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The affirmation of acrylamide as a probable carcinogen by the European Food Safety Authority has reinforced the need to lower acrylamide content in fried potato products. Selected for low reducing sugars and acrylamide-forming potential, recently released cultivars ‘Alpine Russet’, ‘Dakota Trailblazer’, and ‘Ivory Crisp’ were evaluated for their processing quality when grown with varying nitrogen (N) fertilizer regimes. The objective of this study was to determine the effects of N fertilizer rate (34, 135, 202, 269 and 336 kg ha−1) on tuber glucose and acrylamide concentration following processing of new cultivars relative to standard cultivars ‘Russet Burbank’ and ‘Snowden’ at harvest, and after 3, 6 and 9 months of storage at 7.2 °C over 2 years. Glucose and acrylamide responses to N rate were similar for chip cultivars, which linearly decreased in 2011, and quadratically increased then decreased in 2012 with increasing N rate. The N rate effect on French fry glucose concentration varied by cultivar and either decreased or did not respond to elevated N rate. Glucose and acrylamide concentrations of chip cultivars generally increased during storage, with a dramatic increase in ‘Snowden’ resulting from senescence sweetening after 9 months of storage. Environmental conditions significantly affected glucose and acrylamide responses of French fry cultivars to storage time. Glucose and acrylamide concentrations of all French fry cultivars generally increased during storage in 2011. In contrast, glucose concentrations of French fry cultivars were stable or increased, while acrylamide concentrations generally decreased during storage in 2012. The relationship between chip color and glucose concentration was significant, but differed by year. Glucose and acrylamide concentrations of French fry and chip cultivars were significantly correlated (R2 = 0.52 and 0.66, in 2011 and 2012, respectively). Generally, acrylamide in fried potato products can be minimized by using low reducing sugar cultivars supplied with a N fertilizer rate that optimizes yield and quality during growing seasons with minimal environmental stress. [ABSTRACT FROM AUTHOR]

Nitrite plays a major role in inhibiting the growth of foodborne pathogens, including Clostridium botulinum (C. botulinum) that causes botulism, a life-threatening disease. Nitrite serves as a color-fixing agent in processed meat products. However, N-nitroso compounds can be produced from nitrite, which are considered as carcinogens. Thus, consumers desire processed meat products that contain lower concentrations (below conventional concentrations of products) of nitrite or no nitrite at all, although the portion of nitrite intake by processed meat consumption in total nitrite intake is very low. However, lower nitrite levels might expose consumers to risk of botulism poisoning due to C. botulinum or illness caused by other foodborne pathogens. Hence, lower nitrite concentrations in combination with other factors such as low pH, high sodium chloride level, and others have been recommended to decrease the risk of food poisoning. In addition, natural compounds that can inhibit bacterial growth and function as color-fixing agents have been developed to replace nitrite in processed meat products. However, their antibotulinal effects have not been fully clarified. Therefore, to have processed meat products with lower nitrite concentrations, low pH, high sodium chloride concentration, and others should also be applied together. Before using natural compounds as replacement of nitrite, their antibotulinal activities should be examined. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the seasonal variations of mercury levels and human health risk in vegetables that were collected from farmland, home garden, and plastic greenhouse in summer and winter 2016 in Arid Oasis (Shihezi city), Xinjiang, Northwest China. The results showed that the levels of mercury in fresh vegetables were lower in winter (0.003–0.025 mg·kg−1) than in summer (0.001–0.035 mg·kg−1). Single factor pollution (P) in vegetables indicated that all vegetables were polluted in diverse levels. The exceeding rate in different vegetables was 0.00% to 88.89% in summer and 0.00% to 100% in winter compared with limits of pollutants in vegetables. The value of bio-concentration factor (BCF) revealed that the mercury absorption capacity of 10 species vegetables decreased in the following order:pea seedling>spinage>caraway>lettuces>pakchoi>celery>crowndaisy chrysanthemum>chives>spinach>shallot. The daily intake (DI) and target hazard quotient (THQ) of mercury for children (2–12 years), young adults (18–45 years), and quinquagenarian (>45 years) indicated that non-carcinogenic values were below the threshold values except one sampling sit from farmland around the industrial parks. Furthermore, the THQ of open field in summer was higher than plastic greenhouse in winter. Under the same pollution level, children had more non-carcinogenic risk than young adults and quinquagenarian. [ABSTRACT FROM PUBLISHER]

Chicken egg fetal livers were evaluated for histopathological changes produced by four genotoxic hepatocarcinogens: 2-acetylaminofluorene (AAF), aflatoxin B 1 (AFB 1 ), benzo[a]pyrene (BaP), diethylnitrosamine (DEN); four structurally related non- or weakly- carcinogenic comparators: fluorene (FLU), aflatoxin B 2 (AFB 2 ), benzo[e]pyrene (BeP), N-nitrosodiethanolamine (NDELA); two epigenetic hepatocarcinogens: clofibric acid (CFA), phenobarbital (PB); and the non-carcinogen, D-mannitol (MAN). CFA, PB and MAN were also assessed for formation of DNA adducts using the 32 P nucleotide postlabeling (NPL) assay and for DNA breaks using the comet assay. CFA was also assessed in enhanced comet assay for oxidative DNA damage induction. Eggs were dosed on days 9- 11 of incubation. For genotoxicity evaluation, livers were collected 3 h after the last dose. Liver qualitative histopathology assessment was performed on days 12 and 18 of incubation. CFA was negative for DNA adducts but yielded clear evidence of DNA breaks due to oxidative stress. PB and MAN produced no DNA adducts or breaks. Liver to body weight ratios were not affected in most groups, but were decreased in DEN groups, and increased after PB dosing. Livers from control groups, FLU, AFB 2 , BeP, NDELA, CFA, and MAN groups, displayed a typical hepatocellular trabecular pattern at both time points. In contrast, the four genotoxic carcinogens induced time- and dose- related interference with fetal liver cell processes of proliferation, migration and differentiation, leading to hepatocellular and cholangiocellular pleomorphic dysplasia and re-(de-) differentiation with distortion of the trabecular pattern. In addition, dosing with the high dose of DEN produced gallbladder agenesis. PB induced hepatocellular hypertrophy, interference with migration, expressed as distortion of the trabecular pattern, and a moderate cholangiocellular dysplasia. In summary, histopathological analysis of chicken fetal livers revealed developmental anomalies, as well as genotoxicity-induced and, in the case of PB, adaptive morphological changes. Thus, the model provides histopathological outcomes of molecular effects. [ABSTRACT FROM AUTHOR]

