Alcohol and Acetaldehyde in African Fermented Milk Mursik--A Possible Etiologic Factor for High Incidence of Esophageal Cancer in Western Kenya (original) (raw)
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Alcoholism: Clinical and Experimental Research, 1999
Background: Acctaldehydc, the first metabolite of alcohol, has been proposed to be the carcinogenic substance behind ethanol-related oral cancers. High levels of acetaldehyde are formed from ethanol in saliva by the oral flora, but so far the role of certain microbial species responsible for this phenomenon is not known. Yeasts are common commensals of the oral cavity that have alcohol-oxidizing enzymes, thus providing a potential source of acetaldehyde from ethanol. The aim of this study was to examine the contribution of oral yeasts to the production of ethanol-derived acetaldehyde in the oral cavity. Methods: Fifty-five saliva samples were divided into two groups, high and low, based on the in vitro salivary acetaldehyde production capacity from ethanol. Yeasts were isolated and identified from these samplcs, and their acetaldehyde production capacity was determined gas chromatographically by incubating intact cells with ethanol at the physiological pH of 7.4. Results: Yeast colonization was found in 78% of the high acetaldehyde-producing salivas, compared with 47% in thc low acetaldehyde-producing salivas (p = 0.026). Among carriers, the density of yeasts was higher in the high than in low acetaldehyde producers (p = 0.025). Candida albicans was the main species isolated (88% of all oral isolates). Moreover, C. albicans strains isolated from the high acetaldehydeproducing salivas formed significantly higher acetaldehyde levels from ethanol than C. albicans strains from low-acctaldehydc-producing salivas (73.1 nmol ach/lOe6 colony-forming units vs. 43.2 nmol ach/lOe6 colony-forming units,p = 0.035). Conclusions: This study shows that some C. albicans strains have a marked capacity to produce toxic and Carcinogenic acetaldehyde from ethanol in vitro. Because the in vitro production of salivary acetaldehyde has becn previously shown to correlate with in vivo acetaldehyde production, our finding could be an important microbial pathogenetic factor underlying cancer of the oral cavity associated with ethanol drinking.
Acetaldehyde production from ethanol and glucose by non-Candidaalbicans yeasts in vitro
Oral Oncology, 2009
Background: Major environmental risk factors for upper digestive tract cancers are tobacco smoking, alcohol intake and poor oral hygiene. They all result in increased acetaldehyde (ACH) levels in saliva which has been shown to be carcinogenic. During alcohol challenge the oral microbiota is the main determinant of the local ACH concentration. Many bacteria and Candida albicans have been shown to be capable of ACH production. Moreover, chronic candidal mucositis can be carcinogenic. The ability of non-C. albicans Candida to produce ACH has not been studied. Aim: The aim of this study was to explore the ability of non-C. albicans Candida species to produce ACH in vitro during ethanol and glucose incubation. Methods: A total of 30 non-C. albicans Candida isolates and one C. albicans reference strain were used. The cells were exposed to 11 mM of ethanol and to 100 mM glucose in vitro. ACH was measured by gas chromatography. Results: All Candida isolates produced significant amounts of ACH in ethanol incubation. C. tropicalis isolates were the highest (252.3 lM) and C. krusei isolates were the lowest (54.6 lM) producers of ACH from ethanol. Only C. glabrata produced significant amounts of ACH by fermentation from glucose. Conclusion: Colonization of oral mucosa with a non-C. albicans species such as C. glabrata, capable of producing carcinogenic amounts of ACH from both ethanol and glucose, may contribute to the development of oral cancer.
Toxicology Reports, 2020
Greek fermentation and distillation industries produce traditional spirit beverages, such as tsipouro and tsikoudia, consumed both in bottles and bulk quantities by the general population or tourists. The same spirits are also produced by individuals at home since previous centuries, as a part of the local culture but mainly due to the Greek agricultural sector unique characteristics (small cultivation areas with great number of farmers). In this study, the concentrations of carcinogenic compounds: ethanol and acetaldehyde; and noncarcinogenic: higher alcohols (1-propanol, isobutanol, and isoamyl alcohol), esters (ethyl acetate), and methanol were measured to estimate the potential cancer risk and daily intake of these compounds. The margin of exposure (MOE) of carcinogenic compounds was found to be less than 500 (mean value), well below the toxic threshold of 10,000, above which there is not public concern, as suggested by the European Food Safety Authority. Additionally, through risk assessment of noncarcinogenic compounds, we identified two specific compounds in-bulk spirits (produced by individuals), namely ethyl acetate and isobutanol, with health risk index (HRI) greater than 1 (indicating a possibility to induce side effects by consumption of high amounts). Our results indicate that bottled spirits, which are produced in a controlled environment (alcohol industries), showed higher human safety level in terms of both carcinogenic and noncarcinogenic risk assessment studies, comparing to bulk beverages produced by individuals (with out strict regulations).
