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Dietary acrylamide and cancer risk: An updated meta-analysis
International Journal of Cancer
Abstract
The debate on the potential carcinogenic effect of dietary acrylamide is open. In consideration of the recent findings from large prospective investigations, we conducted an updated meta-analysis on acrylamide intake and the risk of cancer at several sites. Up to July 2014, we identified 32 publications. We performed meta-analyses to calculate the summary relative risk (RR) of each cancer site for the highest vs. lowest level of intake and for an increment of 10 µg/day of dietary acrylamide, through fixed-effects or random-effects models, depending on the heterogeneity test. Fourteen cancer sites could be examined. No meaningful associations were found for most cancers considered. The summary RRs for high vs. low acrylamide intake were 0.87 for oral and pharyngeal, 1.14 for esophageal, 1.03 for stomach, 0.94 for colorectal, 0.93 for pancreatic, 1.10 for laryngeal, 0.88 for lung, 0.96 for breast, 1.06 for endometrial, 1.12 for ovarian, 1.00 for prostate, 0.93 for bladder, and 1.13 for lymphoid malignancies. The RR was of borderline significance only for kidney cancer (RR=1.20; 95% confidence interval, CI, 1.00-1.45). All the corresponding continuous estimates ranged between 0.95 and 1.03, and none of them was significant. Among never-smokers, borderline associations with dietary acrylamide emerged for endometrial (RR=1.23; 95% CI, 1.00-1.51) and ovarian (RR=1.39; 95% CI, 0.97-2.00) cancers. This systematic review and meta-analysis of epidemiological studies indicates that dietary acrylamide is not related to the risk of most common cancers. A modest association for kidney cancer, and for endometrial and ovarian cancers in never smokers only, cannot be excluded. This article is protected by copyright. All rights reserved.
... All of these studies used a dietary assessment method to estimate dietary acrylamide exposure except for one study performed in a Swedish population where acrylamide exposure was assessed through both dietary intake and hemoglobin adducts (20). So far, a few systematic reviews and meta-analyses based on epidemiological studies were performed to synthesize the body of evidence in this field (42)(43)(44)(45)(46)(47)(48). In the most recent and comprehensive meta-analysis published in 2015, no association between high dietary acrylamide exposure and the risk of several cancers was noted, except for a modest increased risk of renal cancer (46), which was not observed in another metaanalysis investigating dietary acrylamide exposure and renal cell carcinoma (44). ...
... So far, a few systematic reviews and meta-analyses based on epidemiological studies were performed to synthesize the body of evidence in this field (42)(43)(44)(45)(46)(47)(48). In the most recent and comprehensive meta-analysis published in 2015, no association between high dietary acrylamide exposure and the risk of several cancers was noted, except for a modest increased risk of renal cancer (46), which was not observed in another metaanalysis investigating dietary acrylamide exposure and renal cell carcinoma (44). With the exception of a recent study investigating the relationship between dietary acrylamide exposure and female reproductive cancers, observing a relatively linear increased risk for ovarian and endometrial cancer (42), no dose-response metaanalysis exist for other cancer forms. ...
... Overall, our results of no association between high dietary acrylamide exposure and different site-specific cancers in the general population confirm the findings of previous metaanalyses that did not perform dose-response meta-analysis (22,44,46,48). On the other hand, Pelucchi et al. (46) found a slight increased risk of renal cell carcinoma by 20% in relation to high dietary acrylamide (RR 1.20; 95% CI 1.00-1.45). ...
Diet is a main source of acrylamide exposure to humans. Existing observational data on the relationship between dietary exposure to acrylamide and risk of cancer are inconsistent. We performed a systematic review and dose-response meta-analysis of epidemiological studies evaluating the association between dietary acrylamide exposure and several site-specific cancer. A systematic literature search was conducted in PubMed, Scopus, and Web of Science databases until March 7, 2022. Studies were eligible if they were carried out in non-occupationally exposed adults, assessed dietary acrylamide exposure (μg/day) and reported risk estimates of cancer incidence (all but gynecological cancers). Using a random-effects model, we performed a meta-analysis of site-specific cancer risk comparing the highest vs. lowest category of dietary acrylamide exposure. We also carried out a one-stage dose-response meta-analysis assessing the shape of the association. Out of 1,994 papers screened, 31 were eligible (total of 16 studies), which included 1,151,189 participants in total, out of whom 48,175 developed cancer during the median follow-up period of 14.9 years (range 7.3–33.9). The mean estimated dose of dietary acrylamide across studies was 23 μg/day. Pooled analysis showed no association between the highest vs. lowest dietary acrylamide exposure and each site-specific cancer investigated, with no evidence of thresholds in the dose-response meta-analysis. There were also no associations between dietary acrylamide exposure and the risk of cancers when stratifying by smoking status, except for increased risk of lung cancer in smokers. In conclusion, high dietary acrylamide exposure was not associated with an increased risk of site-specific non-gynecological cancer.
