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Aflatoxins, a group of toxic secondary metabolites produced by Aspergillus species, pose significant threats to human health due to their potent carcinogenic, mutagenic, and immunosuppressive properties. Chronic exposure to these contaminants, commonly found in staple foods such as maize and groundnuts, has been linked to an increased risk of liver cancer, growth impairment, and immune dysfunction. Several agents, such as calcium montmorillonite clay and Lactobacillus rhamnosus GG, have shown promise in reducing aflatoxin bioavailability and alleviating its toxic effects. Additionally, dietary supplements such as chlorophyllin, selenium, and N-acetylcysteine have demonstrated potential as adjuvants to counteract aflatoxin-induced oxidative stress and support liver function. In this treatise, some of the most discussed approaches to mitigating aflatoxin effects are explored in terms of their efficacy, safety, and potential mechanisms of action, which include direct aflatoxin binding, detoxification, cellular antioxidative, and hepatocellular protection properties. However, the effectiveness of these strategies can be influenced by various factors, such as dose, duration of exposure, and individual susceptibility. Therefore, further research is needed to optimize these interventions and develop new, targeted therapies for the prevention and treatment of aflatoxin-related diseases. This review aims to provide a comprehensive analysis of 18 pharmaceutical, nutraceutical, supplement, and probiotic strategies currently available for mitigating the deleterious effects of chronic aflatoxin exposure in humans and animal models. [ABSTRACT FROM AUTHOR]

Purpose of review: Aflatoxin B1 (AFB1) has been categorized as a Group I carcinogen by the International Agency for Research on Cancer (IARC). Considering its significant public health implications, it is crucial to have a comprehensive understanding of the different routes of exposure and biomarkers of aflatoxin. Recent findings: The main mechanisms by which aflatoxins cause harm to the body are oxidative stress, immune suppression, and DNA damage. More attention has recently been paid to investigating exposure through occupational and transplacental routes. Aflatoxin exposure is linked to unfavorable pregnancy outcomes, like low birth weight, according to the recent literature currently available on human studies. As aflatoxin can cause a variety of mutations and DNA damage, the AFB1-N7 guanine adduct has gained special interest in cancer research and toxicity. The most commonly used biomarker currently for determining chronic and consistent exposure to this carcinogen is aflatoxin B1-lysine serum albumin adduct in human blood samples (2–3 months). Recent research also investigates the potential for using hair analysis to study chronic exposure. Summary: The three main routes of aflatoxin exposure are dietary, occupational, and transplacental. Biomarkers can be found in a variety of biological samples, such as blood, hair, faeces, milk, urine, and bronchalveolar lavage. Surprisingly, there is an absence of cutoff limits for aflatoxin levels in biological fluids concerning adverse health effects in humans. Given the potential carcinogenic effects and the significant public health implications of aflatoxin, prioritizing the identification of new biomarkers for evaluating chronic exposure is crucial. [ABSTRACT FROM AUTHOR]

Background: Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer commonly used in a wide variety of products, including medical devices. It is rapidly metabolized in the liver into various metabolites upon absorption through oral ingestion, dermal absorption, and inhalation. DEHP is classified as a non-genotoxic hepatocarcinogen in rodents, as its chronic exposure has been associated with the development of liver cancer in these animals, but most genotoxicity studies have been negative. Epidemiologic studies in humans suggest that long-term high intakes of DEHP may be a risk factor for liver dysfunction. The repeated-dose liver micronucleus (RDLMN) assay is a well-established method for assessing chromosomal changes caused by hepatic genotoxins and/or carcinogens. It is particularly valuable for detecting substances that undergo metabolic activation, especially when the metabolite has a short half-life or does not reach the bone marrow effectively. Therefore, we investigated whether the RDLMN assay could detect DEHP-induced micronucleus formation in the liver following a 14 or 28-day treatment. Results: We report that the RDLMN assay demonstrated an increased frequency of hepatic micronuclei in rats exposed to DEHP for 14 or 28 days. The increases in micronuclei correlated with hepatomegaly, an established response to phthalates in the liver. Conversely, no such increases were observed in the micronucleus assay using bone marrow from these rats. Conclusion: The detection of DEHP-induced micronuclei by the RDLMN assay suggests that this assay could detect the potential genotoxicity and hepatocarcinogenicity of DEHP. It also demonstrated the utility of the RDLMN assay in identifying metabolically activated hepatic carcinogens. [ABSTRACT FROM AUTHOR]

Muthalamada in the Western Ghats has been a prominent mango-cultivating region of Asia for the last three decades. In the present study, soil samples from Muthalamada mango orchards were analysed for pesticide contents and estimated associated cancer risk indices. Sixteen pesticides, including organochlorines, organophosphates, synthetic pyrethroids, and carbamates were detected in the region. The concentration of chlorpyrifos (2.05–720.27 mg/kg) was the highest level reported from any agroecosystem in India. Community health risk assessment indicates high carcinogenic risk and greater susceptibility in children. The study demonstrates the need for immediate interventions to reduce the ecological and human cancer risks in the mango orchards. [ABSTRACT FROM AUTHOR]

Legacy tailings from decommissioned mines are known to negatively impact human health and environmental quality. In this study, potentially toxic elements (PTEs) including Cr, Cu, Ni, Pb, and Zn concentrations in tailings from a Selebi-Phikwe mine, Botswana, were assessed for contamination and health risk via multiple exposure pathways in adults and children. Tailings samples from the defunct mine were analyzed for total elemental composition using inductively coupled plasma‒optical emission spectrometry. The results show a decreasing order of mean content of Co (2106 mg/kg) > Ni (1805 mg/kg) > Cr (139 mg/kg) > Co (97 mg/kg) > Zn (53 mg/kg) > Pb (14 mg/kg). The I-geo values show varying degrees of Cr, Cu, Ni, and Zn contamination. Dermal contact (54.5%) was the primary exposure pathway of noncarcinogenic risk for adults, and oral ingestion (95.7%) was the primary exposure route for children. The PTEs posed very low to no noncarcinogenic risks. As a single element, the mean hazard index (HI) for adults and children followed a similar trend: Cr > Cu > Ni > Pb > Zn. However, the carcinogenic risk of Cr, Cu, Ni, and Pb exposure in children was high and unacceptable. For adults, the carcinogenic risks of Cr, Cu, and Ni were high and unacceptable. Overall, children were generally more vulnerable to the adverse effects of PTE exposure. A study of this nature is essential for routine environmental monitoring and assessment and fundamental for planning and reinforcing existing pollution control measures. [ABSTRACT FROM AUTHOR]

Benzene is widely recognized as a potential carcinogen. Furthermore, the deficiency of specific nutrients may render individuals more vulnerable to cancer. For instance, β-cryptoxanthin, which possesses anti-inflammatory, antioxidant, and anticancer properties, has been identified as one such nutrient. Elevated benzene levels and reduced β-cryptoxanthin levels are reportedly correlated with an augmented susceptibility to cancer. To date, whether these 2 substances are linked with one another in the above correlation is yet to be determined. This study included 1358 participants with data on the serum concentration of β-cryptoxanthin as well as benzene and its derivatives. The data were sourced from the 2003–2004 National Health and Nutrition Examination Survey, a cross-sectional survey of the noninstitutionalized US population. Headspace solid-phase microextraction with gas chromatography and mass spectrometry was used to measure serum benzene and its derivatives, while high-performance liquid chromatography using multiwavelength photodiode-array absorbance detection was employed to quantify serum β-cryptoxanthin. In this study, male and female participants showed average β-cryptoxanthin levels of 9.10 ± 6.35 and 9.92 ± 8.95 ug/dL, respectively (p = 0.049). Styrene exhibited the strongest correlation with the change in β-cryptoxanthin concentration (β = −3.30, p for trend <0.001) upon comparing highest-quartile participants with those in the lowest quartile, followed by benzene (β = −2.95, p for trend <0.001), toluene (β = −2.90, p for trend <0.001), and ethylbenzene (β = −1.43, p for trend = 0.09). Subgroup analysis by sex displayed a statistically significant negative correlation of β-cryptoxanthin with benzene, styrene, and toluene in both the unadjusted and multivariate-adjusted models. The sera of noninstitutionalized US individuals exhibit a negative association of β-cryptoxanthin levels with benzene and its derivatives. Styrene demonstrates the strongest link with a substantial decline in serum β-cryptoxanthin levels, followed by benzene, toluene, and ethylbenzene. [ABSTRACT FROM AUTHOR]

