"Characterization of residential proximity to sources of environmental carcinogens in clusters of Acute Lymphoblastic Leukemia in San Luis Potosi, Mexico".

BACKGROUND: Acute Lymphoblastic Leukemia (ALL) is the most prevalent neoplasia in children and teenagers in Mexico. Although epidemiological data supports that children's residence close to emissions from vehicular traffic or industrial processes increases the risk of ALL; and the IARC states that benzene, PAHs, and PM 2.5 are well-known environmental carcinogens, there is a gap in linking these carcinogenic hazards with the sources and their distribution from scenario perspective. AIM: To identify ALL clusters in the population under 19 years of age and characterize the environment at the neighborhood level by integrating information on sources of carcinogenic exposure using spatial analysis techniques in the Metropolitan Area of San Luis Potosi, Mexico. METHODS: Using the Kernel Density test, we designed an ecological study to identify ALL clusters from incident cases in the population under 19 years of age. A multicriteria analysis was conducted to characterize the risk at the community level from carcinogenic sources. A hierarchical cluster analysis was performed to characterize risk at the individual level based on carcinogenic source count within 1 km for each ALL case. RESULTS: Eight clusters of carcinogenic sources were located within the five identified ALL clusters. The multicriteria analysis showed high-risk areas (by density of carcinogenic source) within ALL clusters. CONCLUSIONS: This study has a limited source and amount of available data on ALL cases, so selection bias is present as well as the inability to rule out residual confounding factors, since covariates were not included. However, in this study, children living in environments with high vehicular density, gas stations, brick kilns, incinerators, commercial establishments burning biomass, or near industrial zones may be at higher risk for ALL.

Lead facilitates foci formation in a Balb/c-3T3 two-step cell transformation model: role of Ape1 function.

Several possible mechanisms have been examined to gain an understanding on the carcinogenic properties of lead, which include among others, mitogenesis, alteration of gene expression, oxidative damage, and inhibition of DNA repair. The aim of the present study was to explore if low concentrations of lead, relevant for human exposure, interfere with Ape1 function, a base excision repair enzyme, and its role in cell transformation in Balb/c-3T3. Lead acetate 5 and 30 µM induced APE1 mRNA and upregulation of protein expression. This increase in mRNA expression is consistent throughout the chronic exposure. Additionally, we also found an impaired function of Ape1 through molecular beacon-based assay. To evaluate the impact of lead on foci formation, a Balb/c-3T3 two-step transformation model was used. Balb/c-3T3 cells were pretreated 1 week with low concentrations of lead before induction of transformation with n-methyl-n-nitrosoguanidine (MNNG) (0.5 µg/mL) and 12-O-tetradecanoylphorbol-13-acetate (TPA) (0.1 µg/mL) (a classical two-step protocol). Morphological cell transformation increased in response to lead pretreatment that was paralleled with an increase in Ape1 mRNA and protein overexpression and an impairment of Ape1 activity and correlating with foci number. In addition, we found that lead pretreatment and MNNG (transformation initiator) increased DNA damage, determined by comet assay. Our data suggest that low lead concentrations (5, 30 µM) could play a facilitating role in cellular transformation, probably through the impaired function of housekeeping genes such as Ape1, leading to DNA damage accumulation and chromosomal instability, one of the most important hallmarks of cancer induced by chronic exposures.

Estudio epidemiológico de arsénico en agua subterránea para consumo humano en el territorio del Cluster Lechero Regional, Argentina / Epidemiological study of arsenic in groundwater for human consumption in the territory of the Cluster Lechero Regional, Argentina

En diversas regiones del mundo se han encontrado acuíferos, destinados para el consumo humano, con niveles de arsénico que sobrepasan los límites recomendados por las agencias ambientales o fijados por la legislación, lo que representa un grave problema de salud pública. En el noroeste de la provincia de Santa Fe y sur de Santiago del Estero, área en estudio, los antecedentes indican la existencia de acuíferos con concentraciones de minerales que superan ampliamente los valores recomendados para consumo humano. Estos niveles de salinidad aumentan con la profundidad, y se detecta además, la presencia de tóxicos como el arsénico, siendo un factor condicionante para el aprovechamiento del agua subterránea. En el territorio del Cluster Lechero Regional, se estudió la composición salina del agua subterránea y, en particular, la concentración de arsénico, con el objetivo de establecer niveles de toxicidad y el potencial desarrollo de enfermedades crónicas. Los resultados muestran elevada salinidad y una concentración media de arsénico en la zona de 0,203 mg/L. Estimamos que, para una población de riesgo de 57.436 habitantes que no tienen acceso a sistemas de agua de red, expuestos teóricamente a la concentración de arsénico hallada en este estudio, se manifiesten 500 casos de cáncer atribuibles a este nivel de exposición en los próximos años. La población infantil comprendida entre 0 y 2 años de edad (3.690 niños de la región) podría desarrollar lesiones dérmicas y efectos neurológicos de distinta magnitud.