There is a geographic inequality in the incidence of colorectal cancer, lowest in developing countries, and greatest in developed countries. This disparity suggests an environmental contribution to cancer resistance in endemic populations. Enterotoxigenic bacteria associated with diarrheal disease are prevalent in developing countries, including enterotoxigenic E. coli (ETEC) producing heat-stable enterotoxins (STs). STs are peptides that are structurally homologous to paracrine hormones that regulate the intestinal guanylyl cyclase C (GUCY2C) receptor. Beyond secretion, GUCY2C is a tumor suppressor universally silenced by loss of expression of its paracrine hormone during carcinogenesis. Thus, the geographic imbalance in colorectal cancer, in part, may reflect chronic exposure to ST-producing organisms that restore GUCY2C signaling silenced by hormone loss during transformation. Here, mice colonized for 18 weeks with control E. coli or those engineered to secrete ST exhibited normal growth, with comparable weight gain and normal stool water content, without evidence of secretory diarrhea. Enterotoxin-producing, but not control, E. coli, generated ST that activated colonic GUCY2C signaling, cyclic guanosine monophosphate (cGMP) production, and cGMP-dependent protein phosphorylation in colonized mice. Moreover, mice colonized with ST-producing E. coli exhibited a 50% reduction in carcinogen-induced colorectal tumor burden. Thus, chronic colonization with ETEC producing ST could contribute to endemic cancer resistance in developing countries, reinforcing a novel paradigm of colorectal cancer chemoprevention with oral GUCY2C-targeted agents. [ABSTRACT FROM AUTHOR]

The high success of silver nanoparticles (AgNPs), mainly associated with their proved antimicrobial properties, has led to an increasing spread in our close environment. Although many studies have been carried out to detect potential toxicity of AgNPs, most of them have been developed under unrealistic exposure conditions. In terms of human risk, the evaluation of long-term exposures to subtoxic doses of NPs remains a challenge. Here, we have determined different transformation-related end points under a scenario of 6 weeks long-term exposure to low noncytotoxic AgNPs concentrations (0.5 and 1 μg/mL) in Caco-2 cells. A significant uptake of AgNPs was demonstrated by using confocal microscopy showing a high presence of AgNPs in both the cytoplasm and the nucleus. As for the assayed parameters of cell transformation such as ability to growth without requiring adherence to a surface (soft-agar assay), the secretion of extracellular matrix metalloproteinase to the medium (zymography), migration capacity and ability of the secretome of exposed cells to promote tumor growth, significant effects were detected in all cases, with the exception of the extracellular matrix metalloproteinases (MMP2 and MMP9) secretion. Our results point out the potential carcinogenic risk associated with AgNPs exposure under long-term exposure conditions, as well as the importance of using realistic exposure scenarios to test nanomaterials. [ABSTRACT FROM PUBLISHER]

This study was conducted in order to estimate the carcinogenic risk of heavy metals exposure via the consumption of groundwater and bottled water for the population of Covenant University and Canaanland, Ota, Ogun state using Perkin Elmer Optima 8000 ICP-OES. The chronic daily intake (CDI) in all the samples ranged from 0.005 and and 0.014μgL-1kg-1d-1which was found to be negligible of potential risk on the inhabitants of different age groups. The carcinogenic Risk (R) for all the samples ranged between 0.01 and 0.025 μgL-1d-1. The R for all the age groups was found to be less than the acceptable level of EPA. The highest carcinogenic risk in Arsenic was found in children, which could be attributed to their lower body weight. However, all the values measured were observed to be below the recommended level by USEPA and WHO respectively. [ABSTRACT FROM AUTHOR]

Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First- and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed. [ABSTRACT FROM AUTHOR]

DNA methylation is an epigenetic modification of DNA molecule that plays a vital role in gene expression regulation. It is not only involved in many basic biological processes, but also considered an important factor for tumorigenesis and other human diseases. Study of DNA methylation has been an active field in cancer epigenomics research. With the advances of high-throughput technologies and the accumulation of enormous amount of data, method development for analyzing these data has gained tremendous interests in the fields of computational biology and bioinformatics. In this review, we systematically summarize the recent developments of computational methods and software tools in high-throughput methylation data analysis with focus on two aspects: differential methylation analysis and tumor purity estimation in cancer studies. [ABSTRACT FROM AUTHOR]