Increased levels of the non-essential hazardous metalloid arsenic (As) in rice grains pose a threat to human health and the sustainability of the rice industry. In several counties, the average As contamination in polished rice has been detected to range from 0.002 to 0.39 mg/kg, which is above the safe limit of 1 mg/kg as recommended by the World Health Organisation. Beyond this limit, the digestive tract, circulatory system, skin, liver, kidney, nervous system and heart can be affected. Humans can develop cancer from consuming or inhaling As. In addition, long-term exposure to drinking water contaminated with arsenic has also been linked to a dose-response relationship with an increased risk of hypertension and diabetes mellitus. Rice has been shown to be an indirect source of arsenic accumulation in human bodies. Under flooded paddy soil, trivalent arsenate (AsIII) occupies 87-94% of the total As, while under non-flooded soil, pentavalent arsenate (AsV) predominates (73-96% of the total As). This review aims to provide a thorough and interdisciplinary understanding of the behaviour of As in the paddy soil and transportation to rice grain and further investigate efficient ways to limit arsenic contamination. Supplementation of soil with specific mineral nutrients such as iron (Fe), sulphur (S) and silicon (Si) can significantly decrease the arsenic accumulation in rice grain by minimising its uptake and translocation. The hydrogen bonding potentials of uronic acids, proteins and amino sugars on the extracellular surface of soil microorganisms facilitate the detoxification of arsenic species. Further, rice is absorbed less when exposed to aerobic water management practices than anaerobic ones since it reduces the build-up of As in rice, and the solution is immobilised as in the soil. [ABSTRACT FROM AUTHOR]

In drinking water distribution systems, the oxidation of zerovalent chromium, Cr(0), in iron corrosion scales by chlorine residual disinfectant is the dominant reaction to form carcinogenic hexavalent chromium, Cr(VI). This study investigates inhibitive corrosion control strategies through adjustments of chemical water parameters (i.e., pH, silicate, phosphate, calcium, and alkalinity) on Cr(VI) formation through oxidation of Cr(0)(s) by free chlorine under drinking water conditions. The results show that an increase in pH, silicate, alkalinity, and calcium suppressed Cr(VI) formation that was mainly attributed to in situ surface precipitation of new Cr(III) solids on the surface of Cr(0)(s), including Cr(OH)3(s), Cr2(SiO3)3(s), CrPO4(s), Cr2(CO3)3(s), and Cr10Ca(CO3)16(s). The Cr(III) surface precipitates were much less reactive with chlorine than Cr(0)(s) and suppressed the Cr redox reactivity. The concentration of surface Cr(III) solids was inversely correlated with the rate constant of Cr(VI) formation. Adding phosphate either promoted or inhibited the Cr(VI) formation, depending on the phosphate concentration. This study provides fundamental insight into the Cr(VI) formation mechanisms via Cr(0) oxidation by chlorine and the importance of surface precipitation of Cr(III) solids with different corrosion control strategies and suggests that increasing the pH/alkalinity and addition of phosphate or silicate can be effective control strategies to minimize Cr(VI) formation.

Abstract Background Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer commonly used in a wide variety of products, including medical devices. It is rapidly metabolized in the liver into various metabolites upon absorption through oral ingestion, dermal absorption, and inhalation. DEHP is classified as a non-genotoxic hepatocarcinogen in rodents, as its chronic exposure has been associated with the development of liver cancer in these animals, but most genotoxicity studies have been negative. Epidemiologic studies in humans suggest that long-term high intakes of DEHP may be a risk factor for liver dysfunction. The repeated-dose liver micronucleus (RDLMN) assay is a well-established method for assessing chromosomal changes caused by hepatic genotoxins and/or carcinogens. It is particularly valuable for detecting substances that undergo metabolic activation, especially when the metabolite has a short half-life or does not reach the bone marrow effectively. Therefore, we investigated whether the RDLMN assay could detect DEHP-induced micronucleus formation in the liver following a 14 or 28-day treatment. Results We report that the RDLMN assay demonstrated an increased frequency of hepatic micronuclei in rats exposed to DEHP for 14 or 28 days. The increases in micronuclei correlated with hepatomegaly, an established response to phthalates in the liver. Conversely, no such increases were observed in the micronucleus assay using bone marrow from these rats. Conclusion The detection of DEHP-induced micronuclei by the RDLMN assay suggests that this assay could detect the potential genotoxicity and hepatocarcinogenicity of DEHP. It also demonstrated the utility of the RDLMN assay in identifying metabolically activated hepatic carcinogens.

Increased levels of the non-essential hazardous metalloid arsenic (As) in rice grains pose a threat to human health and the sustainability of the rice industry. In several counties, the average As contamination in polished rice has been detected to range from 0.002 to 0.39 mg/kg, which is above the safe limit of 1 mg/kg as recommended by the World Health Organisation. Beyond this limit, the digestive tract, circulatory system, skin, liver, kidney, nervous system and heart can be affected. Humans can develop cancer from consuming or inhaling As. In addition, long-term exposure to drinking water contaminated with arsenic has also been linked to a dose-response relationship with an increased risk of hypertension and diabetes mellitus. Rice has been shown to be an indirect source of arsenic accumulation in human bodies. Under flooded paddy soil, trivalent arsenate (AsIII) occupies 87-94% of the total As, while under non-flooded soil, pentavalent arsenate (AsV) predominates (73-96% of the total As). This review aims to provide a thorough and interdisciplinary understanding of the behaviour of As in the paddy soil and transportation to rice grain and further investigate efficient ways to limit arsenic contamination. Supplementation of soil with specific mineral nutrients such as iron (Fe), sulphur (S) and silicon (Si) can significantly decrease the arsenic accumulation in rice grain by minimising its uptake and translocation. The hydrogen bonding potentials of uronic acids, proteins and amino sugars on the extracellular surface of soil microorganisms facilitate the detoxification of arsenic species. Further, rice is absorbed less when exposed to aerobic water management practices than anaerobic ones since it reduces the build-up of As in rice, and the solution is immobilised as in the soil.