In various regions of the world, it has been found aquifers, destined for human consumption, with arsenic levels that exceed the limits recommended by the environmental agencies or required by law, so that represents a serious public health problem. In the northwest of the province of Santa Fe and the south of Santiago del Estero, defined study area, the background information indicates the existence of aquifers with concentrations of minerals that far exceeded the recommended values for human consumption. These levels of salinity increases with depth and, in addition, it was detected the presence of toxic substances such as arsenic, being a conditioning factor for the groundwater use. In the territory of the Cluster Lechero Regional, the composition of the saline groundwater was analized and, in particular, the concentration of arsenic was assessed, with the aim of setting levels of toxicity and the potential development of chronic diseases. Results showed high salinity and an average concentration of arsenic in the area of 0.203 mg/L. We believe that for a high risk population of 57,436 inhabitants, with no access to a water system network, and theoretically exposed to the concentration of arsenic found in this study, it would be expected 500 cases of cancer attributable to this level of exposure, in the next years. Children between 0 and 2 years old (3,690 children from the region) could develop skin lesions and neurological effects of different magnitude.

Aflatoxins ingestion and canine mammary tumors: There is an association?

The aim of this study was to determine the presence of mycotoxins on dogs feed and to explore the potential association between mycotoxins exposure and the chance of mamary tumors in a case-control study. The study included 256 female dogs from a hospital population, 85 with mammary tumors (case group) and 171 without mammary tumors (control group). An epidemiological questionnaire was applied to both groups, and the data were analyzed by the EpiInfo statistical package. For the study, 168 samples of the feed offered to dogs were analyzed for the presence of aflatoxins, fumonisins and zearalenone by high-performance liquid chromatography. Mycotoxins were found in 79 samples (100%) in the case group and 87/89 (97.8%) in the control group. Mycotoxins were detected in all types of feed, regardless feed quality. Level of aflatoxin B1 (p = 0.0356, OR = 2.74, 95%, CI 1.13 to 6.60), aflatoxin G1 (AFG1) (p = 0.00007, OR = 4.60, 95%, CI = 2.16 to 9.79), and aflatoxin G2 (AFG2) (p = 0.0133, OR = 9.91, 95%, CI 1.21 to 81.15) were statistically higher in case of mammary cancer. In contrast, neutering was a protective factor for mammary cancer (p = 0.0004, OR = 0.32, 95%, CI = 0.17 to 0.60).

Aflatoxin M1 in raw milk from different regions of São Paulo state--Brazil.

A total of 635 raw milk samples from 45 dairy farms, from three regions of São Paulo state - Brazil, were evaluated during 15 months for aflatoxin M1 (AFM1). AFM1 was determined by high performance liquid chromatograph with fluorescence detection. AFM1 was detected (>0.003 µg kg(-1)) in 72.9%, 56.3% and 27.5% of the samples from Bauru, Araçatuba and Vale do Paraíba regions, respectively. The mean AFM1 contamination considering all the samples was 0.021 µg kg(-1). Furthermore, the concentration of AFM1 was quite different among Bauru (0.038 µg kg(-1)), Araçatuba (0.017 µg kg(-1)) and Vale do Paraíba (<0.01 µg kg(-1)) regions. Only three samples (0.5%) had higher contamination than the tolerated limit in Brazil (0.50 µg kg(-1)) and 64 samples (10.1%) had a higher contamination than the maximum limit as set by the European Union (0.050 µg kg(-1)). The estimated AFM1 daily intake was 0.358 and 0.120 ng kg(-1) body weight per day for children and adults, respectively.

Polycyclic aromatic hydrocarbons in milk powders marketed in Argentina and Brazil.