Traditional and commercial alcohols and esophageal cancer risk in Kenya
International Journal of Cancer
Squamous cell esophageal cancer is common throughout East Africa, but its etiology is poorly understood. We investigated the contribution of alcohol consumption to esophageal cancer in Kenya, based on a hospital-based casecontrol study conducted from 08/2013 to 03/2018 in Eldoret, western Kenya. Cases had an endoscopy-confirmed esophageal tumor whose histology did not rule out squamous cell carcinoma. Age and gender frequency-matched controls were recruited from hospital visitors/patients without digestive diseases. Logistic regression was used to calculate odds ratios (ORs) and their 95% confidence intervals (CI) adjusting for tobacco (type, intensity) and 6 other potential confounders. A total of 422 cases (65% male, mean at diagnosis 60 (SD 14) years) and 414 controls were included. ORs for ever-drinking were stronger in ever-tobacco users (9.0, 95% CI: 3.4, 23.8, with few tobacco users who were never drinkers) than in nevertobacco users (2.6, 95% CI: 1.6, 4.1). Risk increased linearly with number of drinks: OR for >6 compared to >0 to ≤2 drinks/ day were 5.2 (2.4, 11.4) in ever-tobacco users and 2.1 (0.7, 4.4) in never-tobacco users. Although most ethanol came from low ethanol alcohols (busaa or beer), for the same ethanol intake, if a greater proportion came from the moonshine chang'aa, it was associated with a specific additional risk. The population attributable fraction for >2 drinks per day was 48% overall and highest in male tobacco users. Alcohol consumption, particularly of busaa and chang'aa, contributes to half of the esophageal cancer burden in western Kenya.
Carcinogenicity of acetaldehyde in alcoholic beverages: risk assessment outside ethanol metabolism
Addiction, 2009
Aims In addition to being produced in ethanol metabolism, acetaldehyde occurs naturally in alcoholic beverages. Limited epidemiological evidence points to acetaldehyde as an independent risk factor for cancer during alcohol consumption, in addition to the effects of ethanol. This study aims to estimate human exposure to acetaldehyde from alcoholic beverages and provide a quantitative risk assessment.Methods The human dietary intake of acetaldehyde via alcoholic beverages was estimated based on World Health Organization (WHO) consumption data and literature on the acetaldehyde contents of different beverage groups (beer, wine, spirits and unrecorded alcohol). The risk assessment was conducted using the European Food Safety Authority's margin of exposure (MOE) approach with benchmark doses obtained from dose–response modelling of animal experiments. Life-time cancer risk was calculated using the T25 dose descriptor.Results The average exposure to acetaldehyde from alcoholic beverages was estimated at 0.112 mg/kg body weight/day. The MOE was calculated to be 498, and the life-time cancer risk at 7.6 in 10 000. Higher risk may exist for people exposed to high acetaldehyde contaminations, as we have found in certain unrecorded alcohol beverages in Guatemala and Russia, for which we have demonstrated possible exposure scenarios, with risks in the range of 1 in 1000.Conclusions The life-time cancer risks for acetaldehyde from alcoholic beverages greatly exceed the usual limits for cancer risks from the environment set between 1 : 10 000 and 1 : 1 000 000. Alcohol consumption has thus been identified as a direct source of acetaldehyde exposure, which in conjunction with other sources (food flavourings, tobacco) results in a magnitude of risk requiring intervention. An initial public health measure could be to reduce the acetaldehyde content in alcoholic beverages as low as technologically possible, and to restrict its use as a food flavour additive.