Introduction The underlying factors of oral squamous cell cancers (OSCC) have been elucidated, but studies have focused little on etiological differences in affected oral cavity sites. The aim of this retrospective study was to clarify the role of carcinogen exposure in OSCC of different oral cavity areas. Methods A cross-sectional study of patients with primary OSCC was conducted retrospectively, based on patient records from Helsinki University Hospital, Finland, between January 2016 and December 2020. The patients’ self-reported history of tobacco smoking and alcohol use was explained by tumor site, age, sex, tumor size, and lymph node status in a logistic regression model. The information on smoking and alcohol use was compiled from a patient background form. Results In 519 patients, tumors occurred most often in the tongue (51%), gingiva (21%), or floor of the mouth (FOM; 15%). FOM had 26-fold greater odds for a history of smoking and alcohol use than other tumor sites (OR=25.78; 95% CI: 8.02–82.95; p

Abstract Bread is one of the most consumed foods all over the world. Several contaminants are identified in bread. Polycyclic aromatic hydrocarbons (PAHs) is one of these contaminants. This systematic study evaluates the amount of four carcinogenic PAHs (PAH4) in various types of breads. To conduct this study, a comprehensive search was carried out using keywords of polycyclic aromatic hydrocarbons, PAHs, PAH4, and bread, with no time limitations. 17 articles were selected and fully evaluated. The observed range of PAH4 concentrations in bread varied from non-detected (ND) to 20.66 µg/kg. In the sample preparation process for analysis, an ultrasonic bath was predominantly utilized. Most chromatographic methods are able to measure PAHs in food, but the GC-MS method has been used more. To mitigate PAH levels in bread, it is suggested to incorporate antioxidants during the bread-making process. Furthermore, the type of bread, the type of fuel used to bake the bread, the temperature and the cooking time were some of the factors affecting the amount of PAH. Restricting these factors could significantly reduce PAH content. Regarding the risk assessment conducted in the manuscript, it was determined that industrial breads are usually considered safe. However, some traditional breads may pose risks in terms of their potential PAH content.

Bread is one of the most consumed foods all over the world. Several contaminants are identified in bread. Polycyclic aromatic hydrocarbons (PAHs) is one of these contaminants. This systematic study evaluates the amount of four carcinogenic PAHs (PAH4) in various types of breads. To conduct this study, a comprehensive search was carried out using keywords of polycyclic aromatic hydrocarbons, PAHs, PAH4, and bread, with no time limitations. 17 articles were selected and fully evaluated. The observed range of PAH4 concentrations in bread varied from non-detected (ND) to 20.66 µg/kg. In the sample preparation process for analysis, an ultrasonic bath was predominantly utilized. Most chromatographic methods are able to measure PAHs in food, but the GC-MS method has been used more. To mitigate PAH levels in bread, it is suggested to incorporate antioxidants during the bread-making process. Furthermore, the type of bread, the type of fuel used to bake the bread, the temperature and the cooking time were some of the factors affecting the amount of PAH. Restricting these factors could significantly reduce PAH content. Regarding the risk assessment conducted in the manuscript, it was determined that industrial breads are usually considered safe. However, some traditional breads may pose risks in terms of their potential PAH content. [ABSTRACT FROM AUTHOR]

INTRODUCTION The underlying factors of oral squamous cell cancers (OSCC) have been elucidated, but studies have focused little on etiological differences in affected oral cavity sites. The aim of this retrospective study was to clarify the role of carcinogen exposure in OSCC of different oral cavity areas. METHODS A cross-sectional study of patients with primary OSCC was conducted retrospectively, based on patient records from Helsinki University Hospital, Finland, between January 2016 and December 2020. The patients' self-reported history of tobacco smoking and alcohol use was explained by tumor site, age, sex, tumor size, and lymph node status in a logistic regression model. The information on smoking and alcohol use was compiled from a patient background form. RESULTS In 519 patients, tumors occurred most often in the tongue (51%), gingiva (21%), or floor of the mouth (FOM; 15%). FOM had 26-fold greater odds for a history of smoking and alcohol use than other tumor sites (OR=25.78; 95% CI: 8.02-82.95; p<0.001). Gingival and buccal sites were associated significantly less with smoking and alcohol use (OR=0.43, 95% CI: 0.28-0.67; p<0.001 and OR=0.47; 95% CI: 0.25-0.92; p<0.026, respectively). Patients of older age were less likely to have a history of smoking and alcohol use (AOR=0.95; 95% CI: 0.94-0.97; p<0.001) than younger patients. Tumor size (T3-4) and FOM increased the odds for history of smoking and alcohol use (AOR=1.73; 95% CI: 1.15-2.60; p=0.009 and AOR=26.15; 95% CI: 8.01-84.84; p<0.001, respectively). CONCLUSIONS OSCC of oral cavity sites has notable differences in etiology. FOM seems to be related almost exclusively to conventional smoking and heavy alcohol use. [ABSTRACT FROM AUTHOR]

Skin cancer is a global and increasingly prevalent issue, causing significant individual and economic damage. UV filters in sunscreens play a major role in mitigating the risks that solar ultraviolet ra-diation poses to the human organism. While empirically effective, multiple adverse effects of these compounds are discussed in the media and in scientific research. UV filters are blamed for the dis-ruption of endocrine processes and vitamin D synthesis, damaging effects on the environment, induction of acne and neurotoxic and carcinogenic effects. Some of these allegations are based on scientific facts while others are simply arbitrary. This is especially dangerous considering the risks of exposing unprotected skin to the sun. In summary, UV filters approved by the respective governing bodies are safe for human use and their proven skin cancer-preventing properties make them in-dispensable for sensible sun protection habits. Nonetheless, compounds like octocrylene and ben-zophenone-3 that are linked to the harming of marine ecosystems could be omitted from skin care regimens in favor of the myriad of non-toxic UV filters. [ABSTRACT FROM AUTHOR]

Background: Non-muscle invasive bladder cancer (NMIBC) patients are affected by a high risk of recurrence. The topography of collagen fibers represents a hallmark of the neoplastic extracellular microenvironment. Objective: Assess the topographic change associated with different stages of bladder cancer (from neoplastic lesions to bona fide tumor) and whether those changes favour the development of NMIBC. Design, Setting, and Participants: Seventy-one clinical samples of urothelial carcinoma at different stages were used. Topographic changes preceding tumor onset and progression were evaluated in the rat bladder cancer model induced by nitrosamine (BBN), a bladder-specific carcinogen. The preclinical model of actinic cystitis was also used in combination with BBN. Validated hematoxylin-eosin sections were used to assess the topography of collagen fibrils associated with pre-tumoral steps, NMIBC, and MIBC. Findings: Linearization of collagen fibers was higher in Cis and Ta vs. dysplastic urothelium, further increased in T1 and greatest in T2 tumors. In the BBN preclinical model, an increase in the linearization of collagen fibers was established since the beginning of inflammation, such as the onset of atypia of a non-univocal nature and dysplasia, and further increased in the presence of the tumor. Linearization of collagen fibers in the model of actinic cystitis was associated with earlier onset of BBN-induced tumor. Conclusions: The topographic modification of the extracellular microenvironment occurs during the inflammatory processes preceding and favoring the onset of bladder cancer. The topographic reconfiguration of the stroma could represent a marker for identifying and treating the non-neoplastic tissue susceptible to tumor recurrence.

Summary: Background: The International Agency for Research on Cancer (IARC) recently classified opium consumption as carcinogenic to humans. This study aimed to estimate the potential reduction in incident cancers by 2035 in Iran, which accounts for 42% of global opium consumption, through decreasing opium use prevalence. Methods: The population attributable fraction (PAF) of opium-related cancers was projected using national cancer incidence, age- and gender-specific opium use prevalence, relative cancer risks associated with opium use, and annual percentage changes in cancer incidence rates in Iran. Opium-related cancers were defined based on IARC monographs as cancers of lung, larynx, bladder, esophagus, stomach, pancreas, and pharynx. The number of preventable cancer cases under different opium prevalence scenarios was determined by subtracting attributable cases in each year based on current prevalence from those in alternative scenarios. Findings: By 2035, an estimated 3,001,421 new cancer cases are expected in Iran, with 904,013 (30.1%) occurring in opium-related sites. Maintaining the current opium prevalence (5.6%) is projected to cause 111,130 new cancer cases (3.7% of all cancers, 12.3% of opium-related). A 10%, 30%, and 50% reduction in opium prevalence could prevent 9,016, 28,161, and 49,006 total incident cancers by 2035 in Iran, respectively. Reducing opium use prevalence by 10%–50% is projected to have the highest impact on lung cancer (prevention of 2,946–15,831 cases), stomach cancer (prevention of 2,404–12,593 cases), and bladder cancer (prevention of 1,725–9,520 cases). Interpretation: Our results highlight the significant benefits that can be achieved through effective cancer prevention policies targeting opium use in Iran. Neglecting this risk factor is estimated to pose a significant burden on cancer incidence in the next decade in this population. Funding: None.