The aim of this study was to quantify polycyclic aromatic hydrocarbon (PAH) levels in milk powder samples commercialised in Argentina and Brazil during 2012. Thirty-one samples were available from the retail market. An HPLC method for the determination of PAHs was applied involving a clean-up step with silica cartridges. Recoveries were greater than 79% for all PAHs analysed. Reproducible determination with adequate detection and quantification limits (LOD and LOQ) were attained by HPLC with fluorescence detection for 14 PAHs. Acenaphthylene was determined with a UV-VIS detector. There is no significant difference in any PAHs or in the sum of them between the Argentinean and Brazilian samples. Therefore, the samples were evaluated together. The highest concentration of benzo(a)pyrene (BaP) detected was 0.57 µg kg⁻¹ in milk powder. Contamination of samples expressed as the sum of 15 analysed PAHs varied between 11.8 and 78.4 µg kg⁻¹ and as PAH4 (BaP, chrysene, benzo(a)anthracene and benzo(b)fluoranthene) was between 0.02 and 10.16 µg kg⁻¹. The correlation coefficient for PAH2 (BaP and chrysene) and PAH4 groups was 0.95, for PAH2 and PAH8 it was 0.71, and for PAH4 and PAH8 it was 0.83. All the samples were below the regulatory limit for BaP, but 65% of commercial milk powders do not comply with the European Union limit for PAH4. This is the first report of PAH contamination in powder milk from Argentina and Brazil.

Differential effect of DDT, DDE, and DDD on COX-2 expression in the human trophoblast derived HTR-8/SVneo cells.

The purpose of this study was to investigate the effect of 1,1,1-trichloro-2,2-bis-(chlorophenyl)ethane (DDT), 1,1-bis-(chlorophenyl)-2,2-dichloroethene (DDE), and 1,1-dichloro-2,2-bis(chlorophenyl)ethane (DDD) isomers on COX-2 expression in a human trophoblast-derived cell line. Cultured HTR-8/SVneo trophoblast cells were exposed to DDT isomers and its metabolites for 24 h, and COX-2 mRNA and protein expression were assessed by RT-PCR, Western blotting, and ELISA. Prostaglandin E2 production was also measured by ELISA. Both COX-2 mRNA and protein were detected under control (unexposed) conditions in the HTR-8/SVneo cell line. COX-2 protein expression and prostaglandin E2 production but not COX-2 mRNA levels increased only after DDE and DDD isomers exposure. It is concluded that DDE and DDD exposure induce the expression of COX-2 protein, leading to increased prostaglandin E2 production. Interestingly, the regulation of COX-2 by these organochlorines pesticides appears to be at the translational level.

Environmental risk assessment of arsenic and fluoride in the Chaco Province, Argentina: research advances.

The arsenic (As) and fluoride (F⁻) concentration in groundwater and potential adverse human health risk was investigated in the Central-West Region of the Chaco Province, northern Argentina. The mean concentration of As in shallow groundwater was 95 µg/L, where 76% of samples exceeded the World Health Organization (WHO) guideline value of 10 µg/L, while in deep groundwater it was 90 µg/L, where 63% samples exceeded 10 µg/L. For As health risk assessment, the average daily dose, hazard quotient (HQ), and cancer risk were calculated. The values of HQ were found to be >1 in 77% of samples. This level of contamination is considered to constitute a high chronic risk compared with U.S. Environmental Protection Agency (EPA) guidelines. Further, a significant portion of the population has lifetime carcinogenic risk >10⁻4 and may suffer from cancer. A positive correlation was observed between As and F⁻ in groundwater. The Código Alimentario Argentino (CAA) suggested a limit of F⁻ in drinking water as low as 0.8 mg/L under tropical environmental conditions; however, in shallow (39%) and deep groundwater (32%), samples exceeded these values. Exposure to F⁻ was calculated and compared with the adequate intake of minimal safe level exposure dose of 0.05 mg/kg/d and it was noted that 42% of population may be at high risk of fluorosis. Chronic exposure to high As and F⁻ levels in this population represents a concern due to possible adverse health effects attributed to these elements.