... This epoxide is highly reactive and attacks DNA to form an adduct at the nitrogen 7 of guanine (N 7 -GA-Gua), which indicates a potential carcinogenic pathway [24]. The dose-response relationships of cancers associated with dietary AA are uncertain [25]. However, while some authors have reported weak or no statistical significance between dietary AA exposure and cancer, others have reported a significant increase in endometrial, kidney, and ovarian cancers [26,27]. ...
... This study investigated the association between dietary AA exposure and the risk of kidney, ovarian, and uterine cancers. We were motivated by meta-analyses that reported a modest increase in the risk of renal cancer [41] and a recent study that suggested a positive linear relationship between dietary AA exposure and the risk of ovarian and uterine cancers [25]. We synthesized the evidence on the association between dietary AA exposure and the risk and burden of these cancers based on the prevalence, mortality, YLL, and YLD of these cancers in Ethiopia, Kenya, Ghana, and Nigeria from 2015 to 2019 from the Global Burden of Disease (GBD) Compare database [33]. ...
Acrylamide (AA) is a food processing byproduct that forms at high temperatures and is classified as a probable human carcinogen. Previous studies have linked AA to kidney, uterus, and ovary cancer burdens, but its study in African countries remains underexplored. This study systematically used six recent articles on dietary AA concentration data from scholarly databases using specific search terms. We also collected health metrics secondary data from the Institute of Health Metrics and Evaluation and other sources for the period 2015–2019. We used a Monte-Carlo simulation to integrate the dietary AA exposure, risks, and health metrics to estimate the cancer burdens. The results showed that the modal healthy life years lost ranged from 0.00488 (Ghana) to 0.218 (Ethiopia) per 100,000 population. The median statistic indicated 1.2 and 26.10 healthy life years lost for Ghana and Ethiopia, respectively, due to the three cancer types. The four-country study areas' total disability-adjusted life years (DALYs) were 63.7 healthy life-year losses. Despite the limitations of the non-standardized age-related food consumption data and the few inclusive articles, the probabilistic approach may account for the uncertainties and provide valid conclusions.
... However, bread can be a significant source of potentially harmful compounds formed during processing, such as acrylamide, heterocyclic amines, and polycyclic aromatic hydrocarbons [3][4][5][6]. These compounds are formed in any carbohydrate food during dry heating to temperatures >120 C, as occurs in frying and baking, and are among However, since the initial IARC statement 30 y ago, results from epidemiologic studies assessing the association between dietary acrylamide exposure and cancer risk have been inconclusive [11][12][13][14][15][16][17]. Despite the inconsistent findings from epidemiologic studies on the association between acrylamide exposure from foods and cancer in humans, both the United States NTP and the Joint FAO/WHO Expert Committee on Food Additives consider acrylamide to be a concern to human health [18]. ...
... Regarding dietary acrylamide exposure and cancer risk, results from cohort studies are inconclusive. Some meta-analyses have reported higher cancer risk [11,14,15] whereas several other systematic reviews and meta-analyses demonstrated that most cohort studies show no increased cancer risk associated with dietary acrylamide exposure [12,13,16,17]. Thus, despite having been determined to be "probably carcinogenic to humans" by the IARC in 1994 [7] and "reasonably anticipated to be a human carcinogen" according to the NTP's report on carcinogens [8], published data on dietary acrylamide intake and cancer risk in humans suggest that risks are low. ...