According to the European Agency for Safety and Health at Work (EU - OSHA) and the Roadmap on Carcinogens about 120,000 work - related cancer cases occur each year as a result exposure to carcinogens at the workplace in the EU, leading to approximately 80,000 fatalities annually. Occupational risk assessment is used as a criterion for occupational safety. At the cement manufacturing sector, it was revealed that the main hazard is exposure to carcinogen substances such as respirable crystalline SiO2. In the present work, two methods were used for risk assessment in a cement production enterprise: the classical Fine - Kinney method and Flexible risk assessment method developed by Reinhold and Tint. The results of the joint application of these two methods show the advantages and disadvantages of each of them and point to the need to combine more than one method to effectively cover aspects of risk assessment. It was made the evaluation of applied existing control measures, as well as new measures for better protection have been proposed. [ABSTRACT FROM AUTHOR]

Arsenic exhibits varying degrees of toxicity depending on its many chemical forms. The carcinogenic properties of arsenic have already been established. However, the precise processes underlying the development of diseases following acute or chronic exposure to arsenic remain poorly known. Most of the existing investigation has focused on studying the occurrence of cancer following significant exposure to elevated levels of arsenic. Nevertheless, multiple investigations have documented diverse health consequences from prolonged exposure to low levels of arsenic. Inorganic arsenic commonly causes lung, bladder, and skin cancer. Some investigations have shown an association between arsenic in drinking water and prostate cancer, but few investigations have focused on exploring this connection. There is currently a lack of relevant animal models demonstrating a clear link between inorganic arsenic exposure and the development of prostate cancer. Nevertheless, studies using cellular model systems have demonstrated that arsenic can potentially promote the malignant transformation of human prostate epithelial cells in vitro. The administration of elevated levels of arsenic has been demonstrated to elicit cell death in instances of acute experimental exposure. Conversely, in cases of chronic exposure, arsenic prompts cellular proliferation and sustains cellular viability, thereby circumventing the constraints imposed by telomere shortening and apoptosis. Furthermore, cells consistently exposed to the stimulus exhibit an augmented ability to invade surrounding tissues and an enhanced potential to form tumors. This review aims to portray mechanistic insights into arsenic-induced prostate cancer. [ABSTRACT FROM AUTHOR]

The kinetically-derived maximal dose (KMD) is defined as the maximal external dose at which kinetics are unchanged relative to lower doses, e.g., doses at which kinetic processes are not saturated. Toxicity produced at doses above the KMD can be qualitatively different from toxicity produced at lower doses. Here, we test the hypothesis that neoplastic lesions reported in the National Toxicology Program's (NTP) rodent cancer bioassay with ethylbenzene are a high-dose phenomenon secondary to saturation of elimination kinetics. To test this, we applied Bayesian modeling on kinetic data for ethylbenzene from rats and humans to estimate the Vmax and Km for the Michaelis–Menten equation that governs the elimination kinetics. Analysis of the Michaelis–Menten elimination curve generated from those Vmax and Km values indicated KMD ranges for venous ethylbenzene of 8–17 mg/L in rats and 10–18 mg/L in humans. Those venous concentrations are produced by inhalation concentrations of around 200 ppm ethylbenzene, which is well above typical human exposures. These KMD estimates support the hypothesis that neoplastic lesions seen in the NTP rodent bioassay occur secondary to saturation of ethylbenzene elimination pathways and are not relevant for human risk assessment. Thus, ethylbenzene does not pose a credible cancer risk to humans under foreseeable exposure conditions. Cancer risk assessments focused on protecting human health should avoid endpoint data from rodents exposed to ethylbenzene above the KMD range and future toxicological testing should focus on doses below the KMD range. [ABSTRACT FROM AUTHOR]

Background: Exposures to polyaromatic hydrocarbons (PAHs) contribute to cancer in the fire service. Fire investigators are involved in evaluations of post-fire scenes. In the US, it is estimated that there are up to 9000 fire investigators, compared to approximately 1.1 million total firefighting personnel. This exploratory study contributes initial evidence of PAH exposures sustained by this understudied group using worn silicone passive samplers. Objectives: Evaluate PAH exposures sustained by fire investigators at post-fire scenes using worn silicone passive samplers. Assess explanatory factors and health risks of PAH exposure at post-fire scenes. Methods: As part of a cross-sectional study design, silicone wristbands were distributed to 16 North Carolina fire investigators, including eight public, seven private, and one public and private. Wristbands were worn during 46 post-fire scene investigations. Fire investigators completed pre- and post-surveys providing sociodemographic, occupational, and post-fire scene characteristics. Solvent extracts from wristbands were analyzed via gas chromatography-mass spectrometry (GC-MS). Results were used to estimate vapor-phase PAH concentration in the air at post-fire scenes. Results: Fire investigations lasted an average of 148 minutes, standard deviation ± 93 minutes. A significant positive correlation (r=0.455, p

Polycyclic aromatic hydrocarbons (PAHs) are considered as harmful pollutants for the environment and human health system. The most prevalent PAHs in the environment is benzo[a]pyrene when present in high concentrations are potentially hazardous because it is carcinogenic. The objective of the current study was to identify and screen benzo[a]pyrene-degrading bacterial strain that is adapted for various environmental and nutritional requirements in order to determine how well they can decompose the benzo[a]pyrene. The results showed that, after 45 days of incubation at 140 rpm in a temperature-controlled shaker, benzo[a]pyrene (initial concentration of 1000 mg/L) was degraded 87.5% by the isolated strain LOBP-19A at 37 °C, pH 9 in the presence of glucose (1%), and peptone (0.5%) from. Isolated strain performed worse when temperature and pH are different from optimal conditions. Enzymes were screened using bacterial strain (LOBP-1A) and also produced biosurfactant by different method. GCMS studied and characterized metabolites of benzo[a]pyrene of LOBP-19A strain are 1-(3-methylbutyl)-2,3,4,6-tetramethylbenzene, Tetrazole, 1-(2-flourophenyl)-5-[4-(1,1-dimethylethyl) benzythio], 1,4-Benzenediol,2,6-bis(1,1-dimethylethyl)-(CAS), Octadecanoic acid trimethylsilyl ester and 1-naphthalene-sulfonic acid. The isolated strain was identified as Stutzerimonas stutzeri (LOBP-19A) OP389146 based their 16s-rRNA sequencing. Thus the current study demonstrated the great potential of isolated bacterial strain for use in water bodies and field scale bioremediation of benzo[a]pyrene and PAHs contaminated sites.

