aflatoxin-m1 and Carcinoma--Hepatocellular

Considering the genotoxic and cancerogenic nature of aflatoxin M1 (AFM1), its presence in milk and dairy products may pose health risks for consumers. The chronic exposure was calculated using a two-dimensional (second order) Monte Carlo model. Results of 13 722 milk and dairy product samples analysed in the 2015-2022 period were used. Milk and dairy products intake information was collected with a Food Frequency Questionnaire (FFQ) validated by a 24-h recall-based method. Risk characterization was done by calculation of the Margin of Exposure (MOE) and by calculation of AFM1 induced number of hepatocellular carcinoma (HCC) cases. Mean AFM1 Estimated Daily Intake (EDI) was highest in children at 0.336 (CI: 0.294-0.385) ng kg

Topics: Adolescent; Adult; Aflatoxin M1; Animals; Carcinoma, Hepatocellular; Child; Dietary Exposure; Female; Food Contamination; Humans; Liver Neoplasms; Male; Milk; Serbia

For 60 y, it has been known that aflatoxin B1 (AFB1), a mycotoxin produced by Aspergillus fungi in certain food and feed crops, causes hepatocellular carcinoma (liver cancer; HCC) in humans. The annual global burden of AFB1-related HCC has been estimated. However, much less is known about the potential carcinogenic impact of a metabolite of AFB1 called aflatoxin M1 (AFM1), which is secreted in milk when dairy animals consume AFB1-contaminated feed. The cancer risk of AFM1 to humans from milk consumption has not yet been evaluated.. We sought to estimate the global risk of AFM1-related liver cancer through liquid milk consumption, accounting for possible synergies between AFM1 and chronic infection with hepatitis B virus (HBV) in increasing cancer risk.. We conducted a quantitative cancer risk assessment by analyzing extensive datasets of national population sizes, dairy consumption patterns, AFM1 concentrations in milk in 40 nations, and chronic HBV prevalence. Two separate cancer risk assessments were conducted: assuming a possible synergy between AFM1 and HBV in increasing cancer risk in a manner similar to that of AFB1 and HBV, and assuming no such synergy.. If there is no synergy between AFM1 and HBV, AFM1 may contribute ∼0.001% of total annual HCC cases globally. If there is synergy between AFM1 and HBV infection, AFM1 may contribute ∼0.003% of all HCC cases worldwide. In each case, the total expected AFM1-attributable cancer cases are ∼13-32 worldwide.. AFM1 exposure through liquid milk consumption does not substantially increase liver cancer risk in humans. Policymakers should consider this low risk against the nutritional benefits of milk consumption, particularly to children, in a current global situation of milk being discarded because of AFM1 concentrations exceeding regulatory standards.

Topics: Aflatoxin B1; Aflatoxin M1; Animal Feed; Animals; Carcinoma, Hepatocellular; Food Contamination; Humans; Incidence; Liver Neoplasms; Milk

Topics: Adult; Aflatoxin M1; Animals; Carcinoma, Hepatocellular; Dietary Exposure; Female; Food Contamination; Greece; Humans; Liver Neoplasms; Male; Milk; Risk Assessment; Serbia; Students; Yogurt; Young Adult

Aflatoxin M₁ (AFM₁), a human carcinogen, is found in milk products and may have potentially severe health impacts on milk consumers. We assessed the risk of cancer and stunting as a result of AFM₁ consumption in Nairobi, Kenya, using worst case assumptions of toxicity and data from previous studies. Almost all (99.5%) milk was contaminated with AFM₁. Cancer risk caused by AFM₁ was lower among consumers purchasing from formal markets (0.003 cases per 100,000) than for low-income consumers (0.006 cases per 100,000) purchasing from informal markets. Overall cancer risk (0.004 cases per 100,000) from AFM₁ alone was low. Stunting is multifactorial, but assuming only AFM₁ consumption was the determinant, consumption of milk contaminated with AFM₁ levels found in this study could contribute to 2.1% of children below three years in middle-income families, and 2.4% in low-income families, being stunted. Overall, 2.7% of children could hypothetically be stunted due to AFM₁ exposure from milk. Based on our results AFM₁ levels found in milk could contribute to an average of -0.340 height for age z-score reduction in growth. The exposure to AFM₁ from milk is 46 ng/day on average, but children bear higher exposure of 3.5 ng/kg bodyweight (bw)/day compared to adults, at 0.8 ng/kg bw/day. Our paper shows that concern over aflatoxins in milk in Nairobi is disproportionate if only risk of cancer is considered, but that the effect on stunting children might be much more significant from a public health perspective; however, there is still insufficient data on the health effects of AFM₁.