... Their consumption accelerates oxidative degradation of membrane lipids, forming hazardous reactive oxygen species and impairs the membrane functions, inactivates membrane-bound receptors or enzymes, and disturbs ions permeability and fluidity, which eventually leads to membrane rupture [6]. These lipid oxidation products have been established to have mutagenic [7], carcinogenic [8] and cytotoxic, genotoxic [9,10] properties and constitute a risk factor to human health. Some researchers have attributed degraded compounds in the frying oil to heterocyclic amines or polycyclic aromatic hydrocarbons formed from meat [11] or acrylamide formed in carbohydrate-rich foods [8]. ...
... These lipid oxidation products have been established to have mutagenic [7], carcinogenic [8] and cytotoxic, genotoxic [9,10] properties and constitute a risk factor to human health. Some researchers have attributed degraded compounds in the frying oil to heterocyclic amines or polycyclic aromatic hydrocarbons formed from meat [11] or acrylamide formed in carbohydrate-rich foods [8]. ...
Within a space of three decades, after fast foods consumption became so rampant in southeastern Nigeria, there exists a conspicuous sharp increase in undetailed/unrecorded health complications such as diabetes, hypertension, stroke, cardiovascular disorders, cancer, vascular inflammation, hematological complications and worst of it all untimely death. These have necessitated the need for an in-depth research on any link between these health impediments and the consumption of highly oxidized fatty acids via intake of roasted and ready-made deep-fried fast food as the root cause. The aim of this present research work is to determine the levels of lipid peroxidation products in most roasted and deep-fried fast foods eaten in southeastern Nigeria using thiobarbituric acid reactive substances (TBARS), conjugated dienes, and hydroperoxide as bio-markers. Our observation reveals that the concentrations of products of lipid peroxidation in deep-fried fast foods were significantly higher than that of roasted fast foods. Our results further depict that fried egg recorded the highest mean value of TBARS among fried food samples, but a non-significant decrease in comparison with the used frying oil, while the other samples exhibited varied values of TBARS in increasing order of fried egg > plantain chips > akara > yam chips>chin-chin > bonus > potatoes chips> doughnut > puff-puff. Moreover, among roasted foods suya meat exhibited the highest concentration of TBARS followed by groundnut and pork meat. This research work indicates that glacial acetic acid/water solvent mixture extracted a significant concentration of conjugated dienes from roasted bread fruit, baked cake, and fried doughnut, in comparison with methanol/chloroform extracts that gave the highest extractive mean values of conjugated dienes for roasted bambara nut, groundnut, and suya meat.
... Many findings from large longitudinal studies have recently been published including, among others, the European Prospective Investigation on Cancer and Nutrition (EPIC) and the Nurses' Health Service (NHS). In particular, the EPIC study published findings for oesophageal, pancreatic, and endometrial cancer, which included over 500,000 participants [2][3][4]. ...
... Acrylamide was first reported in products by the Swedish National Food Administration in 2002. The acrylamide is the by-product of the roasting process that develops through the Chemical reaction towards the amino acid asparagine, this same response caused bowering of the food during baking, frying, and roasting, by reducing sugar (glucose or fructose) [2]. The levels of acrylamide in cooked meals are therefore determined by parameters including cooking temperatures, heating duration, moisture content as well as the reduction of sugar as well as aspartic acid in the raw foods. ...
Acrylamide is a yellowish, odorless solid that is water-soluble and is used in a variety of organic solvents and organic chemical compounds. It is used as a precursor or substitute for water-soluble thickeners in a variety of applications. It is very toxic and hence carcinogenic, and it is administered as a watery solution. Aside from exposure to the industry and cigarettes, food appears to be the most common source of human exposure. Cancer has remained the second-leading cause of death, with a global increase in the number of cases. Increasing the cancer burden necessitates the use of cancer preventive methods. Because of the present results of several future investigations, specialists have conducted a new meta-analysis on the usage of acrylamide-related illness incidence in various areas. Authors discovered 32 publications on their own. The researchers conducted a meta-analysis utilizing corrected or spontaneous modeling, based on the heterogeneous method, to assess the overall chance for each cancer site for highest versus lowest consumption levels, including an increase in nutritional acrylamide by 10 mg/day. Acrylamide has been classified by the International Agency for Research on Cancer as a human category 2A carcinogen, based on evidence of acrylamide carcinogenicity in animals.