Aflatoxins (AFs) are the most potent and ubiquitously found mycotoxins, capable of causing contamination in agricultural products. Aflatoxin B1 (AFB1) is the most toxic and primarily produced Aflatoxin and will be a real threat to the safety of food and feeds. The current study searched for the potential of Lactic acid bacteria (LAB) isolated from animal excreta for AFB1 mitigation. Three LAB out of 56 isolates were found to exhibit more than 50% sorbent action with AFB1 in phosphate-buffered saline (PBS) and were identified as Lactococcuslactis strain CF_6 (OP183481) (65.38%), Lacticaseibacillus casei strain CW_3 (OP183482)(52.63%) and Lactobacillus acidophilus strain CE_4 (OP183483)(63.13%). More than 60% of the total AFB1 removal was observed in 2 hr of incubation, and maximum sorbent action was found at a pH 6-7 range at 37oC for 24 hours. In the Scanning Electron Microscope (SEM) analysis, heat-killed cells showed a significant increase in cell surface binding area, which improved the surface binding for all isolates except L. casei strain CW_3; however, it proves that LAB surface binding is strain-specific rather than heat treatment. Moreover, the rise in AFB1 concentration improved the rate of the sorbent action but did not observe any substantial changes in total AFB1 detoxification. So, it is concluded that the animal excreta may be a versatile source of probiotic LAB for AFB1 detoxification by surface binding.

Convincing data regarding carcinogenic substances is very useful for handling materials correctly to avoid exposure to cancer-triggering substances in the body. To collect as much carcinogen data as possible, low-requirement carcinogen detection setups need to be developed. In this study, the first steps in the development of carcinogen detection through functional protein expression assessment are reported. Hydrazine sulfate, one of the well-known carcinogens chosen as a model material, was tested on germination of Raphanus sativus L., with various concentrations, namely 0 (control), 1, 10, and 100 mM. This plant was selected due to its characteristics showing a stable germination rate over a wide range of temperatures. Within a predetermined germination time, seeds and/or sprouts were observed and germination rate, protein concentration, and alkaline phosphatase activity were measured. The results showed that hydrazine sulfate slowed seed germination, and increased 72-h protein concentration but decreased alkaline phosphatase activity in the control group. This suggests that changes in alkaline phosphatase activity in seeds during germination have the potential to be a marker for cancer. In this research, it can be concluded that the method used can be applied as a first step to assess the carcinogenicity of a compound.

Aflatoxins (AFs) are the most potent and ubiquitously found mycotoxins, capable of causing contamination in agricultural products. Aflatoxin B1 (AFB1) is the most toxic and primarily produced Aflatoxin and will be a real threat to the safety of food and feeds. The current study searched for the potential of Lactic acid bacteria (LAB) isolated from animal excreta for AFB1 mitigation. Three LAB out of 56 isolates were found to exhibit more than 50% sorbent action with AFB1 in phosphate-buffered saline (PBS) and were identified as Lactococcuslactis strain CF&lowbar;6 (OP183481) (65.38%), Lacticaseibacillus casei strain CW&lowbar;3 (OP183482)(52.63%) and Lactobacillus acidophilus strain CE&lowbar;4 (OP183483)(63.13%). More than 60% of the total AFB1 removal was observed in 2 hr of incubation, and maximum sorbent action was found at a pH 6-7 range at 37o C for 24 hours. In the Scanning Electron Microscope (SEM) analysis, heat-killed cells showed a significant increase in cell surface binding area, which improved the surface binding for all isolates except L. casei strain CW&lowbar;3; however, it proves that LAB surface binding is strain-specific rather than heat treatment. Moreover, the rise in AFB1 concentration improved the rate of the sorbent action but did not observe any substantial changes in total AFB1 detoxification. So, it is concluded that the animal excreta may be a versatile source of probiotic LAB for AFB1 detoxification by surface binding. [ABSTRACT FROM AUTHOR]

Radon is a known carcinogen and a by-product of degrading naturally occurring radioactive elements. The North Shore Micmac District Council (NSMDC) board of directors, in Eastern New Brunswick, Canada, were aware of this issue and saw a need for increased radon testing and awareness in their communities. The initial plan was to administer a testing blitz across communities to gauge the current levels of radon exposure in both residential and band-owned structures. This, with Elder consultation and a participant health survey, would create a data set used to guide future strategies effectively and better direct resources to mitigate the leading cause of lung cancer in non-smokers. These plans were put in place prior to the COVID-19 pandemic that began in March 2020. The subsequent provincial levels of restriction could not have been predicted. The ever-changing pandemic-related restrictions, and public health's focus on a new deadly pathogen, led to difficulties managing and following through on many health and wellness projects. These circumstances led to a unique situation that delayed results, prolonged exposure to a known carcinogen, and may have consequences in the long term. Few procedures, treatments, or medications do not have side effects, and even warranted pandemic-related measures affect other aspects of health. [ABSTRACT FROM AUTHOR]

Background/Aim: Patients with radiation sensitive Fanconi anemia (FA) are presenting with cancers of the oral cavity, oropharynx, and other anatomic locations. Materials and Methods: Animal models for cancer in FA mice used orthotopic tumors from wild type mice. We derived a cancer cell line from Fanca--/-- mice by topical application of the chemical carcinogen dimethyl benzanthracene (DMBA). Results: A Fanca--/-- mouse rhabdomyosarcoma was derived from a Fanca--/-- (129/Sv) mouse. The in vitro clonogenic survival of the Fanca--/-- clone 6 cancer cell line was consistent with the FA genotype. Transplanted tumors demonstrated hypoxic centers surrounded by senescent cells. Conclusion: This Fanca--/-- mouse syngeneic cancer should provide a valuable resource for discovery and development of new normal tissue radioprotectors for patients with FA and cancer. [ABSTRACT FROM AUTHOR]

Direct DNA double-strand breaks result in phosphorylation of H2AX, a variant of the histone H2 protein. Phosphorylated H2AX (γH2AX) may be a potential indicator in the evaluation of genotoxicity and hepatocarcinogenicity. In this study, γH2AX and Ki-67 were detected in the short-term responses (24 h after chemical administration) to classify genotoxic hepatocarcinogens (GHs) from non-GH chemicals. One hundred and thirty-five 6-week-old Crl: CD(SD) (SPF) male rats were treated with 22 chemicals including 11 GH and 11 non-GH, sacrificed 24 h later, and immunostained with γH2AX and Ki-67. Positivity rates of these markers were measured in the 3 liver ZONEs 1–3; portal, lobular, and central venous regions. These values were input into 3 machine learning models—Naïve Bayes, Random Forest, and k-Nearest Neighbor to classify GH and non-GH using a 10-fold cross-validation method. All 11 and 10 out of 11 GH caused significant increase in γH2AX and Ki-67 levels, respectively (P  < .05). Of the 3 machine learning models, Random Forest performed the best. GH were identified with 95.0% sensitivity (76/80 GH-treated rats), 90.9% specificity (50/55 non-GH-treated rats), and 90.0% overall correct response rate using γH2AX staining, and 96.2% sensitivity (77/80), 81.8% specificity (45/55), and 90.4% overall correct response rate using Ki-67 labeling. Random Forest model using γH2AX and Ki-67 could independently predict GH in the early stage with high accuracy. [ABSTRACT FROM AUTHOR]