DNA methylation has been proved to play important roles in cell development and complex diseases through comparative studies of DNA methylation profiles across different tissues and samples. Current studies indicate that the regulation of DNA methylation to gene expression depends on the genomic locations of CpGs. Common DNA methylation patterns shared across different cell types and tissues are abundant, and they are likely involved in the basic functions of cell development, such as housekeeping functions. By way of contrast, cell type-specific DNA methylation patterns show distinct functional relevance with cell type specificity. Additionally, abnormal DNA methylation patterns are extensively involved in tumour development. Pan-cancer methylation patterns reveal common mechanisms and new similarities of different cancers, while cancer-specific patterns are relating to tumour heterogeneity and patient survival. Moreover, DNA methylation patterns in specific cancer are relevant with diverse regulatory elements such as enhancers and long non-coding RNAs. In this review, we survey the recent advances on DNA methylation patterns in normal or tumour states to illustrate their potential roles in cell development and cell canceration. [ABSTRACT FROM AUTHOR]

Aberrant DNAmethylation is considered to be one of themost common hallmarks of cancer. Several recent advances in assessing the DNAmethylome provide great promise for deciphering the cancer-specific DNAmethylation patterns. Herein, we present the current key technologies used to detect high-throughput genome-wide DNAmethylation, and the available cancerassociatedmethylation databases. Additionally, we focus on the computationalmethods for preprocessing, analyzing and interpreting the cancermethylome data. It not only discusses the challenges of the differentiallymethylated region calling and the predictionmodel construction but also highlights the biomarker investigation for cancer diagnosis, prognosis and response to treatment. Finally, some emerging challenges in the computational analysis of cancermethylome data are summarized. [ABSTRACT FROM AUTHOR]

It is well known that the occupational exposure to contaminants and carcinogens leads to the development of cancer in exposed workers. In the 18th century, Percivall Pott was the first to hypothesize that chronic exposure to dust in the London chimney sweeps was associated with an increased risk of developing cancer. Subsequently a growing body of evidence indicated that other physical factors were also responsible for oncogenic mutations. Over the past decades, many carcinogens have been found in the occupational environment and their presence is often associated with an increased incidence of cancer. Occupational exposure involves several factors and the association between carcinogens, occupational exposure and cancer is still unclear. Only a fraction of factors is recognized as occupational carcinogens and for each factor, there is an increased risk of cancer development associated with a specific work activity. According to the International Agency for Research on Cancer (IARC), the majority of carcinogens are classified as 'probable' and 'possible' human carcinogens, while, direct evidence of carcinogenicity is provided in epidemiological and experimental studies. In the present review, exposures to benzene, pesticides and mineral fibers are discussed as the most important cancer risk factors during work activities. [ABSTRACT FROM AUTHOR]

Erythrocyte-based PIG-A assay is sensitive and reliable in detecting exposure to mutagenetic agents in animal studies, but there are few data from human populations. In this study, we employed a method for detecting CD59 phenotypic variants, resulting from mutation in the PIG-A gene, in human red blood cells (RBCs), and determined the CD59-deficient RBC (RBCCD59−) frequencies in 217 subjects from general population. The majority of subjects had a relatively low mutant frequencies (MFs) (average, 5.25 ± 3.6 × 10−6, median, 4.38 × 10−6, for all subjects), but with males having a significantly greater MFs (5.97 ± 4.0 × 10−6) than females (4.19 ± 2.5 ×10−6). There was no correlation between MFs and age. In addition, MFs showed no difference between smoker and nonsmoker, and also no association with smoke duration in male subjects. However, there was a significant correlation between cigarette-pack-years which indicated that the MF was only slightly elevated with the increase of cigarette-pack-years. Moreover, intraindividual variations were investigated in three volunteer subjects over 300 days, and the MFs were relatively stable and repeatable. Furthermore, a pilot study by using white blood cell (WBC) assay based on labeling with FLAER was performed in volunteer subjects. The MFs of FLAER-deficient WBC (WBCFLAER−) and RBCCD59− were consistently elevated in two subjects. Our findings provide baseline data that will be helpful in designing further studies using the PIG-A assay to monitor the genotoxic effects of carcinogens in human populations. Environ. Mol. Mutagen. 57:589-604, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Exposure of humans to erionite fibers of suitable morphology and dimension has been unambiguously linked to the occurrence of malignant mesothelioma. For this reason, a morphological, morphometrical, mineralogical, and chemical investigation was performed on two representative samples of potential carcinogenic, fibrous erionite from Lessini Mounts, northeastern (NE) Italy, which has not apparently been examined previously. The first sample is erionite-Ca with an extremely fibrous, hair-like and flexible appearance, and growth in intimate association with levyne. The second sample is erionite-Ca with prismatic to acicular crystals and rigid behavior, enriched in K+and Ca2+extra-framework cations. Although erionite is a nominally Fe-free phase, iron (Fe) was detected in low amounts in all the analyzed crystals. In both the investigated samples, erionite is present as individual fibers of respirable size. Considering that the toxicity and carcinogenic potential of erionite is associated with its size parameters, together with its in vivo durability and high surface area, most of the investigated fibers may also be potentially carcinogenic. The presence of erionite in extensively quarried and largely employed volcanic rocks, suggesting the need for detailed health-based studies in the region. [ABSTRACT FROM AUTHOR]

