC Curve , Sensitivity and SpecificityABSTRACT
BACKGROUND: Helicobacter pylori infection is usually acquired during childhood and is a known risk factor for the development of gastric malignancies in adulthood. It has been reported that early age at first infection may determine a neoplastic outcome in adults. The purpose of this study was to determine the prevalence of Helicobacter pylori infection in children residing in areas with high (Pasto) and low risk (Tumaco) of gastric cancer in Colombia to evaluate whether differences in the age of acquisition of H. pylori infection were present in the two populations. MATERIALS AND METHODS: The study sample was based on a census taken in 1999. Using the (13)C-urea breath test, we compared the prevalence of H. pylori infection among children aged 1-6 years. RESULTS: Among 345 children in Pasto, 206 (59.7%) were H. pylori-positive, compared with 188 (58.6%) among 321 children in Tumaco. The two populations share a common pattern of very early age at infection and marked increase in prevalence during the first 4 years of life. No differences in any one year were observed when comparing the two groups. CONCLUSIONS: The prevalence of infection was similarly high and increased with age in both populations. In these populations the age of acquisition of H. pylori after 1 year of age does not appear to be a primary factor responsible for the differences in the rates of gastric cancer incidence in adults. Previous findings in adults showed lower prevalence of the most virulent genotypes in Tumaco compared to Pasto, and bacterial virulence may play a key role in determining cancer outcome.
Subject(s)
Helicobacter Infections/epidemiology , Helicobacter pylori/isolation & purification , Stomach Neoplasms/epidemiology , Age of Onset , Anthropometry , Breath Tests , Child , Child, Preschool , Colombia/epidemiology , Cross-Sectional Studies , Female , Helicobacter Infections/diagnosis , Helicobacter Infections/microbiology , Humans , Infant , Male , Prevalence , Risk Factors , Stomach Neoplasms/diagnosisABSTRACT
OBJECTIVE: The aim of this study was to prospectively follow a cohort of children without Helicobacter pylori infection and to compare growth velocity in the children who become infected during follow-up with that of children who remained infection-free. METHODS: Three hundred forty-seven children in general good health, aged 12 to 60 months, who tested negative for H. pylori by the 13C-urea breath test, from three daycare centers in a lower-middle class borough of Cali, Colombia, were monitored for 2.5 years. Anthropometric measurements were performed every 2 months and breath tests every 4 months. Linear mixed models were used to analyze growth velocity in relation to onset of H. pylori infection. RESULTS: One hundred five (30.3%) children who were uninfected at the start of the study became infected during follow-up. Growth velocity in infected children was reduced by 0.042 +/- 0.014 cm/mo (P = 0.003) (approximately 0.5 cm/yr) after adjusting for age. The rate of deceleration in growth velocity was relatively constant over time. CONCLUSIONS: Among these lower-middle class children aged 12 to 60 months from a population with high prevalence of H. pylori infection, a new and sustained infection was followed by significant growth retardation.
Subject(s)
Growth , Helicobacter Infections/physiopathology , Helicobacter pylori , Body Height , Breath Tests , Carbon Isotopes , Child, Preschool , Cohort Studies , Colombia , Family Characteristics , Female , Growth Disorders/microbiology , Helicobacter Infections/diagnosis , Helicobacter Infections/epidemiology , Humans , Infant , Male , Prospective Studies , Socioeconomic Factors , Urea/analysisABSTRACT
Infection with Helicobacter pylori has been recognized as a cause of gastric carcinoma. Although the neoplasia is always detected in adults, the infection starts in childhood. It has been reported that early age at first infection is a determinant of gastric cancer risk. In this study, we examined the histopathology of the gastric mucosa in infected children from a population at high risk for gastric cancer (Pasto, Colombia) and compared it with that of a lower-risk population (New Orleans, LA). Gastric biopsies obtained from antrum and corpus were stained with hematoxylin and eosin and Steiner's silver method. Immunohistochemical stains were used to identify B lymphocytes (CD20), T lymphocytes (CD3 and CD8), macrophages (CD68), and polymorphonuclear neutrophil myeloperoxidase. Morphometric techniques were used to evaluate the immunohistochemical stains. In both populations, the inflammatory lesions were seen predominantly in the antrum. Compared with children from the lower-risk populations, children from the higher-risk population exhibited more severe polymorphonuclear neutrophil infiltration, stromal and intraepithelial lymphocyte infiltration, mucus depletion, and H. pylori colonization density. Regenerative activity was significantly more marked in the lower-risk population. Morphometric analysis of immunohistochemical stains showed increased representation of T lymphocytes and macrophages in the higher-risk population. Most T lymphocytes stained positive for CD8, a marker of suppressor/cytotoxic cells. B lymphocytes were relatively more abundant in the lower-risk population. The possibility that the aforementioned characteristics of H. pylori infection in children are related to cancer risk in adults is discussed.