Background: This study aimed to evaluate the carcinogenic and non-carcinogenic health risks of heavy metals in seven types of tobacco widely consumed in the east of the country through inhalation exposure. Methods: This descriptive-analytical study was conducted from April 2022 to October 2022 in the city of Bojnord, Iran on sook of seven popular tobacco brands. Metal concentrations in sook of tobacco were determined using inductively coupled plasma-optical emission spectroscopy. In order to analyze the data and ensure the accuracy of the results, the amount of metals in the samples was repeated three times, and their average was analyzed. Monte Carlo software was used to assess possible risks. Results: The results of this study showed heavy metal concentrations in sook tobaccos were, respectively, Fe>Zn>Mn>Ba>Pb>Ni>Cu>Mo>Cr>As>Cd. The concentration of heavy metals such as arsenic, cadmium and molybdenum in Alrah brand tobacco was higher than other types of tobacco. So that the amounts of heavy metals including arsenic, cadmium and molybdenum for this brand were 14.2±0.05, 10.4±0.06 and 11.6±0.04 micrograms per gram, respectively. The hazard index (HI) values for different types of tobacco, including Al-Rah, Amordadsub, Al-Fakher, Al-Rubi, Mazaya, traditional flavorless, and Nakhle, were 2.64, 2.41, 2.05, 1.7, 1.49, 1.46, and 1.44, respectively. The lifetime cancer risk (ILCR) for Amordadsub, Al-Rah, Nakhla, Mazaya, Al-Rubi, Al-Fakher, and traditional flavorless tobaccos was 2.8×10-3, 2.43×10-3, 1.72×10-3, 1.58×10-3, 1.43×10-3, 9.58×10-4, and 8.08×10-4, respectively. Lead in Alrah tobacco sook had the highest non-carcinogenic risk value with a value of 1.59. Conclusion: According to the obtained results, Alrah tobacco sook has a higher cancer and non-cancer risk than regular tobacco and can cause non-carcinogenic and carcinogenic risks for consumers. Thus, it is necessary to regularly monitor the quality of prevalent tobacco to reduce delete human health risks.

Abstract Despite great medical advances, oncological research is still looking for novel therapeutic approaches due to the limitation of conventional therapeutic agents. Virotherapy is one of these new emerging therapeutic approaches that attract attention with their widespread applications. Virotherapy use lives oncolytic viruses or genetically engineered viruses that selectively infect the tumor cells, replicate, and disrupt the cancerous cells that also induce their anticancer activity by stimulating the host antitumor immune response. Moreover, viruses are widely used as target delivery vectors for specifically delivering different genes, therapeutic agents, and immune‐stimulating agents. In addition to having antitumor activity by themselves in combination with conventional therapeutic agents like immune therapy and chemotherapy, Virotherapy agents also elicit promising outcomes. Therefore, in addition to their promising result in monotherapy use, virotherapy agents can also be used in combination with conventional cancer therapy, epigenetic modulators, and even microRNAs without any cross‐resistance, which allows the patient not to be deprived of her routine medicine. Still, this combination therapy reduces the adverse effect of the conventional therapies. All together suggest that virotherapy agents as novel potential agents in the field of cancer therapy.

Radon is a known carcinogen and a by-product of degrading naturally occurring radioactive elements. The North Shore Micmac District Council (NSMDC) board of directors, in Eastern New Brunswick, Canada, were aware of this issue and saw a need for increased radon testing and awareness in their communities. The initial plan was to administer a testing blitz across communities to gauge the current levels of radon exposure in both residential and band-owned structures. This, with Elder consultation and a participant health survey, would create a data set used to guide future strategies effectively and better direct resources to mitigate the leading cause of lung cancer in non-smokers. These plans were put in place prior to the COVID-19 pandemic that began in March 2020. The subsequent provincial levels of restriction could not have been predicted. The ever-changing pandemic-related restrictions, and public health’s focus on a new deadly pathogen, led to difficulties managing and following through on many health and wellness projects. These circumstances led to a unique situation that delayed results, prolonged exposure to a known carcinogen, and may have consequences in the long term. Few procedures, treatments, or medications do not have side effects, and even warranted pandemic-related measures affect other aspects of health.

AbstractOver time, paint chemistry has changed, posing health hazards to house painters. Surveys and interviews scheduled on work profiles determined the exposure to solvents in commercial painting. This research paper aims to identify the respiratory and lungs issues among painters due to their occupation. With this aim, this also explore the worker’s experiences with various types of paints regarding health implications. The current study is related to research on the health issues of paint workers. Subjects for the study were chosen by the use of cluster sampling from several places in three districts of Uttar Pradesh, India. An interview schedule was developed to collect relevant and maximum information. The study used a sample size of 150 that was not pre-determined. All the respondents were from the labour class and worked with paints. A schedule of the interview was developed to gather information about the painters’ demographic profile and current respiratory health status. Statistical approaches such as Standard Deviation, ANOVA and Pearson’s correlation were used for analysis. The study revealed that painters are exposed to paints and face various health issues. Majority of the respondents (50.7%) belongs to lower economic status, followed by upper lower (33.3%), and only 4% of them belong to the upper class. We found a significant difference between the respondent’s age and respiratory health. This data indicates that respondents who faced high respiratory issues belong to the age group of 61–75 years, and minimum problems were observed in the age group of 19–32 years. This data shows highly significant differences between age groups, and the problem occurs with the respiratory system in painters. The result indicates that wearing the mask was significantly associated with respiratory problems like cough (p = .004), chest tightness (p = .009), and whistling sound from the chest (p = .000). A perfect positive significant correlation between working year, days, and duration with different lung problems were identified. A perfect positive association (0.443**) was also identified between years of work and cough difficulties, indicating that workers who have worked for prolonged periods were more susceptible to cough. Cough problems were highly associated with painters who worked more days per week. Cough issues were perfectly and significantly associated (0.232**) with painters who use masks while working. The chest sound or whistling gets more intense as the cough problem worsens. Moreover, there was a positive and significant association between discomfort during breathing and working years (.340**), working days in a week (.195*), and working duration (.594**). This study highlighted the risk and problems among painters due to pain, including breathing problems, prolonged cough, chest discomfort, and almost all lung problems.

Background: Angiotensin-converting enzyme inhibitors (ACE-I) and their pharmacologically related sartans have been associated with an increased cancer incidence in several clinical observations. In 2018, sartans were revealed as being significantly contaminated with nitrosamines. Nitrosamines are potent human mutagens that can be formed ex vivo and, more concerningly, also in vivo from nitrosatable drug precursors. Their formation in sartans may justify the reported cancer risk and, by analogy, this may also apply to ACE-Is. Materials and methods: We investigated a commonly used ACE-I, ramipril (RAM). We checked its susceptibility to in vivo interaction with nitrite, potentially resulting in the generation of mutagenic N-nitrosamines. To that end, in silico simulation of mutagenicity of RAM nitroso-derivatives was performed using VEGA-GUI software. Then, the Nitrosation Assay Procedure was conducted which served as a model of endogenous reaction. The resulting post-nitrosation mixtures were subjected to a bacterial reverse mutation test employing Salmonella typhimurium strains TA98 and TA100 with and without metabolic activation. Results: Our results showed that studied samples did not induce point mutations in the test bacteria, regardless of the catalytic cytochrome activity. Conclusion: We concluded that RAM endogenous nitrosation is not the reason for increased cancer incidence. However, other ACE-Is must be verified in a similar manner. [ABSTRACT FROM AUTHOR]

Globally, bladder cancer has been identified as one of the most frequent occupational cancers, but our understanding of occupational bladder cancer risk in Iran is less advanced. This study aimed to assess the risk of bladder cancer in relation to occupation in Iran. We used the IROPICAN case‐control study data including 717 incident cases and 3477 controls. We assessed the risk of bladder cancer in relation to ever working in major groups of the International Standard Classification of Occupations (ISCO‐68) while controlling for cigarette smoking, opium consumption. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CI). In men, decreased ORs for bladder cancer were observed in administrative and managerial workers (OR 0.4; CI: 0.2, 0.9), and clerks (OR 0.6; CI: 0.4, 0.9). Elevated ORs were observed in metal processors (OR 5.4; CI: 1.3, 23.4), and workers in occupations with likely exposure to aromatic amines (OR 2.2; CI: 1.2, 4.0). There was no evidence of interactions between working in aromatic amines‐exposed occupations and tobacco smoking or opium use. Elevated risk of bladder cancer in men in metal processors and workers likely exposed to aromatic amines aligns with associations observed outside Iran. Other previously confirmed associations between high‐risk occupations and bladder cancer were not observed, possibly due to small numbers or lack of details on exposure. Future epidemiological studies in Iran would benefit from the development of exposure assessment tools such as job exposure matrices, generally applicable for retrospective exposure assessment in epidemiological studies. [ABSTRACT FROM AUTHOR]