Chi-square analysis of the reduction of ATP levels in L-02 hepatocytes by hexavalent chromium

This study explored the reduction of adenosine triphosphate (ATP) levels in L-02 hepatocytes by hexavalent chromium (Cr(VI)) using chi-square analysis. Cells were treated with 2, 4, 8, 16, or 32 μM Cr(VI) for 12, 24, or 36 h. Methyl thiazolyl tetrazolium (MTT) experiments and measurements of intracellular ATP levels were performed by spectrophotometry or bioluminescence assays following Cr(VI) treatment. The chi-square test was used to determine the difference between cell survival rate and ATP levels. For the chi-square analysis, the results of the MTT or ATP experiments were transformed into a relative ratio with respect to the control (%). The relative ATP levels increased at 12 h, decreased at 24 h, and increased slightly again at 36 h following 4, 8, 16, 32 μM Cr(VI) treatment, corresponding to a "V-shaped" curve. Furthermore, the results of the chi-square analysis demonstrated a significant difference of the ATP level in the 32-μM Cr(VI) group (P < 0.05). The results suggest that the chi-square test can be applied to analyze the interference effects of Cr(VI) on ATP levels in L-02 hepatocytes. The decreased ATP levels at 24 h indicated disruption of mitochondrial energy metabolism and the slight increase of ATP levels at 36 h indicated partial recovery of mitochondrial function or activated glycolysis in L-02 hepatocytes.

Chi-square analysis of the reduction of ATP levels in L-02 hepatocytes by hexavalent chromium.

This study explored the reduction of adenosine triphosphate (ATP) levels in L-02 hepatocytes by hexavalent chromium (Cr(VI)) using chi-square analysis. Cells were treated with 2, 4, 8, 16, or 32 µM Cr(VI) for 12, 24, or 36 h. Methyl thiazolyl tetrazolium (MTT) experiments and measurements of intracellular ATP levels were performed by spectrophotometry or bioluminescence assays following Cr(VI) treatment. The chi-square test was used to determine the difference between cell survival rate and ATP levels. For the chi-square analysis, the results of the MTT or ATP experiments were transformed into a relative ratio with respect to the control (%). The relative ATP levels increased at 12 h, decreased at 24 h, and increased slightly again at 36 h following 4, 8, 16, 32 µM Cr(VI) treatment, corresponding to a "V-shaped" curve. Furthermore, the results of the chi-square analysis demonstrated a significant difference of the ATP level in the 32-µM Cr(VI) group (P < 0.05). The results suggest that the chi-square test can be applied to analyze the interference effects of Cr(VI) on ATP levels in L-02 hepatocytes. The decreased ATP levels at 24 h indicated disruption of mitochondrial energy metabolism and the slight increase of ATP levels at 36 h indicated partial recovery of mitochondrial function or activated glycolysis in L-02 hepatocytes.

CAREX Nicaragua and Panama: Worker exposures to carcinogenic substances and pesticides.

This study provides data on numbers of workers exposed at work to selected carcinogens and pesticides in Nicaragua (35 substances) and Panama (31), based on a modification of the CAREX data system. Population censuses provided industry- and sex-specific workforce numbers. The activity- and sex-specific proportions of exposed workers were estimated by experts from governmental agencies, workers' organizations, and employers' representatives. Finally, the numbers of those occupied in each activity/sex category were multiplied by the proportions of those exposed in the same categories, yielding numbers of those exposed in these categories for each agent. The study revealed high proportions (> 9%) of occupationally exposed workers in both countries for solar radiation and diesel engine emissions; environmental tobacco smoke in Panama; and some pesticides in Nicaragua. A high proportion of exposed was found for men for lead (12%), silica dust (10%), and hexavalent chromium (10%) in Panama.

Early changes induced by short-term low-dose cadmium exposure in rat ventral and dorsolateral prostates.

Prostate cancer (PCa) is the most commonly diagnosed cancer in men. The etiology of PCa in humans is multifactorial and includes age, ethnicity, environmental factors, and other unknown causes. Epidemiological and experimental evidence has shown that cadmium is associated with PCa both in humans and rodents. This metal can act as an endocrine disruptor during prostate development, and it induces prostate lesions late in life. In this study, we investigated the effects of low-dose cadmium on rat prostate morphology during puberty. Two-month-old male Wistar rats were randomized into two experimental groups: cadmium-treated and control. The ventral and dorsolateral prostates were dissected, weighed, and immunohistochemically stained with specific antibodies against Ki-67 and the androgen receptor (AR). The concentration of cadmium was measured in the blood and prostate, and testosterone concentration was measured from the plasma. Our results show that cadmium concentration was increased in both the blood and the prostate of cadmium-treated rats, but there were no changes in the prostatic weight, epithelial cell height, or testosterone levels. However, AR immunostaining and epithelial cell proliferation (Ki-67 index) were increased in both prostates with an increase in apoptosis only in the dorsal lobe. Furthermore, atypical hyperplasic proliferative lesions were found in the dorsolateral lobe after cadmium exposure. Cadmium treatment reduced collagen fiber absolute volume in both prostates. Thus, low-doses of cadmium, even for a short period of time, can interfere with prostate epithelium-stroma homeostasis, and this disruption might be an important factor in the onset of prostate lesions late in life.