Alcohol and Alcoholism, 2000
Many human gastrointestinal facultative anaerobic and aerobic bacteria possess alcohol dehydrogenase (ADH) activity and are therefore capable of oxidizing ethanol to acetaldehyde. We examined whether human gastrointestinal lactobacilli (three strains), bifidobacteria (five strains) and probiotic Lactobacillus GG ATCC 53103 are also able to metabolize ethanol and acetaldehyde in vitro. Acetaldehyde production by bacterial suspensions was determined by gas chromatography after a 1-h incubation with 22 mM ethanol. To determine the acetaldehyde consumption, the suspensions were incubated with 50 µM or 500 µM acetaldehyde as well as with 500 µM acetaldehyde and 22 mM ethanol, i.e. under conditions resembling those in the human colon after alcohol intake. The influence of growth media and bacterial concentration on the ability of lactobacilli to metabolize acetaldehyde and to produce acetate from acetaldehyde were determined. ADH and aldehyde dehydrogenase (ALDH) activities were determined spectrophotometrically. Neither measurable ADH nor ALDH activities were found in aerobically grown Lactobacillus GG ATCC 53103 and Lactobacillus acidophilus ATCC 4356 strains. All the lactobacilli and bifidobacteria strains revealed a very limited capacity to oxidize ethanol to acetaldehyde in vitro. Lactobacillus GG ATCC 53103 had the highest acetaldehyde-metabolizing capacity, which increased significantly with increasing bacterial concentrations. This was associated with a marked production of acetate from acetaldehyde. The type of the growth media had no effect on acetaldehyde consumption. Addition of ethanol to the incubation media diminished the acetaldehyde-metabolizing capacity of all strains. However, in the presence of ethanol, Lactobacillus GG ATCC 53103 still demonstrated the highest capacity for acetaldehyde metabolism of all strains. These data suggest a beneficial impact of Lactobacillus GG ATCC 53103 on high gastrointestinal acetaldehyde levels following alcohol intake. The possible clinical implications of this finding remain to be established in in vitro studies.
Food and Chemical Toxicology, 2008
Acetaldehyde is a volatile compound naturally found in alcoholic beverages, and it is regarded as possibly being carcinogenic to humans (IARC Group 2B). Acetaldehyde formed during ethanol metabolism is generally considered as a source of carcinogenicity in alcoholic beverages. However, no systematic data is available about its occurrence in alcoholic beverages and the carcinogenic potential of human exposure to this directly ingested form of acetaldehyde outside ethanol metabolism. In this study, we have analysed and evaluated a large sample collective of different alcoholic beverages (n = 1555). Beer (9 ± 7 mg/l, range 0-63 mg/l) had significantly lower acetaldehyde contents than wine (34 ± 34 mg/l, range 0-211 mg/l), or spirits (66 ± 101 mg/l, range 0-1159 mg/l). The highest acetaldehyde concentrations were generally found in fortified wines (118 ± 120 mg/l, range 12-800 mg/l). Assuming an equal distribution between the beverage and saliva, the residual acetaldehyde concentrations in the saliva after swallowing could be on average 195 lM for beer, 734 lM for wine, 1387 lM for spirits, or 2417 lM for fortified wine, which are above levels previously regarded as potentially carcinogenic. Further research is needed to confirm the carcinogenic potential of directly ingested acetaldehyde. Until then, some possible preliminary interventions include the reduction of acetaldehyde in the beverages by improvement in production technology or the use of acetaldehyde binding additives. A re-evaluation of the 'generally recognized as safe' status of acetaldehyde is also required, which does not appear to be in agreement with its toxicity and carcinogenicity.
The contribution of acetaldehyde from alcohol to cancer: a review and exposure estimate for Germany
Aims: The consumption of alcoholic beverages has been identified as carcinogenic by the International Agency for Research on Cancer. We aim to summarize the evidence on acetaldehydeas the main mechanism underlying this relation, because humans are exposed to acetaldehyde both through ingestion of acetaldehyde present in alcoholic beverages and acetaldehyde produced through ethanol metabolism. Methods: A literature review of alcohol, acetaldehyde and cancer was used as input for a risk assessment for acetaldehyde derived from alcohol consumption for Germany. Results: There is increasing evidence that acetaldehyde is carcinogenic. Risk assessment scenarios were below the 1:10,000 lifetime risk for cancer threshold (average scenario 8/10,000; extreme scenario 4/1,000), which is considered public health relevant. Conclusion: Acetaldehyde exposure from alcohol alone warrants interventions based on the precautionary principle of public health. It is recommended that high alcohol consumption should be reduced and acetaldehyde levels in alcoholic beverages should be reduced as low as technologically possible, along with the implementation of maximum limits.
Antioxidants
Alcohol consumption is associated with oxidative stress and an increased risk of carcinoma of the upper aero-digestive tract (UADT). Recently, it has been found that some microorganisms in the human oral cavity may locally metabolize ethanol, forming acetaldehyde, a carcinogenic metabolite of alcohol. In a cohort of patients first visited for UADT cancers, we estimated their alcohol consumption by measuring Ethyl Glucuronide/EtG (a long-lasting metabolite of ethanol) in the hair and carbohydrate-deficient transferrin/CDT (short-term index of alcohol intake) in the serum. Moreover, we analyzed, by culture-based methods, the presence of Neisseria subflava, Streptococcus mitis, Candida albicans, and glabrata (microorganisms generating acetaldehyde) in the oral cavity. According to the EtG values, we correlated drinking alcohol with endogenous oxidative stress and the investigated microorganism’s presence. We found that 55% of heavy drinkers presented microorganisms generating acetaldeh...