Introduction: De novo mutations contribute to a large proportion of sporadic psychiatric and developmental disorders, yet the potential role of environmental carcinogens as drivers of causal de novo mutations in neurodevelopmental disorders is poorly studied. Methods: To explore environmental mutation vulnerability of disease-associated gene sets, we analyzed publicly available whole genome sequencing datasets of mutations in human induced pluripotent stem cell clonal lines exposed to 12 classes of environmental carcinogens, and human lung cancers from individuals living in highly polluted regions. We compared observed rates of exposureinduced mutations in disease-related gene sets with the expected rates of mutations based on control genes randomly sampled from the genome using exact binomial tests. To explore the role of sequence characteristics in mutation vulnerability, we modeled the effects of sequence length, gene expression, and percent GC content on mutation rates of entire genes and gene coding sequences using multivariate Quasi-Poisson regressions. Results: We demonstrate that several mutagens, including radiation and polycyclic aromatic hydrocarbons, disproportionately mutate genes related to neurodevelopmental disorders including autism spectrum disorders, schizophrenia, and attention deficit hyperactivity disorder. Other disease genes including amyotrophic lateral sclerosis, Alzheimer's disease, congenital heart disease, orofacial clefts, and coronary artery disease were generally not mutated more than expected. Longer sequence length was more strongly associated with elevated mutations in entire genes compared with mutations in coding sequences. Increased expression was associated with decreased coding sequence mutation rate, but not with the mutability of entire genes. Increased GC content was associated with increased coding sequence mutation rates but decreased mutation rates in entire genes. Discussion: Our findings support the possibility that neurodevelopmental disorder genetic etiology is partially driven by a contribution of environment-induced germ line and somatic mutations. [ABSTRACT FROM AUTHOR]

Background: This study aimed to evaluate the carcinogenic and non-carcinogenic health risks of heavy metals in seven types of tobacco widely consumed in the east of the country through inhalation exposure. Methods: This descriptive-analytical study was conducted from April 2022 to October 2022 in the city of Bojnord, Iran on sook of seven popular tobacco brands. Metal concentrations in sook of tobacco were determined using inductively coupled plasmaoptical emission spectroscopy. In order to analyze the data and ensure the accuracy of the results, the amount of metals in the samples was repeated three times, and their average was analyzed. Monte Carlo software was used to assess possible risks. Results: The results of this study showed heavy metal concentrations in sook tobaccos were, respectively, Fe>Zn>Mn>Ba>Pb>Ni>Cu>Mo>Cr>As>Cd. The concentration of heavy metals such as arsenic, cadmium and molybdenum in Alrah brand tobacco was higher than other types of tobacco. So that the amounts of heavy metals including arsenic, cadmium and molybdenum for this brand were 14.2±0.05, 10.4±0.06 and 11.6±0.04 micrograms per gram, respectively. The hazard index (HI) values for different types of tobacco, including Al-Rah, Amordadsub, Al-Fakher, Al-Rubi, Mazaya, traditional flavorless, and Nakhle, were 2.64, 2.41, 2.05, 1.7, 1.49, 1.46, and 1.44, respectively. The lifetime cancer risk (ILCR) for Amordadsub, Al-Rah, Nakhla, Mazaya, Al-Rubi, Al-Fakher, and traditional flavorless tobaccos was 2.8×10-3, 2.43×10-3, 1.72×10-3, 1.58×10-3, 1.43×10-3, 9.58×10-4, and 8.08×10-4, respectively. Lead in Alrah tobacco sook had the highest non-carcinogenic risk value with a value of 1.59. Conclusion: According to the obtained results, Alrah tobacco sook has a higher cancer and non-cancer risk than regular tobacco and can cause non-carcinogenic and carcinogenic risks for consumers. Thus, it is necessary to regularly monitor the quality of prevalent tobacco to reduce delete human health risks. [ABSTRACT FROM AUTHOR]

Inflammation in the tumor microenvironment is a hallmark of cancer and is recognized as a key characteristic of carcinogens. However, the failure of resolution of inflammation in cancer is only recently being understood. Products of arachidonic acid and related fatty acid metabolism called eicosanoids, including prostaglandins, leukotrienes, lipoxins, and epoxyeicosanoids, critically regulate inflammation, as well as its resolution. The resolution of inflammation is now appreciated to be an active biochemical process regulated by endogenous specialized pro-resolving lipid autacoid mediators which combat infections and stimulate tissue repair/regeneration. Environmental and chemical human carcinogens, including aflatoxins, asbestos, nitrosamines, alcohol, and tobacco, induce tumor-promoting inflammation and can disrupt the resolution of inflammation contributing to a devastating global cancer burden. While mechanisms of carcinogenesis have focused on genotoxic activity to induce mutations, nongenotoxic mechanisms such as inflammation and oxidative stress promote genotoxicity, proliferation, and mutations. Moreover, carcinogens initiate oxidative stress to synergize with inflammation and DNA damage to fuel a vicious feedback loop of cell death, tissue damage, and carcinogenesis. In contrast, stimulation of resolution of inflammation may prevent carcinogenesis by clearance of cellular debris via macrophage phagocytosis and inhibition of an eicosanoid/cytokine storm of pro-inflammatory mediators. Controlling the host inflammatory response and its resolution in carcinogen-induced cancers will be critical to reducing carcinogen-induced morbidity and mortality. Here we review the recent evidence that stimulation of resolution of inflammation, including pro-resolution lipid mediators and soluble epoxide hydrolase inhibitors, may be a new chemopreventive approach to prevent carcinogen-induced cancer that should be evaluated in humans.

Mycotoxins are secondary toxic metabolites synthesized by numerous filamentous fungi including members of the genus Fusarium, Penicillium, Drechslera, Aspergillus, Claviceps, Monascum, Alternaria, Cephalosporium, Nigrospora, and Trichoderma. Among them, Aspergillus and Fusarium species are major plant pathogens recognized to induce infection and produce mycotoxins in food crops. More than 400 mycotoxins have been documented and among them, aflatoxin, fumonisins, trichothecenes, zearalenone, ochratoxin A, citrinin, ergot alkaloids, and patulin are the most prominent compounds linked to a variety of human and animal health disorders. Genus Fusarium and Aspergillus belong to a saprophytic group, which can infect and contaminate many crops at pre and post-harvest stages. Mycotoxins can have a variety of negative effects on health in both humans and animals. Mycotoxins and their metabolites can cause severe acute poisoning, which can result in death, as well as long-term negative health effects, such as cancer and immune-suppressive disorders in living beings (animals and humans). Mycotoxin contamination of agricultural goods has gained global significance, due to its toxic effects on living beings, as well as its importance to international trade. Our objective is to provide a consolidated information on the potential mycotixs in food grains and their significant impact on the health of the human beings.