Subject(s)
Gastritis/microbiology , Gastritis/pathology , Helicobacter Infections/pathology , Helicobacter pylori , Stomach Neoplasms/microbiology , B-Lymphocytes/pathology , Biopsy , CD3 Complex/analysis , CD8 Antigens/analysis , Child , Child, Preschool , Colombia/epidemiology , Epithelium/pathology , Female , Gastric Mucosa/pathology , Humans , Immunohistochemistry , Infant , Louisiana , Macrophages/pathology , Male , Neutrophils/enzymology , Neutrophils/pathology , Peroxidase/analysis , Risk Factors , Stomach Neoplasms/epidemiology , T-Lymphocytes/immunology , T-Lymphocytes/pathologyABSTRACT
A case-control study of oral and pharyngeal cancer involving interviews with 108 cases and 286 controls was carried out in the University Hospital of Montevideo, Uruguay. The study was restricted to males and cases afflicted with lip, salivary gland and nasopharyngeal cancer were excluded. Point estimates of RR associated with smoking variables, alcohol variables, nutritional items and ingestion of hot infusions of the herb Ilex Paraguapensis (Mate) were obtained by logistic regression analysis. Dark tobacco smokers showed a RR 3.4 times higher than light tobacco users and heavy drinkers or wine displayed an OR of 17.2. Mate exposure showed a significant dose-response, after adjustement for age, tobacco and alcohol intake, with a fivefold increase in risk for heavy consumers. Joint exposure to black tobacco and wine displayed very high risks and no significant interactions were observed. The results suggest that the high rates of oropharyngeal cancer could be explained by the multiplicative effect of black tobacco smoking , wine drinking and mate ingestion (AU)
Subject(s)
Humans , Male , Oropharyngeal Neoplasms/etiology , Mouth Neoplasms/etiology , Pharyngeal Neoplasms/etiology , Tobacco Use Disorder/adverse effects , Risk Factors , Wine/adverse effects , Ilex paraguariensis/adverse effects , Alcohol Drinking/adverse effects , UruguayABSTRACT
One hundred seven patients afflicted with incident laryngeal cancer and 290 controls with diseases considered not related to tobacco and alcohol exposure were interviewed in the University Hospital of Montevideo, Uruguay. The study followed a case-referent design, and epidemiologic analysis was carried out at the Louisiana State University, New Orleans. Dark tobacco smoking was the strongest risk factor, with an RR 2.5 times higher than that showed by light (flue-cured) tobacco smokers and 35 times that of non-smokers. Alcohol exposure displayed lesser effects but its interaction with tobacco smoking resulted in very high risks (more than 100 times higher). Among particular types of alcoholic beverages, red wine showed RR's similar to those displayed by hard liquor consumption. The habit of drinking a local tea called mate was associated with a threefold increase in risk, after controlling for the effects of age and tobacco and alcohol consumption. Infrequent consumption of vegetables and fruits showed RR on the order of 2.7, suggesting a role of diet in the causation of laryngeal cancer (AU)