Previous studies on university students have indicated a significant decline in the consumption of fruits and vegetables complemented by an increase in energy-dense foods. The food toxicant, acrylamide, typically occurs in carbohydrate-rich, energy-dense foods that have been heated. Hence, this work presents an estimated dietary acrylamide exposure for university students in Trinidad and Tobago. A 2-day dietary recall method was used to obtain the food consumption information from 683 university students of differing sociodemographic backgrounds. The acrylamide exposure was estimated using a deterministic approach. The median acrylamide intake was estimated to be 1.39 µg/kg bw/day. The estimated mean acrylamide dietary intakes for the female and male population were 1.40 and 1.37 µg/kg bw/day, respectively. Coffee was determined to be the major dietary contributor to acrylamide exposure. However, bread was the food item that was most frequently consumed among the students. Using multiple linear regression, a possible correlation was detected between the acrylamide exposure and these variables: dietary habits (mostly eat out; p < 0.05), and Indian ethnicity (p < 0.10). Using the margin of exposure approach, dietary acrylamide exposure was found to be a health concern with regards to neurotoxicity and carcinogenicity. An evaluation of the procedures and results from this pilot study was carried out for the potential of conducting a full-scale research project.

BACKGROUND: Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are two families of persistent organic pollutants that are dangerous as they remain in the atmosphere for long periods and are toxic for humans and animals. They are found all over the world, including the penguins of Antarctica. One of the mechanisms that explains the toxicity of these compounds is related to oxidative stress. The main idea of this theoretical research is to use conceptual density functional theory as a theory of chemical reactivity to analyze the oxidative stress that PCBs and PBDEs can produce. The electron transfer properties as well as the interaction with DNA nitrogenous bases of nine PCBs and ten PBDEs found in Antarctic penguins are investigated. From this study, it can be concluded that compounds with more chlorine or bromine atoms are more oxidizing and produce more oxidative stress. These molecules also interact directly with the nitrogenous bases of DNA, forming hydrogen bonds, and this may be an explanation for the toxicity. Since quinone-type metabolites of PCBs and PBDEs can cause neurotoxicity, examples of quinones are also investigated. Condensed Fukui functions are included to analyze local reactivity. These results are important as the reactivity of these compounds helps to explain the toxicity of PCBs and PBDEs.
METHODS: All DFT computations were performed using Gaussian16 at M06-2x/6-311 + g(2d,p) level of theory without symmetry constraints. Electro-donating (ω-) and electro-accepting (ω +) powers were used as global response functions and condensed Fukui functions as local parameters of reactivity.

UNASSIGNED: The carcinogenic properties of arsenic make it one of the most hazardous chemicals globally. Nevertheless, the exact level of human exposure to arsenic and the associated risks of cancer and non-cancer effects through different pathways in Ethiopia are still uncertain.
UNASSIGNED: The primary aim of this study was to evaluate the risk of both cancer and non-cancer outcomes among children and adults who have been exposed to arsenic through drinking water in the Adami Tulu Jido Kombolcha district of Ethiopia.
UNASSIGNED: For this study, a longitudinal study design was employed. A total of 45 groundwater sources were sampled using the census sampling method. The concentrations of total arsenic were measured using Agilent 7900 series inductively coupled plasma mass spectrometry. Carcinogenic and noncarcinogenic risk assessments were conducted by calculating lifetime cancer risk and hazard quotients. Microsoft Office Excel was utilized to calculate human health risk indices, and descriptive statistical analysis were performed using SPSS software.
UNASSIGNED: Our findings revealed that during the dry season, the mean arsenic concentration in the groundwater samples was 11.15 ± 9.38 µg/L, while during the rainy season, it was 10.67 ± 8.16 µg/L. The total cancer risk for children, resulting from oral ingestion and skin contact, was 1.15 × 10-2 and 1.07 × 10-2 during the dry and rainy seasons, respectively. For adults, the total cancer risk from oral ingestion and skin contact during the dry and rainy seasons was 4.95 × 10-3 and 4.59 × 10-3, respectively. Furthermore, the total hazard quotients for children via oral ingestion and skin absorption were 25.9 and 24.0 during the dry and rainy seasons, respectively. For adults, the total hazard quotients from ingestion and dermal contact during the dry and rainy seasons were 11 and 10, respectively.
UNASSIGNED: The findings indicate that the risks of cancer and non-cancer effects resulting from arsenic exposure through ingestion and dermal exposure were found to exceed the acceptable thresholds in both seasons. These results emphasize the urgent need for focused attention on the study population in the study area due to the high likelihood of experiencing adverse health outcomes.