... These studies faced challenges in accurately estimating acrylamide intake, leading to potential biases [9]. Some studies suggested modest associations with cancers of the kidney [15], endometrium, ovary, premenopausal Proceedings 2024, 109, 11 3 of 10 breast [16,17], and squamous cell esophageal cancer in never-smokers [18]. Meta-analyses provided mixed results [9], with some finding no association between dietary acrylamide and renal cell carcinoma in never smokers [19]. ...
This study examines the acrylamide levels in a range of roasted coffee samples from Bahrain, with a particular focus on traditionally very light roasted coffees. Acrylamide, classified as a Group 2A carcinogen by the International Agency for Research on Cancer (IARC), is formed during the roasting process as a byproduct of the reaction between amino acids and reducing sugars present in coffee beans. The acrylamide levels were quantified using the standard method EN 16618:2015, which employs liquid chromatography in combination with tandem mass spectrometry (LC-MS/MS). The results demonstrated that the acrylamide levels in very light-roasted coffee samples (646 µg/kg, n = 4), which exhibited characteristics similar to green coffee, were significantly above the European Union (EU) benchmark level for roasted coffee of 400 µg/kg. In contrast, medium-roasted coffee samples (154 µg/kg, n = 4) and dark-roasted coffee samples (62 µg/kg, n = 2) did not exceed the benchmark level. These findings indicate a potential health risk associated with the consumption of very light-roasted coffee, emphasizing the need for awareness and possible mitigation strategies to reduce acrylamide exposure in traditional Arabic coffee practices.
... Furthermore, dietary practices, such as the excessive consumption of high-temperature foods, particularly those prepared through frying, barbecuing, or prolonged meat cooking, as well as nitrite-laden foods, are closely linked to the incidence of gastric cancer [7][8][9]. Notably, barbecued meat generates polycyclic aromatic hydrocarbons, such as acrylamide and heterocyclic amines, which possess mutagenic and carcinogenic properties in animals, thereby promoting the initiation and progression of gastric cancer [10]. Moreover, the enigmatic pathogenesis of gastric cancer, coupled with the fact that the majority of cases are diagnosed at an advanced stage, significantly compromises patient survival and quality of life [11]. ...
In this editorial, we delve into the article and offer valuable insights into a crucial aspect of gastric cancer aetiology. Gastric cancer is a malignancy emanating from the epithelial lining of the gastric mucosa and one of the most prevalent forms of cancer worldwide. The development of gastric cancer is associated with multiple risk factors, including Helicobacter pylori infection, advanced age, a diet rich in salt, and suboptimal eating patterns. Despite notable reductions in morbidity and mortality rates, gastric cancer remains a formidable public health concern, impacting patients' lives. Advanced glycation end products (AGEs) are complex compounds arising from nonenzymatic reactions within living organisms, the accumulation of which is implicated in cellular and tissue damage; thus, the levels are AGEs are correlated with the risk of diverse diseases. The investigation of AGEs is of paramount importance for the treatment of gastric cancer and can provide pivotal insights into disease pathogenesis and preventive and therapeutic strategies. The reduction of AGEs levels and suppression of their accumulation are promising avenues for mitigating the risk of gastric cancer. This approach underscores the need for further research aimed at identifying innovative interventions that can effectively lower the incidence and mortality rates of this malignancy.
... It also forms in foods during high-temperature cooking processes such as frying, roasting and baking. Breads, breakfast cereals, crackers, French fries, potato chips, cookies, prune juice and canned black olives are the primary contributors of acrylamide (45)(46)(47) . • Arsenic: a naturally occurring element, found in air, rocks, soil, water, plants and animals, as well as in industrial and agricultural substances, has been classified as carcinogenic by the World Health Organization (WHO) and the United States (US) National Toxicology Program (32,48,49) . ...