Bioaccumulation of six heavy metals (Mn, Fe, Co, Ni, Cu, Zn) in the muscle of highly consumed fish species ( Mastacembelus armatus) were measured using atomic absorption spectrometer. Fe (213.29 mg/kg dry weight) concentration was the most, followed by Zn (186.19 mg/kg dry weight), Ni (58.98 mg/kg dry weight), Cu (41.36 mg/kg dry weight), Co (9.06 mg/kg dry weight) and Mn (9.03 mg/kg dry weight). Estimated daily intake of heavy metals was calculated by mean fish consumption rate 19.5 × 10 kg/day, on the basis of a calculation of the amount of fish consumed by adult individuals (male and female). The studied fish species pose non carcinogenic risk for Co and Ni [target hazard quotient (THQ) > 1] only. Hazard index (HI) was high. Carcinogenic risk (TR) posed by this fish for male and female was 3.43 × 10 and 3.91 × 10, respectively for Ni (the carcinogenic potency slope factor was available for Ni only). The study is an alert indicating that inhabitants who consume these fishes (particularly females) were at risk of Co and Ni toxicity. In India recommended guidelines have yet not been established for these heavy metals, which is essential for setting of toxicological standards. [ABSTRACT FROM AUTHOR]

A detailed understanding of the relationship between radiation-induced breast cancer and obesity is needed for appropriate risk management and to prevent the development of a secondary cancer in patients who have been treated with radiation. Our goal was to develop an animal model to study the relationship by combining two existing Sprague-Dawley rat models of radiation-induced mammary carcinogenesis and diet-induced obesity. Female rats were fed a high-fat diet for 4 weeks and categorized as obesity prone or obesity resistant based on their body weight at 7 weeks of age, at which time the rats were irradiated with 4 Gy. Control rats were fed a standard diet and irradiated at the same time and in the same manner. All rats were maintained on their initial diets and assessed for palpable mammary cancers once a week for the next 30 weeks. The obesity-prone rats were heavier than those in the other groups. The obesity-prone rats were also younger than the other animals at the first detection of mammary carcinomas and their carcinoma weights were greater. A tendency toward higher insulin and leptin blood levels were observed in the obesity-prone rats compared to the other two groups. Blood angiotensin II levels were elevated in the obesity-prone and obesity-resistant rats. Genes related to translation and oxidative phosphorylation were upregulated in the carcinomas of obesity-prone rats. Expression profiles from human breast cancers were used to validate this animal model. As angiotensin is potentially an important factor in obesity-related morbidities and breast cancer, a second set of rats was fed in a similar manner, irradiated and then treated with an angiotensin-receptor blocker, losartan and candesartan. Neither blocker altered mammary carcinogenesis; analyses of losartan-treated animals indicated that expression of renin in the renal cortex and of Agtr1a (angiotensin II receptor, type 1) in cancer tissue was significantly upregulated, suggesting the presence of compensating mechanisms for blocking angiotensin-receptor signaling. Thus, obesity-related elevation of insulin and leptin blood levels and an increase in available energy may facilitate sustained protein synthesis in cancer cells, which is required for rapid cancer development. [ABSTRACT FROM AUTHOR]

DNA repair genes play critical roles in response to carcinogen-induced and anticancer therapy-induced DNA damage. Benzo[a]pyrene (BaP), the most carcinogenic polycyclic aromatic hydrocarbon (PAH), is classified as a group 1 carcinogen by International Agency for Research on Cancer. The aims of this study were to (1) evaluate the effects of BaP on DNA repair activity and expression of DNA repair genes in vitro and (2) examine the role of xeroderma pigmentosum, complementation group D (XPD) mRNA expression in human head and neck cancers. Host cell reactivation assay showed that BaP inhibited nucleotide excision repair in H1299 lung cancer cells. DNA repair through the non-homologous end-joining pathway was not affected by BaP. Real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR) and Western blot demonstrated that XPD was downregulated by BaP treatment. BaP exposure did not apparently affect expression of another 11 DNA repair genes. BaP treatment increased the DNA damage marker γ-H2AX and ultraviolet (UV) sensitivity, supporting an impairment of DNA repair in BaP-treated cells. XPD expression was also examined by quantitative RT-PCR in 68 head and neck cancers, and a lower XPD mRNA level was found in smokers’ cancer specimens. Importantly, reduced XPD expression was correlated with patient 5-year overall survival rate (35 vs. 56%) and was an independent prognostic factor (hazard ratio: 2.27). Data demonstrated that XPD downregulation was correlated with BaP exposure and human head and neck cancer survival. [ABSTRACT FROM AUTHOR]

In today's fast paced world, due to time crunch people are using packaged readymade food and water on a scale never seen before. Most of the packed food material, water and other beverages are served or sealed in plastic containers, plastic dissolves in miniscule quantities over a long period of time, which can lead to carcinogenic effects like respiratory, gastric tumours etc. Various short term and long-term research works are being done on this alarming condition. This article tries to throw some light on this Global health phenomena. The American Cancer Society estimates that 6% of cancers are related to environmental causes (https://www.polymersolutions.com). [ABSTRACT FROM AUTHOR]

Vacuum metallurgy separation (VMS) is a technically feasible method to recover Pb, Cd and other heavy metals from crushed e-wastes. To further determine the environmental impacts and safety of this method, heavy metals exposure, noise and thermal safety in the ambiance of a vacuum metallurgy separation system are evaluated in this article. The mass concentrations of total suspended particulate (TSP) and PM10 are 0.1503 and 0.0973 mg m−3 near the facilities. The concentrations of Pb, Cd and Sn in TSP samples are 0.0104, 0.1283 and 0.0961 μg m−3, respectively. Health risk assessments show that the hazard index of Pb is 3.25 × 10−1 and that of Cd is 1.09 × 10−1. Carcinogenic risk of Cd through inhalation is 1.08 × 10−5. The values of the hazard index and risk indicate that Pb and Cd will not cause non-cancerous effects or carcinogenic risk on workers. The noise sources are mainly the mechanical vacuum pump and the water cooling pump. Both of them have the noise levels below 80 dB (A). The thermal safety assessment shows that the temperatures of the vacuum metallurgy separation system surface are all below 303 K after adopting the circulated water cooling and heat insulation measures. This study provides the environmental information of the vacuum metallurgy separation system, which is of assistance to promote the industrialisation of vacuum metallurgy separation for recovering heavy metals from e-wastes. [ABSTRACT FROM AUTHOR]