Wood-based panels, which contain wood raw materials along with urea-formaldehyde (UF) or phenol-formaldehyde (PF) resins, can increase the indoor air concentration of formaldehyde. Formaldehyde can stimulate the upper respiratory mucosa and cross-linking reaction with cell proteins and DNA, and this can result in degeneration and necrosis of respiratory cells and damaged cell proliferation. Formaldehyde can induce health hazards such as nasal cancer, leukemia, and destruction of the reproductive system. Acetaldehyde dehydrogenase 5 (ADH5) in the body cooperates with Fanconi anaemia complementation group D2 (FANCD2) to quickly metabolize formaldehyde into formate and maintain the balance of endogenous formaldehyde. However, when both ADH5 and FANCD2 proteins have defects or mutations, damaged DNA repair failure and cell proliferation induce a variety of health diseases. The damage has been found in the upper respiratory area, not on distal body tissues such as liver, kidney, and bone marrow. Meanwhile epidemiological survey has not shown a positive correlation between formaldehyde and health hazards. It is recommended that the use of wood formaldehyde-based products should be reduced, and pathogenesis genes and damage repair mechanism should be studied systematically and deeply to develop gene drugs to remove excess formaldehyde and activate the damage gene repair mechanism in the future.

IntroductionDe novo mutations contribute to a large proportion of sporadic psychiatric and developmental disorders, yet the potential role of environmental carcinogens as drivers of causal de novo mutations in neurodevelopmental disorders is poorly studied.MethodsTo explore environmental mutation vulnerability of disease-associated gene sets, we analyzed publicly available whole genome sequencing datasets of mutations in human induced pluripotent stem cell clonal lines exposed to 12 classes of environmental carcinogens, and human lung cancers from individuals living in highly polluted regions. We compared observed rates of exposure-induced mutations in disease-related gene sets with the expected rates of mutations based on control genes randomly sampled from the genome using exact binomial tests. To explore the role of sequence characteristics in mutation vulnerability, we modeled the effects of sequence length, gene expression, and percent GC content on mutation rates of entire genes and gene coding sequences using multivariate Quasi-Poisson regressions.ResultsWe demonstrate that several mutagens, including radiation and polycyclic aromatic hydrocarbons, disproportionately mutate genes related to neurodevelopmental disorders including autism spectrum disorders, schizophrenia, and attention deficit hyperactivity disorder. Other disease genes including amyotrophic lateral sclerosis, Alzheimer’s disease, congenital heart disease, orofacial clefts, and coronary artery disease were generally not mutated more than expected. Longer sequence length was more strongly associated with elevated mutations in entire genes compared with mutations in coding sequences. Increased expression was associated with decreased coding sequence mutation rate, but not with the mutability of entire genes. Increased GC content was associated with increased coding sequence mutation rates but decreased mutation rates in entire genes.DiscussionOur findings support the possibility that neurodevelopmental disorder genetic etiology is partially driven by a contribution of environment-induced germ line and somatic mutations.

The incidence of breast cancer is often associated with geographic variation which indicates that a person's surrounding environment can be an important etiological factor in cancer development. Environmental risk factors can include exposure to sewage- or wastewater, which consist of a complex mixture of pathogens, mutagens and carcinogens. Wastewater contains primarily carbonaceous, nitrogenous and phosphorus compounds, however it can also contain trace amounts of chemical pollutants including toxic metal cations, hydrocarbons and pesticides. More importantly, the contamination of drinking water by wastewater is a potential source of exposure to mammary carcinogens and endocrine disrupting compounds. Organic solvents and other pollutants often found in wastewater have been detected in various tissues, including breast and adipose tissues. Furthermore, these pollutants such as phenolic compounds in some detergents and plastics, as well as parabens and pesticides can mimic estrogen. High estrogen levels are a well-established risk factor for estrogen-receptor (ER) positive breast cancer. Therefore, exposure to wastewater is a risk factor for the initiation, progression and metastasis of breast cancer. Carcinogens present in wastewater can promote tumourigenesis through various mechanisms, including the formation of DNA adducts, gene mutations and oxidative stress. Lastly, the presence of endocrine disrupting compounds in wastewater can have negative implications for ER-positive breast cancers, where these molecules can activate ERα to promote cell proliferation, survival and metastasis. As such, strategies should be implemented to limit exposure, such as providing funding into treatment technologies and implementation of regulations that limit the production and use of these potentially harmful chemicals. [Display omitted] • Exposure to wastewater is a risk factor for the initiation, progression and metastasis of breast cancer. • Carcinogens present in wastewater can promote tumourigenesis through pro-tumourigenic mechanisms. • Endocrine disrupting compounds in wastewater has negative implications for ER-positive breast cancer. [ABSTRACT FROM AUTHOR]

Despite great medical advances, oncological research is still looking for novel therapeutic approaches due to the limitation of conventional therapeutic agents. Virotherapy is one of these new emerging therapeutic approaches that attract attention with their widespread applications. Virotherapy use lives oncolytic viruses or genetically engineered viruses that selectively infect the tumor cells, replicate, and disrupt the cancerous cells that also induce their anticancer activity by stimulating the host antitumor immune response. Moreover, viruses are widely used as target delivery vectors for specifically delivering different genes, therapeutic agents, and immune-stimulating agents. In addition to having antitumor activity by themselves in combination with conventional therapeutic agents like immune therapy and chemotherapy, Virotherapy agents also elicit promising outcomes. Therefore, in addition to their promising result in monotherapy use, virotherapy agents can also be used in combination with conventional cancer therapy, epigenetic modulators, and even microRNAs without any cross-resistance, which allows the patient not to be deprived of her routine medicine. Still, this combination therapy reduces the adverse effect of the conventional therapies. All together suggest that virotherapy agents as novel potential agents in the field of cancer therapy. [ABSTRACT FROM AUTHOR]

Simple Summary: Colorectal cancer (CRC) is increasing in low- and middle-income countries, likely due to changing lifestyle habits, including diet. We found that a higher total choline intake was associated with an elevated risk of CRC, as well as glycerophosphocholine (GPC) and sphingomyelin (SM). Conversely, betaine intake was associated with a decreased risk of CRC. Consequently, it is possible to focus on the intake of betaine sources and manage the use of animal products as references for SM or other choline types with risks of CRC. Background: Colorectal cancer (CRC) is increasing in low- and middle-income countries, likely due to changing lifestyle habits, including diet. We aimed to investigate the relationship between dietary betaine, choline, and choline-containing compounds and CRC risk. Methods: We analyzed data from a case–control study, including 865 CRC cases and 3206 controls from Iran. Detailed information was collected by trained interviewers using validated questionnaires. The intake of free choline, phosphocholine (Pcho), glycerophosphocholine (GPC), phosphatidylcholine (PtdCho), and sphingomyelin (SM), as well as of betaine was estimated from food frequency questionnaires and categorized into quartiles. The odds ratios (OR) and 95% confidence intervals (CI) of CRC for choline and betaine quartiles were calculated using multivariate logistic regression by adjusting for potential confounders. Results: We observed excess risk of CRC in the highest versus lowest intake of total choline (OR = 1.23, 95% CI 1.13, 1.33), GPC (OR = 1.13, 95% CI 1.00, 1.27), and SM (OR = 1.14, 95% CI 1.01, 1.28). The intake of betaine exerted an inverse association with CRC risk (OR = 0.91, 95% CI 0.83, 0.99). There was no association between free choline, Pcho, PtdCho, and CRC. Analyses stratified by gender showed an elevated OR of CRC in men for SM intake OR = 1.20, 95% CI 1.03, 1.40) and a significantly decreased CRC risk in women for betaine intake (OR = 0.84, 95% CI 0.73, 0.97). Conclusion: Dietary modifications leading to an increase in betaine sources and managing the use of animal products as references for SM or other choline types might contribute to decreasing the risk of CRC. [ABSTRACT FROM AUTHOR]