UNASSIGNED: Opium consumption has recently been identified as a carcinogen, but the impact of opium use on cancer burden is unknown. We aimed to evaluate the fraction of cancers that could be attributed to opium use alone and in combination with cigarette smoking in a region where opium is widely used.
UNASSIGNED: 50,045 Iranian adults were recruited to this prospective cohort study between 2004 and 2008 and were followed through January 2022. We assessed the association between using opium and/or cigarette smoking and various cancers using proportional hazards regression models. We then calculated population attributable fractions (PAFs) for all cancers and for groups of cancers causally linked to opium and cigarette smoking.
UNASSIGNED: Of the total participants, 8% only used opium, 8.3% only smoked cigarettes, and 9% used both substances. During a median 14 years of follow-up, 2195 individuals were diagnosed with cancer, including 215 opium-related cancers (lung, larynx, and bladder) and 1609 tobacco-related cancers (20 types). Opium use alone was estimated to cause 35% (95% CI: 26%-45%) of opium-related cancers, while smoking cigarettes alone was estimated to cause 9% (6%-12%) of tobacco-related cancers in this population. Using opium and/or cigarettes was estimated to cause 13% (9%-16%) of all cancers, 58% (49%-66%) of opium-related cancers, and 15% (11%-18%) of tobacco-related cancers. Moreover, joint exposure to opium and cigarettes had the greatest impact on cancers of the larynx, pharynx, lung, and bladder, with PAFs ranging from 50% to 77%.
UNASSIGNED: Using opium and smoking cigarettes account for a large proportion of cancers in this population. To reduce the cancer burden, prevention policies should aim to decrease the use of both substances through public awareness campaigns and interventional efforts.
UNASSIGNED: The Golestan Cohort Study work was funded by the Tehran University of Medical Sciences, Cancer Research UK, U.S. National Cancer Institute, International Agency for Research on Cancer. The presented analysis was supported by the International HundredK+ Cohorts Consortium (IHCC).

The risk of developing hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) is reduced by antiviral therapy. Here, we evaluated the chronological trends in HCC development risk starting in 2007, when entecavir reimbursement was first initiated in South Korea. Treatment-naïve patients with chronic hepatitis B (CHB) receiving entecavir 0.5 mg/d were stratified into three groups according to entecavir start time: early (2007-2010), middle (2011-2012) and late (2013-2014) cohorts Among 2442 patients, cumulative probabilities of developing HCC after 1, 3 and 5 years were, respectively, 1.7%, 5.1%, and 8.2% (early cohort; n = 672); 1.5%, 5.1% and 8.9% (middle cohort; n = 757); and 1.2%, 5.3% and 10.6% (late cohort; n = 1013; P > .05 between each pair). Older age, male, positive hepatitis B e antigen, liver cirrhosis, Child-Pugh class B (vs A) and lower platelet count significantly predicted HCC development in univariate analysis (P < .001), whereas entecavir start time (early vs middle vs late cohorts) did not affect the risk of HCC development (P = .457). A multivariate analysis revealed that older age (adjusted hazard ratio [aHR]=1.041), male gender (aHR = 2.069), liver cirrhosis (aHR = 3.771) and Child-Pugh class B (vs A, aHR = 1.548) were independently associated with an increased risk of HCC development, whereas higher platelet count was independently associated with a reduced risk of HCC development (aHR = 0.993; all P < .05). In conclusion, the risk of developing HCC among patients receiving entecavir in South Korea has been stable since 2007. To establish more effective HCC surveillance programs, further studies regarding the carcinogenic roles of nonviral factors are required.

OBJECTIVE: The clinical profile of patients with hepatocellular carcinoma (HCC) may differ depending on the etiology of HCC. There is no study from India comparing the clinical profile of patients of HCC due to hepatitis B virus (HBV) infection with other etiologies.
METHODS: We retrospectively reviewed the records of patients clinically diagnosed as HCC between Nov 2000 and Dec 2012 admitted under a single unit of Department of Gastroenterology at our hospital. We compared the clinical presentation of patients of Hepatitis B virus etiology (HBV group) with other etiologies (Non-HBV group).
RESULTS: One hundred and forty-two patients were included (median age 60 years [range 30-83], 92% males). The etiology was HBV in 56 (39%) and among the non-HBV group (n = 86, 61%) the etiological spectrum was following: alcohol 31 (22%), cryptogenic 26 (18%), HCV 27 (19%), and miscellaneous 2 (1%). The median age of presentation was significantly less for HBV group than in non-HBV (56 [30-77] vs. 62 [42-83] years, P < 0.01). Clinical evidence of cirrhosis was significantly less common in the HBV group than non-HBV group (74% vs 98%, P < 0.01). HBV group had lower CTP score than non-HBV (median CTP score 7 vs 8,P < 0.05). Ascites was more common in non-HBV group than HBV group (65% vs 43%, P = 0.018). The BCLC staging was: A 13%, B 23%, C 35%, and D 29%, and there was no difference in tumor characteristics or BCLC staging between HBV or the non-HBV group.
CONCLUSIONS: HBV is a common cause of HCC in India, accounting for 39% of cases. The tumor characteristics of HCC due to HBV is similar to other etiologies, however, HBV causes HCC at an earlier age, and in less advanced or even absence of cirrhosis, thus further consolidating the directly carcinogenic potential of HBV.