Modulation of methylmercury uptake by methionine: prevention of mitochondrial dysfunction in rat liver slices by a mimicry mechanism.

Methylmercury (MeHg) is an ubiquitous environmental pollutant which is transported into the mammalian cells when present as the methylmercury-cysteine conjugate (MeHg-Cys). With special emphasis on hepatic cells, due to their particular propensity to accumulate an appreciable amount of Hg after exposure to MeHg, this study was performed to evaluate the effects of methionine (Met) on Hg uptake, reactive species (RS) formation, oxygen consumption and mitochondrial function/cellular viability in both liver slices and mitochondria isolated from these slices, after exposure to MeHg or the MeHg-Cys complex. The liver slices were pre-treated with Met (250 µM) 15 min before being exposed to MeHg (25 µM) or MeHg-Cys (25 µM each) for 30 min at 37 °C. The treatment with MeHg caused a significant increase in the Hg concentration in both liver slices and mitochondria isolated from liver slices. Moreover, the Hg uptake was higher in the group exposed to the MeHg-Cys complex. In the DCF (dichlorofluorescein) assay, the exposure to MeHg and MeHg-Cys produced a significant increase in DFC reactive species (DFC-RS) formation only in the mitochondria isolated from liver slices. As observed with Hg uptake, DFC-RS levels were significantly higher in the mitochondria treated with the MeHg-Cys complex compared to MeHg alone. MeHg exposure also caused a marked decrease in the oxygen consumption of liver slices when compared to the control group, and this effect was more pronounced in the liver slices treated with the MeHg-Cys complex. Similarly, the loss of mitochondrial activity/cell viability was greater in liver slices exposed to the MeHg-Cys complex when compared to slices treated only with MeHg. In all studied parameters, Met pre-treatment was effective in preventing the MeHg- and/or MeHg-Cys-induced toxicity in both liver slices and mitochondria. Part of the protection afforded by Met against MeHg may be related to a direct interaction with MeHg or to the competition of Met with the complex formed between MeHg and endogenous cysteine. In summary, our results show that Met pre-treatment produces pronounced protection against the toxic effects induced by MeHg and/or the MeHg-Cys complex on mitochondrial function and cell viability. Consequently, this amino acid offers considerable promise as a potential agent for treating acute MeHg exposure.

Câncer de pulmão ocupacional / Occupational lung cancer

O câncer de pulmão é multicausal. Fatores hereditários, genéticos e ambientais interagem na sua gênese. O principal fator de risco é o tabagismo. Entretanto, o ambiente de trabalho é um local de possível exposição a agentes cancerígenos. Atualmente, a International Agency for Research on Cancer lista 19 substâncias/situações de trabalho/ocupações comprovadamente associadas ao câncer de pulmão (grupo 1). A abordagem da ocupação em pacientes portadores de câncer de pulmão é fraca, impactando negativamente na busca da causalidade e, consequentemente, no desvelamento de casos de câncer ocupacional. Os objetivos desta revisão foram elencar os agentes reconhecidamente indutores de câncer de pulmão, discutir a contribuição da ocupação no desenvolvimento da doença, citar as publicações nacionais sobre o tema e sugerir uma lista de procedimentos que são essenciais para uma adequada investigação da relação de causalidade entre câncer de pulmão e ocupação.

Lung cancer is a multifactorial disease. Hereditary, genetic, and environmental factors interact in its genesis. The principal risk factor for lung cancer is smoking. However, the workplace provides an environment in which there is a risk of exposure to carcinogens. The International Agency for Research on Cancer currently lists 19 substances/work situations/occupations that have been proven to be associated with lung cancer (group 1). Thorough occupational history taking is not widely practiced in patients with lung cancer, which has a negative impact on the investigation of causality and, consequently, on the identification of cases of occupational cancer. The objectives of this review were to list the agents that are recognized as causes of lung cancer, to discuss the contribution of occupation to the development of the disease, to cite national studies on the subject, and to propose a list of procedures that are essential to the appropriate investigation of causality between lung cancer and occupation.