16 surface soil samples were collected from Jiaozhou Bay wetland. The concentrations of 16 polycyclic aromatic hydrocarbons (PAHs) were measured by gas chromatography-mass selective detector (GC/MS). The total concentration of PAHs ranged from 176.1–563.3 ng/g dry weight, with a mean of 345.3 ng/g dry weight. Factor analysis was calculated to apportion sources of PAHs. It was found that the PAHs mainly from coal burning, traffic sources, diesel leakage, coke production, oil exploitation and petroleum leakage. Seven carcinogenic PAHs classified by the IARC were calculated for the health risk assessment. Two groups of people (children and adults) were selected to estimate the carcinogenic risk via ingestion, inhalation, and dermal contact. As a result, the total carcinogenic risks for children and adults were 4.8 × 10−7and 8.8 × 10−7, respectively, and the carcinogenic risks were at acceptable range. Sensitivity analysis was conducted to evaluate the parameters which contributed most to the carcinogenic risk assessment. As as a result, the average lifespan (AT), body weight (BW), BaPeq concentrations (CS), exposure frequency (EF), and exposure duration (ED) contribute most to the carcinogenic risk assessment, and these should be acquired on a site-specific basis. [ABSTRACT FROM AUTHOR]

Air pollution has been recognized as a human carcinogen. Children living in urban areas are a high-risk group, because genetic damage occurring early in life is considered able to increase the risk of carcinogenesis in adulthood. This study aimed to investigate micronuclei (MN) frequency, as a biomarker of DNA damage, in exfoliated buccal cells of pre-school children living in a town with high levels of air pollution. A sample of healthy 3-6-year-old children living in Brescia, Northern Italy, was investigated. A sample of the children's buccal mucosa cells was collected during the winter months in 2012 and 2013. DNA damage was investigated using the MN test. Children's exposure to urban air pollution was evaluated by means of a questionnaire filled in by their parents that included items on various possible sources of indoor and outdoor pollution, and the concentration of fine particulate matter (PM10, PM2.5) and NO2 in the 1–3 weeks preceding biological sample collection. 181 children (mean age±SD: 4.3±0.9 years) were investigated. The mean±SD MN frequency was 0.29±0.13%. A weak, though statistically significant, association of MN with concentration of air pollutants (PM10, PM2.5 and NO2) was found, whereas no association was apparent between MN frequency and the indoor and outdoor exposure variables investigated via the questionnaire. This study showed a high MN frequency in children living in a town with heavy air pollution in winter, higher than usually found among children living in areas with low or medium-high levels of air pollution. [ABSTRACT FROM AUTHOR]

Background The Alberta oil sands are an important economic resource in Canada, but there is growing concern over the environmental and health effects as a result of contaminant releases and exposures. Recent studies have shown a temporal and spatial trend of increased polycyclic aromatic hydrocarbon (PAH) concentrations in sediments and snowpack near the Athabasca oil sands operations (i.e., open pit mines), but thus far similar studies have not been done for the Cold Lake region where steam assisted gravity drainage ( in situ) extraction is performed. Methods Many PAHs are known mutagenic carcinogens, and this study measured soil and atmospheric concentrations of PAHs in the Cold Lake region to assess the excess lifetime cancer risk posed to the First Nations' inhabitants of the region. Using both deterministic and probabilistic risk assessment methods, excess lifetime cancer risks were calculated for exposures from inhalation or inadvertent soil ingestion. Results The mean excess cancer risk for First Nations' people through ingestion who engage in traditional wilderness activities in the Cold Lake region was 0.02 new cases per 100,000 with an upper 95% risk level of 0.07 cases per 100,000. Exposure to PAHs via inhalation revealed a maximum excess lifetime cancer risk of less than 0.1 cases per 100,000. Conclusions Excess lifetime risk values below 1 case per 100,000 is generally considered negligible, thus our analyses did not demonstrate any significant increases in cancer risks associated with PAH exposures for First Nations people inhabiting the Cold Lake region. [ABSTRACT FROM AUTHOR]

Silica has been known to cause silicosis for centuries, and evidence that silica causes lung cancer has accumulated over the last several decades. This article highlights 3 important developments in understanding the health effects of silica and preventing illness and death from silica exposure at work. First, recent epidemiologic studies have provided new information about silica and lung cancer. This includes detailed exposure-response data, thereby enabling the quantitative risk assessment needed for regulation. New studies have also shown that excess lung mortality occurs in silica-exposed workers who do not have silicosis and who do not smoke. Second, the US Occupational Safety and Health Administration has recently proposed a new rule lowering the permissible occupational limit for silica. There are approximately 2 million US workers currently exposed to silica. Risk assessments estimate that lowering occupational exposure limits from the current to the proposed standard will reduce silicosis and lung cancer mortality to approximately one-half of the rates predicted under the current standard. Third, low-dose computed tomography scanning has now been proven to be an effective screening method for lung cancer. For clinicians, asking about occupational history to determine if silica exposure has occurred is recommended. If such exposure has occurred, extra attention might be given to the early detection of silicosis and lung cancer, as well as extra emphasis on quitting smoking. CA Cancer J Clin 2014;64:63-69. © 2013 American Cancer Society, Inc. [ABSTRACT FROM AUTHOR]