Cancer is a complex disease stemming from multiple interactions between genes and the environment, and is regarded as a primary contributor to global mortality. It is a condition in which the irregular and uncontrolled growth and proliferation of certain cells interferes with normal tissue function and has the potential to spread throughout the body. While the most prevalent types of cancer among children are those related to the blood (leukemia - i.e. cancer in the white blood cells (WBC) in the bone marrow), brain and bones, among adults, cancers pertinent to the epithelial tissues are more prevalent. Even though the proposed etiology of cancer is multifactorial, the most commonly known risk factors are genetics (age), physical carcinogens (radiation – ultraviolet and ionizing), chemical carcinogens (unhealthy diet, alcohol consumption, smoking and tobacco use, chemical exposures, plastic containers and storage methods), biological carcinogens (infections, hormones, reduced immunity) and other factors (overweight and obesity, sedentary lifestyle, stress).The 2019 Global Burden of Disease (GBD) study has reported that the total number of cancer deathsglobally attributable to all estimated risk factors was 4.45 million, accounting for 44.4% of all cancerdeaths. According to the International Agency for Research (IARC), by 2022, the estimated numberof new cancer cases was approximately 20 million, with 9.7 million death cases. It is also projectedthat the annual number of new cancer cases will increase to 33.1 million with a corresponding rise incancer-related deaths to 18.2 million by 2050. As for the Eastern Mediterranean Region (EMR), thesituation is similar to the global situation, whereby 781,000 new cases of cancer were reported andcancer accounted for approximately 485,000 deaths in 2022. By 2050, the number of new cases anddeaths is projected to reach 1.77 and 1.21 million, respectively.Successful prevention and management of cancer can benefit from proper identification of the individual’s nutritional status and health condition in order to offer individualized treatment, if needed, and to ensure the provision of their needs. This involves mastering the four steps of the nutrition care process: nutritional assessment, nutritional diagnosis, nutritional intervention and consequently monitoring and evaluation; which are discussed in depth throughout the guide.This guide is intended to serve as a resource for policymakers, healthcare professionals and individuals looking to reduce their risk of cancer or improve treatment outcomes if diagnosed. It also sheds light on the need to develop and incorporate nutritional aspects into national cancer control strategies and plans in countries of the EMR despite the potential challenges being faced in the region.Finally, the guide discusses the most common types of cancer (breast, colorectal, esophageal, gastric,head and neck, hematological, liver, lung, pancreatic and small intestine) by providing a brief overview on their common symptoms and side effects, and adequate dietary intervention.
... Although coffee is proven to have a few antioxidant and anti-carcinogenic compounds, we also know that it correlates with a higher level of sex hormones (testosterone, estradiol), which is associated with an enhanced risk of ovarian cancer [94]. Coffee contains acrylamide which can also affect carcinogenesis [95]. Previous studies have shown an increased risk of ovarian cancer associated with caffeine intake in premenopausal women and no or slight association in postmenopausal women [96]. ...
Ovarian cancer (OC) represents a significant challenge in the realm of gynecological cancers, characterized by poor survival rates and complex etiology. In this review, we delve into the se-lected genetic, environmental, and hormonal factors underpinning OC development. We have reviewed scientific databases searching for ovarian cancer genetic and epigenetic factors. We have included studies based on their relevancy. As a result of exploring ovarian carcinogen-esis, this systematic review contains data collected from 126 various works. The role of prominent genetic players such as BRCA mutations, DNA repair mechanisms, un-derscores the intricate landscape of OC susceptibility. We explore Li-Fraumeni and Lynch syn-drome, which impart a heightened predisposition to OC development. Hormonal factors such as estrogen, progesterone, and androgens are also discussed. Environmental alterations, ranging from lifestyle influences on OC to microbiome dysbiosis and lifestyle factors such as obesity, al-cohol consumption, and physical activity intersect with genetic and epigenetic pathways, shaping the risk landscape for OC. Through a meticulous examination of current literature, this review provides a nuanced under-standing of the multifactorial nature of OC, emphasizing the need for holistic approaches to prevention, diagnosis, and treatment.
... Dietary exposure to acrylamide has been associated with a significant increase in the risk of kidney cancer (Pelucchi et al., 2015), endometrial cancer (Je, 2015), breast cancer (Bellicha et al., 2022;Olsen et al., 2012), and ovarian cancer (Adani et al., 2020). EFSA confirmed that acrylamide in food increases the potential risk of developing cancer for all age groups (EFSA, 2015) and the investigation of the contribution of acrylamide to the burden of disease is highly relevant. ...