Toxicokinetics and toxicological effects of single oral dose of fumonisin B1 containing Fusarium verticillioides culture material in weaned piglets.

Toxicokinetics and the toxicological effects of culture material containing fumonisin B(1) (FB(1)) were studied in male weaned piglets by clinical, pathological, biochemical and sphingolipid analyses. The animals received a single oral dose of 5 mg FB(1)/kg of body weight, obtained from Fusarium verticillioides culture material. FB(1) was detected by HPLC in plasma collected at 1-h intervals up to 6h and at 12-h intervals up to 96 h. FB(1) eliminated in feces and urine was quantified over a 96-h period and in liver samples collected 96 h post-intoxication. Blood samples were obtained at the beginning and end of the experiment to determine serum enzyme activity, total bilirubin, cholesterol, sphinganine (Sa), sphingosine (So) and the Sa/So ratio. FB(1) was detected in plasma between 30 min and 36 h after administration. The highest concentration of FB(1) was observed after 2 h, with a mean concentration of 282 microg/ml. Only 0.93% of the total FB(1) was detected in urine between 75 min and 41 h after administration, the highest mean concentration (561 microg/ml) was observed during the interval after 8 at 24 h. Approximately 76.5% of FB(1) was detected in feces eliminated between 8 and 84 h after administration, with the highest levels observed between 8 and 24 h. Considering the biochemical parameters, a significant increase only occurred in cholesterol, alkaline phosphatase and aspartate aminotransferase activities. In plasma and urine, the highest Sa and Sa/So ratios were obtained at 12 and 48 h, respectively.

Occupational lung cancer.

Lung cancer is a multifactorial disease. Hereditary, genetic, and environmental factors interact in its genesis. The principal risk factor for lung cancer is smoking. However, the workplace provides an environment in which there is a risk of exposure to carcinogens. The International Agency for Research on Cancer currently lists 19 substances/work situations/occupations that have been proven to be associated with lung cancer (group 1). Thorough occupational history taking is not widely practiced in patients with lung cancer, which has a negative impact on the investigation of causality and, consequently, on the identification of cases of occupational cancer. The objectives of this review were to list the agents that are recognized as causes of lung cancer, to discuss the contribution of occupation to the development of the disease, to cite national studies on the subject, and to propose a list of procedures that are essential to the appropriate investigation of causality between lung cancer and occupation.

Biomonitoring of oral epithelial cells in petrol station attendants: comparison between buccal mucosa and lateral border of the tongue.

Owing to the influence of geno- and cytotoxicity on chemical carcinogenesis, studies have demonstrated that petroleum derivatives are able to induce genetic damage and cellular death with conflicting results so far. The aim of the present study was to comparatively evaluate DNA damage (micronucleus) and cellular death (pyknosis, karyolysis and karyorrhexis) in exfoliated oral mucosa cells from gas petrol attendants using two different anatomic buccal sites: cheek mucosa and lateral border of the tongue. A total of 23 gas petrol attendants and 23 health controls (non-exposed individuals) were included in this setting. Individuals had epithelial cells from cheek and lateral border of the tongue mechanically exfoliated, placed in fixative and dropped in clean slides which were checked for the above nuclear phenotypes. The results pointed out significant statistical differences (p<0.05) of micronucleated oral mucosa cells from gas petrol attendants for both oral sites evaluated. In the same way, petroleum derivate exposure was able to increase other nuclear alterations closely related to cytotoxicity such as karyorrhexis, pyknosis and karyolysis, being the most pronunciated effects as those found in the lateral border of the tongue. No interaction was observed between smoking and petroleum exposure. In summary, these data indicate that gas petrol attendants comprise a high risk group for DNA damage and cellular death. It seems that the lateral border of the tongue is a more sensitive site to geno- and cytotoxic insult induced by petroleum derivates.

DNA damage and apoptosis induced by Pteridium aquilinum aqueous extract in the oral cell lines HSG and OSCC-3.