Topics: Adult; Aflatoxin M1; Animals; Carcinoma, Hepatocellular; Child, Preschool; Dietary Exposure; Food Contamination; Growth Disorders; Humans; Income; Kenya; Liver Neoplasms; Milk; Risk Assessment

The present research were tempted to investigate whether Aflatoxin is an additive factor in development of HCC through detecting its metabolite Aflatoxin Ml1 in serum and urine of HCC and cirrhotics in Egypt. Present study comprised (46) Hepatocellular Carcinoma (HCC) patients with mean age (56.28 +/- 8.08), 30 males and 16 females, (12) cirrhotic patients with mean age (47.83 +/- 18.20), 7 males and 5 females and (12) sex and age matched healthy controls. All were exposed to, liver function tests, abdominal ultrasonography and detection of Aflatoxin metabolite M1 in serum and urine by means of the reverse phase HPLC device. Aflatoxin M1 was detected in sera of HCC group, cirrhotics and controls (57.8%) (5.61 +/- 17.21 ng mL(-1)), (91.7%) (19.23 +/- 20.42 ng mL(-1)) and (50%) (0.66 +/- 0.84 ng mL(-1)), respectively and in urine (41.3%) (3.82 +/- 8.03 ng mL(-1)) (91.7%) (43.22 +/- 45.02 ng mL(-1)) and (50%) (0.98 +/- 1.4 ng mL(-1)), respectively representing significant increase in the serum of the cirrhotic group (p < 0.02) and a high significant increase in urine of the cirrhotic group (p < 0.0001). Among HCC group patients, there is high significant value of M1 concentration in urine of upper Egypt residents compared to those of lower Egypt (p < 0.002). The mean value of Aflatoxin M1 concentration among females of the HCC group was significantly higher than that among males (p = 0.006). There is higher statistical significance of aflatoxin prevalence and concentration in serum and urine ofcirrhotics than HCC patients and controls and in concentration in urine of HCC patients from upper than lower Egypt.

Topics: Adult; Aflatoxin M1; Aged; Carcinoma, Hepatocellular; Chromatography, High Pressure Liquid; Egypt; Female; Humans; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Poisons

We followed 145 men with chronic hepatitis B virus (HBV) hepatitis for 10 years to determine whether exposure to aflatoxin, or concomitant exposure to hepatitis C virus (HCV), or family history of hepatocellular carcinoma (HCC) increased the risk of developing HCC. We collected 8 monthly urine samples before beginning follow-up and pooled them to detect aflatoxin metabolite M1 (AFM1). AFM1 was detected in 78 (54%) of the subjects. The risk of HCC was increased 3.3-fold (with a 95% confidence interval of 1.2-8.7) in those with detectable AFM1 (above 3.6 ng/L). This relative risk was adjusted for age and for HCV status. The attributable risk from exposure to detectable AFM1 was 0.553 (0.087, 0.94). The relative risk of fatal cirrhosis for those with elevated AFM1 was 2.8 (0.6, 14.3), and the odds of having a persistently elevated alanine transaminase (ALT) were 2.5-fold greater in those with detectable AFM1 (P =.007). Concomitant infection with HCV increased the risk of HCC 5.8-fold (2. 0-17), adjusted for age and AFM1 status. A family history of HCC increased the risk of HCC 5.6-fold, adjusted for age and AFM1. Four men with detectable AFM1 and HCC all had missense mutation in codon 249 of the p53 gene in cancer tissues. This study shows that exposure to AFM1 can account for a substantial part of the risk of HCC in men with chronic HBV hepatitis and adds importantly to the evidence that HCV and family history of HCC increase the risk of HCC in men with chronic HBV hepatitis.

Topics: Adolescent; Adult; Aflatoxin M1; Aged; Carcinoma, Hepatocellular; Carrier State; Child; Child, Preschool; Cohort Studies; Hepatitis B Surface Antigens; Hepatitis B, Chronic; Humans; Infant; Infant, Newborn; Liver Neoplasms; Male; Middle Aged; Prospective Studies; Risk

A high performance liquid chromatographic (HPLC) method for the analysis of aflatoxin M1 (AFM1) in urine is described. Urine samples were treated with saturated lead acetate and AFM1 was extracted with chloroform. After washing with water to remove impurities the compound was derivatized with trifluoroacetic acid and the AFM1 derivative was analyzed quantitatively by HPLC. The sample pretreatment is simple and more selective. A good line correlation between AFM1 peak height and its concentration was obtained when AFM1 content was in the range of 50-400 pg. The ratio of recovery was 87.42%. Sensitivity is 0.01 ppb. The method is applicable to trace analysis. Results in urine of residents who live in the high/low liver cancer incidence area in Fushui county were the same as that of previous epidemiological investigation.

Topics: Aflatoxin B1; Aflatoxin M1; Aflatoxins; Animals; Carcinoma, Hepatocellular; China; Chromatography, High Pressure Liquid; Humans; Liver Neoplasms; Microchemistry; Quality Control; Tupaia