... However, as recognized by Hogervorst et al. in a recent editorial about dietary acrylamide and human cancer, "the body of evidence is still cloudy" [18]. For prostate cancer (PCa) specifically, previous studies have not found an association between acrylamide intake and the risk of this tumor [19][20][21][22][23][24][25][26][27]. Nevertheless, these studies considered only diet as the source of exposure. ...
Acrylamide is a probable carcinogen. Its main sources are the diet and tobacco. The association between acrylamide intake from the diet and tobacco and prostate cancer (PCa) has not been previously evaluated. We aimed to evaluate the relationship between dietary acrylamide intake and exposure to acrylamide through cigarettes and PCa risk. A population-based case–control (CAPLIFE) study was conducted, including 428 incident PCa cases and 393 controls. Smoking and dietary information, with a validated food frequency questionnaire, was collected. We calculated the amount of acrylamide from both sources, and tertiles (Ts) were created. Multivariable logistic regression and restricted cubic spline models were applied to assess the association between exposure to acrylamide and PCa risk. The median was similar for acrylamide in both dietary and smoking acrylamide among PCa cases and controls. No association was observed between dietary acrylamide intake and overall PCa risk (adjusted ORT3vsT1 = 0.90 (95% CI 0.59, 1.37)). A risk trend was observed for acrylamide exposure from cigarette smoking (p-trend = 0.032), with the highest odds in those subjects with the high exposure to acrylamide through cigarettes (adjusted ORT3vsT1 = 1.67 (95% CI 0.92, 3.04)). The restricted cubic splines suggested a linear relationship. In conclusion, acrylamide from smoking could be positively associated with PCa risk, but no association was observed for dietary acrylamide.
... It has been reported that exposure to acrylamide may cause neurotoxic effects by irritating the eyes, skin, and respiratory tract (Hagmar et al., 2001;Kopanska et al., 2018). Several studies have shown that dietary acrylamide exposure is positively associated (Adani et al., 2020;Hogervost et al., 2008;Wilson et al., 2010), negatively associated (Atabati et al., 2020;Mucci et al., 2003), and not associated with various types of cancer Ikeda et al., 2021;Pelucchi et al., 2015). Gao et al. (2023) indicated that dietary acrylamide exposure may have an effect on the emotional status and neurobehavior of university students in China. ...
This study aimed to determine the acrylamide exposure of pregnant women resulting from the consumption of bread, coffee, and French fries and to evaluate it in terms of carcinogenic and non‐carcinogenic health risks. Retrospective 24‐h food consumption data of pregnant women ( n = 487) was obtained using the Food Frequency Questionnaire (FFQ). Dietary acrylamide exposure was calculated according to a deterministic model, and the data were assessed by hazard index (HI) and carcinogenic risk (CR). The mean daily acrylamide exposure of pregnant women aged 18–30 and ≥31 years and in the 1st, 2nd, and 3rd trimesters was 31.4, 35.4, 38.7, 31.3, and 32.4 μg/day, respectively. The acrylamide exposure data were not significantly different among different age groups and pregnancy periods ( p > .05). Dietary acrylamide exposure in pregnant women of different age groups and trimesters may cause significant and serious health problems in terms of carcinogenic risk. According to their level of contribution to average acrylamide exposure, the foods were ranked as follows: French fries> bread> coffee. There is a significant risk of cancer due to exposure to acrylamide from French fries and bread other than coffee. The findings suggest that pregnant women should avoid consuming French fries, bread, and coffee with high acrylamide levels for both their own health and their newborns' health.
... Moreover, animal studies reported the relationship of acrylamide intake with significant carcinogenic and neurotoxic risk 6,7 . Epidemiological studies have issued conclusive evidence that dietary acrylamide exposure is associated with the risk of cancers in humans 8 ; there are also studies that reported a significant association between dietary acrylamide intake and risk of renal, endometrial, and ovarian cancers 9 . International Agency for Research on Cancer considers acrylamide as a probable human carcinogen 10 . ...