Review of the literature reveals that environmental hazards cause adverse health effects that include sterility, infertility, embryotoxicity, low birth weight, skin lesions, neurodevelopmental defects, immunologic disorders, cancer, and fear of late effects. They have been identified mostly by astute practitioners but also by a bacteriologist, an animal experimentalist, 5 factory workers in childless marriages, and a tipsy bystander in an economically impoverished area of Baltimore. Dust on a parent's work clothes has transported a hazard at work to a hazard at home (lead, asbestos, and chlordecone). Causality is established by showing a dose-response effect and reproducing the effect in studies of other exposed groups or by using another epidemiologic method, eg, prospective instead of retrospective study. Also, the findings should be biologically plausible and not attributable to a concomitant variable such as cigarette smoking. Contrary to front-page newspaper headlines, incidence rates for childhood leukemia are not rising. Preserving specimens for future studies has been valuable: blood from people who were exposed to dioxin in Seveso, Italy; mummified umbilical cords containing methyl mercury at Minamata Bay, Japan; and Guthrie dried blood spots to screen retrospectively for 43 genetic disorders and a specific prenatal cytogenetic abnormality in some children with 1 form of leukemia. Recommendations are given for enhancing interest in environmental hazards and their discovery by clinicians. Pediatrics 2004;113:945-951; case reports, case series, epidemiology, disease clusters, causality., Environmental hazards are usually first de scribed by astute clinicians. The descriptions that follow are in part from personal experience beginning in medical school (radiation-induced teratogenesis), from conferences on the [...]

Menin is a scaffold protein encoded by the multiple endocrine neoplasia type 1 (MEN1) gene in humans, and it interacts with a variety of transcriptional proteins to control active or repressive cellular processes. Here, we show that heterozygous ablation of Men1 in female mice reduces chemical carcinogen-induced liver carcinogenesis and represses the activation of the inflammation pathway. Using ChIP-on-chip screens and ChIP assays, we find that menin occupancy frequently coincides with H3K4me3 at the promoter of many liver cancer-related genes, such as Yes-associated protein (Yap1). Increased menin and Yap1 expression in human hepatocellular carcinoma specimens was associated with poor prognosis. Our findings reveal that menin plays an important epigenetic role in promoting liver tumorigenesis, and support the notion that H3K4me3, which is regulated by the menin-mixedlineage leukemia complex, is a potential therapeutic target in hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

The use of genetically modified (GM) mice to assess carcinogenicity is playing an increasingly important role in the safety evaluation of chemicals. While progress has been made in developing and evaluating mouse models such as the Trp53+/−, Tg.AC and the rasH2, the suitability of these models as replacements for the conventional rodent cancer bioassay and for assessing human health risks remains uncertain. The objective of this research was to evaluate the use of accelerated cancer bioassays with GM mice for assessing the potential health risks associated with exposure to carcinogenic agents. We compared the published results from the GM bioassays to those obtained in the National Toxicology Program's conventional chronic mouse bioassay for their potential use in risk assessment. Our analysis indicates that the GM models are less efficient in detecting carcinogenic agents but more consistent in identifying non-carcinogenic agents. We identified several issues of concern related to the design of the accelerated bioassays (e.g., sample size, study duration, genetic stability and reproducibility) as well as pathway-dependency of effects, and different carcinogenic mechanisms operable in GM and non-GM mice. The use of the GM models for dose-response assessment is particularly problematic as these models are, at times, much more or less sensitive than the conventional rodent cancer bioassays. Thus, the existing GM mouse models may be useful for hazard identification, but will be of limited use for dose-response assessment. Hence, caution should be exercised when using GM mouse models to assess the carcinogenic risks of chemicals. [ABSTRACT FROM AUTHOR]

Background Although sun exposure is a strong risk factor for skin cancer, tanning is very popular among adolescents. Awareness of skin cancer and sun exposure might influence sun protective behaviours in this population. Objectives To investigate the awareness of skin cancer and sun-safe practices among Italian adolescents. Methods A questionnaire about knowledge of skin cancer, perceived severity of sun rays/skin cancer and behaviour toward sun protection was administered to 1204 secondary school students. Predictors of these three components were assessed by case-control analyses considering different combinations of answers. Multiple logistic regression models were used to this scope. Results The majority of participants had heard of skin cancer in the past (97.0%), correctly identified possible causes (58.6%) and names (64.2%) of skin cancers and judged appropriately the perceived danger of sunrays (70.2%) and skin cancer (80.6%). Nonetheless, students' behaviour was poor: only 13.5% stated to always use sun-safe practices and 39.1% never used any. Independent predictors of proper knowledge were: Lyceum school, and family or TV/media as information source; of appropriate perceived severity: Lyceum school, a darker skin type, and dermatologists as information source; of acceptable behaviour: female sex, a darker skin type, and dermatologists or general practitioners (GPs) as information source. Conclusions Despite a fairly good knowledge about skin cancer and sun exposure, students' behaviour was unsatisfactory. Knowledge is not sufficient to produce a positive behaviour, as determinants of these two aspects are different. Dermatologists and GPs should be considered as key-figures for future multicomponent intervention strategies in this field. [ABSTRACT FROM AUTHOR]