BACKGROUND: Bracken fern (Pteridium aquilinum) has been consumed by humans and animals for centuries. However, its consumption is associated with a high incidence of cancer in the upper digestory tract of different species. Although the oral cavity is the first site of contact with ingested toxic substances, the interaction of bracken fern composites with oral cell lines has not yet been studied. METHODS: In order to study the biological responses of oral cells exposed to bracken fern, we evaluated the genotoxic and cytotoxic effects of a bracken fern aqueous extract in oral cell lines. Human submandibular gland (HSG) and human oral epithelium cells (OSCC-3) cells were treated with three different concentrations of the extract. DNA damage was determined by the comet assay, and cellular morphology was examined by light microscopy. Apoptotic changes were evaluated by transmission electron microscopy and TUNEL assay. RESULTS: The comet assay revealed that the extract was genotoxic for both cell lines but the results were not dose-dependent. The morphological and ultrastructural analyses showed that the extract caused conspicuous alterations in both cell types: uncommon chromatin condensation, nuclear picnosis, cellular volume decrease, nuclear envelope disruption, formation of numerous vacuoles of different sizes and apoptotic bodies. The TUNEL assay confirmed apoptosis induction. CONCLUSIONS: These results demonstrate that the extract was cytotoxic to HSG and OSCC-3 cells, and that cellular degeneration occurred mainly by apoptosis. We believe that oral cells could trigger apoptosis after bracken fern induced DNA damage, in order to avoid the malignant transformation.

Genotoxicity in child populations exposed to polycyclic aromatic hydrocarbons (PAHs) in the air from Tabasco, Mexico.

The economy of the state of Tabasco is based on oil extraction. However, this imposes major effects to the environment and communities. Examples are the Polycyclic Aromatic Hydrocarbons (PAHs) that may be found in the soil, water and sediment of the region. Their volatility makes them available to living beings and results in genotoxic activity. The purpose of this study was to quantify the levels of PAHs in the air at several points in the state, and to analyze their relationship with possible damage to DNA on local inhabitants. Single Cell Gel Electrophoresis Assay (Comet Assay) was applied to peripheral blood lymphocytes of five groups of children between six and 15 years of age. PAH samples were analyzed following US/EPA TO-13-A method. Results indicated the presence in the air of most of the 16 PAHs considered as high priority by EPA, some of which have been reported with carcinogenic activity. Differences (p<0.05) were found between PAHs concentration in the gaseous component and in the particulate component of air samples, with the greatest values for the gaseous component. Greatest PAH concentrations were detected in areas with high oil extraction activities. Children groups from high oil activity areas presented genotoxic damage labeled from moderate to high according to DNA migration from nuclei (Tail Length: 14.2 - 42.14 microm and Tail/Head: 0.97 - 2.83 microm) compared with control group (12.25 and 0.63 microm, respectively). The group with greatest cell damage was located in the area with the greatest oil activity. We conclude that the presence of PAHs in the air may represent a health risk to populations that are chronically exposed to them at high oil activity regions.

Micronuclei induced by airborne particulate matter from Mexico City.

Particulate air pollution is an important environmental health risk. In the present study, we have investigated the ability of chemically characterized water and organic-soluble extracts of PM(10) from two different regions of Mexico City to induce micronuclei in a human epithelial cell line. We also evaluated the association between the chemical characteristics of the PM and its genotoxicity. The airborne particulate samples were collected from an industrial and a residential region; a Hi-Vol air sampler was used to collect PM(10) on glass fiber filters. PM mass was determined by gravimetric analysis of the filters. One section of each PM(10) filter was agitated either with deionized water to extract water-soluble compounds or with dichloromethane to prepare organic-soluble compounds. The chemical composition of the extracts was determined by ion and gas chromatography and atomic adsorption spectroscopy. A549-human alveolar epithelial cells were exposed to different concentrations of PM(10) extracts and the cytokinesis blocked micronucleus assay was performed to measure DNA damage. Even though the industrial region had a higher PM concentration, higher amounts of metals and PAHs were found in the residential area. Both industrial and residential extracts induced a significant concentration-related increase in the micronuclei frequency. The PM(10) water-soluble industrial extract induced significantly more micronuclei than the one of the residential region; inversely, the organic residential extract induced more micronuclei than the one from the industrial region. The association between the induction of micronuclei and the chemical components obtained by the comparative analysis of standardized regression coefficients showed that cadmium and PAHs were significantly associated with micronuclei induction. Data indicate that water-soluble metals and the organic-soluble fraction of PM(10) are both important in the production of micronuclei. Effects observed, point to the risk of PM exposure and shows the need of integrative studies.