This study aimed at investigating the association of acrylamide consumption with the incidence of type 2 diabetes (T2D) in adults. The 6022 subjects of the Tehran lipid and glucose study participants were selected. The acrylamide content of food items were summed and computed cumulatively across follow up surveys. Multivariable Cox proportional hazard regression analyses were performed to estimate the hazards ratio (HR) and 95% confidence interval (CI) of incident T2D. This study was done on men and women, respectively aged 41.5 ± 14.1 and 39.2 ± 13.0 years. The mean ± SD of dietary acrylamide intake was 57.0 ± 46.8 µg/day. Acrylamide intake was not associated with the incidence of T2D after adjusting for confounding variables. In women, a higher acrylamide intake was positively associated with T2D [HR (CI) for Q4: 1.13 (1.01–1.27), P trend: 0.03] after adjusting for confounding factors. Our results demonstrated that dietary intake of acrylamide was associated with an increased risk of T2D in women.
... Historically, acrylamide has been regarded as a carcinogen; however, it has also been linked to a number of medical conditions, including thyroid, neurologic, and reproductive system disorders (Pelucchi et al. 2015;Pedersen et al. 2022). Several epidemiologic studies have demonstrated that acrylamide exposure is independently associated with cardiovascular disease , diabetes (Guo et al. 2017), allergic symptoms (Yin et al. 2021), metabolic syndrome (Chu et al. 2017), and body composition (Hung et al. 2021); however, whether these association are positive or inverse is inconsistent. ...
Osteoarthritis (OA) is the most prevalent degenerative joint disease, and acrylamide is a chemical produced when foods are processed at high temperatures. Recent epidemiological research linked acrylamide exposure from the diet and environment to a number of medical disorders. However, whether acrylamide exposure is associated with OA is still uncertain. This study was aimed at assessing the relationship between OA and hemoglobin adducts of acrylamide and its metabolite glycidamide (HbAA and HbGA). Data were taken from four cycles of the US NHANES database (2003–2004, 2005–2006, 2013–2014, 2015–2016). Individuals aged between 40 and 84 years who had complete information on arthritic status as well as HbAA and HbGA levels were eligible for inclusion. Univariate and multivariate logistic regression analysis s was performed to determine associations between study variables and OA. Restricted cubic splines (RCS) were used to examine non-linear associations between the acrylamide hemoglobin biomarkers and prevalent OA. A total of 5314 individuals were included and 954 (18%) had OA. After adjusting for relevant confounders, the highest quartiles (vs. lowest) of HbAA (adjusted odds ratio (aOR) = 0.87, 95% confidence interval (CI), 0.63–1.21), HbGA (aOR = 0.82, 95% CI, 0.60–1.12), HbAA + HbGA (aOR = 0.86, 95% CI, 0.63–1.19), and HbGA/HbAA (aOR = 0.88, 95% CI, 0.63–-1.25) were not significantly associated with greater odds for OA. RCS analysis revealed that HbAA, HbGA, and HbAA + HbGA levels were non-linearly and inversely associated with OA (p for non-linearity < 0.001). However, the HbGA/HbAA ratio displayed a U-shaped relationship with prevalent OA. In conclusion, acrylamide hemoglobin biomarkers are non-linearly associated with prevalent OA in a general US population. These findings implicate ongoing public health concerns for widespread exposure to acrylamide. Further studies are still warranted to address the causality and biologic mechanisms underlying the association.
... Acrylamide, which is produced during roasting coffee beans at high temperatures, may be the mechanism causing this outcome [52]. High acrylamide intake may be scientifically conceivable as a potential risk factor for OC [53]. In addition, caffeine is able to inhibit aromatase activity and increase the secretion of sex hormone-binding globulin altering the hormonal milieu [54,55]. ...
Objective
Currently, the association between smoking, alcohol, and coffee intake and the risk of ovarian cancer (OC) remains conflicting. In this study, we used a two-sample mendelian randomization (MR) method to evaluate the association of smoking, drinking and coffee consumption with the risk of OC and prognosis.
Methods
Five risk factors related to lifestyles (cigarettes per day, smoking initiation, smoking cessation, alcohol consumption and coffee consumption) were chosen from the Genome-Wide Association Study, and 28, 105, 10, 36 and 36 single-nucleotide polymorphisms (SNPs) were obtained as instrumental variables (IVs). Outcome variables were achieved from the Ovarian Cancer Association Consortium. Inverse-variance-weighted method was mainly used to compute odds ratios (OR) and 95% confidence intervals (Cl).