Background More than 10 years have passed since the terrorist attack on the New York City World Trade Center on September 11, 2001. It is well known that long-term carcinogenic bioassays on rodents can predict the potential carcinogenic effects of chemical and physical agents for humans. Objective A life-span carcinogenicity bioassay was conducted on Sprague-Dawley rats at the CMCRC of the Ramazzini Institute to test the potential carcinogenic effects of settled dust collected at the WTC immediately after the terrorist attack. Methods The WTC material tested is a complex mixture of coarse particles (95%) contain pulverized cement, glass fibres, asbestos, lead, polycyclic aromatic hydrocarbons (PAHS), polychlorinated biphenyls (PCBS) and polychlorinated furans, and dioxin. The test matter was suspended in sterile saline and administered by intratracheal instillation (IT) to 8-week-old Sprague-Dawley rats (100 animals/sex), 3-4 days/week for 4 weeks. A group of 200 male and female rats served as controls. The animals were kept under observation until natural death. Results Histopathological evaluation of the lungs (target organ) of instilled control and treated male and female rats, did not show any significant increased incidence of lung tumors. Two hemangiomas (one with endothelial atypia) and one hemangiosarcoma were found in the lungs of treated males. Moreover a modest increased incidence of terminal bronchiolar hyperplasia (TBH) and squamous metaplasia occurred in the lung of treated males and females compared to the controls. Conclusion Hemangioma and hemangiosarcoma are extremely rare tumors in the lung of our colony and we believe they are caused by WTC dust. Am. J. Ind. Med. 56:155-162, 2013. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background As part of an effort to strengthen occupational safety and health programs, the United Arab Emirates (UAE) commissioned a study to estimate the burden of disease attributable to occupational exposure to carcinogens, particulate matter, and noise. Methods We developed an innovative simulation model to estimate the occupational disease burden and facilitate future assessments as more field-based quantitative data become available. Results We determined that, in 2008, an estimated 46 deaths (95% CI: 27-71) and 17,000 health-care facility visits (95% CI: 16,000-18,000), along with 4,500 cases of noise-induced hearing loss, were attributable to the occupational risk factors covered in this study. Lung cancer and leukemia were associated with the highest number of deaths (38), whereas asthma and chronic obstructive pulmonary disease contributed most to the health-care facility visits (nearly 16,900). The highest estimated occupational disease burden is in construction. Conclusion These results will help the UAE to institute new policies for environment, health, and safety management. Am. J. Ind. Med. 55:940-952, 2012. © 2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Hazardous chemicals can be released from artificial turf used in some school playgrounds. To distinguish between Health risk assessment (HRA) exposure scenarios for this study, the ratio of elementary, middle and high schools was considered before final selection. Considering exposure pathways (inhalational, oral and dermal), media and materials were examined, targeting hazardous chemicals released from artificial turf playground-related products. Upon evaluation, the quantity of infill chips was shown to exceed the domestic product content standard (90mg/kg) at eight (16%) out of 50 schools. PAHs were shown to exceed standards (10mg/kg) at two (4%) out of the 50 schools. The excess cancer risk (ECR) of carcinogens was shown to be 1x10-6 in most users for the worst exposure scenario. In children with pica, who represented the most extreme exposure group, the ECR was expected to be as high as 1x10-4, showing the low risk level of carcinogens. The hazard index (HI) for individual chemicals was shown to be low, at around 0.1 or less, except for children with pica, according to the mean exposure scenario of artificial turf playground exposure. However, the HI was shown to exceed 1.0 in children with pica. Therefore, no direct health risk was found in using artificial turf playgrounds and urethane flooring tracks for the mean exposure scenario, except in children with pica. [ABSTRACT FROM AUTHOR]

The article discusses the occupational cancers in Great Britain which includes liver, esophagus and stomach. It states that these cancers arise due to exposure to carcinogenic agents including asbestos, mineral oils, solar radiation and silica. It is estimated that mortality due to occupational disease in Great Britain accounts to four percents.

Background Oral 8-methoxypsoralen-UV-A (PUVA) and narrowband UV-B (NB-UVB or UVB TL-01) are effective and widely used treatments for chronic plaque psoriasis. Although the role of PUVA therapy in skin carcinogenesis in humans with psoriasis has been clearly demonstrated, there is still controversy regarding the risk of skin cancer with NB-UVB. Furthermore, there is no clear evidence about the maximum cumulative number of sessions not to be exceeded in a lifetime. Objectives To assess the respective cutaneous carcinogenic risks of PUVA or NB-UVB in psoriasis; to estimate the respective dose-relationship between skin cancers and PUVA or NB-UVB; to estimate a maximum number of sessions for PUVA or NB-UVB not to be exceeded in a lifetime. Methods A systematic literature search was carried out in Medline, Embase and Cochrane Library databases from1980 to December 2010 in English and French, with the keywords 'Psoriasis' AND 'UVB therapy' AND 'UVA therapy' AND 'cancer' AND 'skin' OR 'neoplasm' OR 'cutaneous carcinoma' OR 'melanoma'. Results Of 243 identified references, 49 published studies were included. Most of them (45/49) concerned PUVA therapy, with 41 assessing the risk of non-melanoma skin cancers (NMSC) following PUVA. All publications referring to the US prospective PUVA follow-up study revealed an increased risk of NMSC with the following characteristics: risk most pronounced for squamous cell carcinomas developing even with low exposures and increasing linearly with the number of sessions, tumors occurring also on non-exposed skin including invasive penile tumors, risk persisting after cessation of treatment. An increased risk of basal cell carcinomas was observed in patients receiving more than hundred PUVA sessions. The four prospective European studies selected in our review and most of the pre-1990 European and US retrospective studies failed to find a link between exposure to PUVA and skin cancer. Only the most recent cohorts, including three large long-term retrospective European studies comparing records with their respective national cancer registries reported on an independent increased risk of NMSC with PUVA, The risk was lower as compared to the US prospective PUVA follow-up study. Six studies assessed the risk of melanoma following PUVA therapy: two of the three US publications coming from the same PUVA prospective follow-up study revealed an increased risk with more than doubled incidence of both invasive and in situ melanoma among patients exposed to at least 200 PUVA treatments compared with patients exposed to lower doses, whereas the three retrospectives European studies, comparing the incidence of melanoma in PUVA users with national cancer registers, did not find any increased risk of melanoma. No increased risk of skin cancer was evidenced in the four studies specifically assessing the potential carcinogenic risk of NB-UVB Conclusion There is an increased risk of skin cancer following PUVA, shown by both US and European studies. The greater risk measured by the US studies may be at least partly explained by high UVA dose exposure and the lighter phototypes of the treated patients. The lack of prospective studies in psoriasis patients treated with NB-UVB constitutes a barrier to the robust assessment of carcinogenic risk of this phototherapy technique. [ABSTRACT FROM AUTHOR]

Effects of all pollutants existing in the Nanjing city drinking water (DWNC) on mouse gene transcription levels were measured to assess the DWNC carcinogenic risks and to identify candidate indicator genes for assessing and early warning the cancer risks. Transcriptional expression levels of 14,000 hepatic genes for the treatment group mice ( Mus musculus, ICR) fed with DWNC for 90 days were detected using the GeneChip Mouse Genome 430A 2.0 array. The analysis indicated that the transcriptional levels of 294 genes were up-regulated and 542 ones were down-regulated. Of these genes, 12 ones identified to be involved in at least five different types of cancers were further analyzed. An interrogation by Kyoto Encyclopedia of Genes and Genomes (KEGG) revealed that three (including ITGAV, CCND1 and SMAD2) of the 12 genes were mapped to pathway in cancer. Gene Ontology (GO) function annotation also showed that they were associated with the functional categories of cell cycle regulation, adhesion, apoptosis, signal transduction and so on which are closely implicated in tumorigenesis and progression. The correlations between the aberrant expressions of them and the genesis and progression of cancers have been further documented by a number of scientific researches. These results might demonstrate that the potential toxicity and carcinogenic risks were associated with DWNC. Moreover, ITGAV, CCND1 and SMAD2 were identified as the most likely candidate indicator genes for the assessment of the combined carcinogenic risk of all pollutants existing in DWNC. [ABSTRACT FROM AUTHOR]

The article presents a study on the impact of biphenyl ethers to the procarcinogens transition to mutagens, and its effect on the hepatic mixed-function oxidase (MFO). The study examined the impact of hepatic MFO on chemical metabolism and its role in the changing of procarcinogens to mutagens in male rats treated with biphenyl ethers. The study shows a substantial role of biphenyl ethers in the hazards of carcinogenicity in humans due to its capability in converting procarcinogens to mutagens.

Previous studies have demonstrated that methapyrilene hydrochloride (MP) is a rat-specific nongenotoxic carcinogen which induces liver tumors in a dose-dependent manner following chronic exposure in the diet. This study was conducted to determine the dose response of MP in the medium-term bioassay and to compare the response to tumor incidence. Two weeks following a single initiating dose of diethylnitrosamine (DEN), male F344 rats were administered MP at doses of 0, 62.5, 125, 250, or 1000 ppm in the diet for 6 weeks. A ½ partial hepatectomy was performed 3 weeks post-DEN. At termination, sections from the remaining three lobes were stained with GST-P antibody. Number and size of foci were measured using an image analysis system with a digitizing board. MP induced a dose-dependent increase in the number of GST-P+ foci/cm2 (0 ppm=0.85 foci/cm2; 62.5 ppm=1.29 foci/cm2; 125 ppm=1.59 foci/cm2; 250 ppm=6.55 foci/cm2; 1000 ppm=28.23 foci/cm2). A significantly greater number of foci were observed in the caudate lobe than in the anterior and posterior lobes. The size of individual foci was largely unaffected. This study demonstrates a strong correlation between foci induction and tumor incidence and suggests that this assay may have utility in predicting dose responses for the chronic bioassay. [ABSTRACT FROM AUTHOR]

Byline: A.F. Malenchenko, S.N. Sushko, I.V. Saltanova The evaluation of dose-effect dependencies in the case of pure irradiation, and evaluation of these dependencies after addition of carcinogen at different times after irradiation, yields information on the particularities of the process of tumour formation under the combined action of radiation and chemical carcinogens. This is the basis for the present work. The dose-time dependency of the frequency of the appearance of adenomas was studied at different times of addition of urethane after irradiation. It was shown that the frequency of tumours is determined both by the radiation dose and the time interval between irradiation and addition of the carcinogen. The data obtained make it possible to analyse the period of conservation of induced damage and the nonlinearity of the process of tumour formation under the combined action of radiation and toxic factors on the organism. The latter is to be taken into account when forecasting the radiation risk under ecological conditions. A mathematical model was constructed to describe the amount of damage recovered by a chemical promoter after a concrete time delay after irradiation.