Results
The two-sample MR analysis supported the causal association of genetically predicted smoking initiation (OR: 1.15 per SD, 95%CI: 1.02–1.29, P = 0.027) and coffee consumption (OR: 1.40 per 50% increase, 95%CI: 1.02–1.93, P = 0.040) with the risk of OC, but not cigarettes per day, smoking cessation, and alcohol consumption. Subgroup analysis based on histological subtypes revealed a positive genetical predictive association between coffee consumption and endometrioid OC (OR: 3.01, 95%CI: 1.50–6.04, P = 0.002). Several smoking initiation-related SNPs (rs7585579, rs7929518, rs2378662, rs10001365, rs11078713, rs7929518, and rs62098013), and coffee consumption-related SNPs (rs4410790, and rs1057868) were all associated with overall survival and cancer-specific survival in OC.
Conclusion
Our findings provide the evidence for a favorable causal association of genetically predicted smoking initiation and coffee consumption with OC risk, and coffee consumption is linked to a greater risk of endometrioid OC.
... celery, lettuce, and spinach) can help prevent KC and UBC while soy consumption may lead to a statistical significant reduction of PC risk [274,275]. In contrast, a Western pattern diet that includes fried foods rich in acrylamide, high fat products and low intake of fruits, vegetables, whole grain and fiber, is directly associated with increased UBC and KC risk [265,276]. Accordingly, a pro-inflammatory diet, which involves red meat, white rice, and white bread, may increase the likelihood of developing PC, KC, and UBC [277]. High glycemic index foods (fast food, potatoes, sports drinks and processed foods) tend to have an unfavorable effect on UBC and KC occurrence [278]. ...
Urologic cancers (UC) account for 13.1% of all new cancer cases and 7.9% of all cancer-related deaths. A growing body of evidence has indicated a potential causal link between obesity and UC. The aim of the present review is to appraise in a critical and integrative manner evidence from meta-analyses and mechanistic studies on the role of obesity in four prevalent UC (kidney-KC, prostate-PC, urinary bladder-UBC, and testicular cancer-TC). Special emphasis is given on Mendelian Randomization Studies (MRS) corroborating a genetic causal association between obesity and UC, as well as on the role of classical and novel adipocytokines. Furthermore, the molecular pathways that link obesity to the development and progression of these cancers are reviewed. Available evidence indicates that obesity confers increased risk for KC, UBC, and advanced PC (20-82%, 10-19%, and 6-14%, respectively), whereas for TC adult height (5-cm increase) may increase the risk by 13%. Obese females tend to be more susceptible to UBC and KC than obese males. MRS have shown that a higher genetic-predicted BMI may be causally linked to KC and UBC but not PC and TC. Biological mechanisms that are involved in the association between excess body weight and UC include the Insulin-like Growth Factor axis, altered availability of sex hormones, chronic inflammation and oxidative stress, abnormal secretion of adipocytokines, ectopic fat deposition, dysbiosis of the gastrointestinal and urinary tract microbiomes and circadian rhythm dysregulation. Anti-hyperglycemic and non-steroidal anti-inflammatory drugs, statins, and adipokine receptor agonists/antagonists show potential as adjuvant cancer therapies. Identifying obesity as a modifiable risk factor for UC may have significant public health implications, allowing clinicians to tailor individualized prevention strategies for patients with excess body weight.
... However, to date, epidemiologic evidence remains scarce. One recent systematic review of cohort studies reported a positive association between dietary acrylamide and the risk of ovarian cancer (11), but most reviews detected no association with the risk of cancer at other sites (12)(13)(14)(15). In particular, to our knowledge, only 5 prospective cohort studies (16)(17)(18)(19)(20) and 1 case-cohort study (whose findings were reported in 2 studies) (21,22) have investigated the associations between dietary acrylamide and risk of breast cancer, which is the most frequent female cancer worldwide (23). ...
Background: Acrylamide is classified as a probable human carcinogen by the IARC but epidemiological evidence on the carcinogenicity of acrylamide from dietary sources is limited. This study aimed to investigate the associations between dietary acrylamide and breast cancer risk in the NutriNet-Santé cohort. Methods: This prospective cohort study included 80,597 French women (mean [SD] age at baseline: 40.8 [14] years) during a mean (SD) follow-up of 8.8 (2.3) years. Acrylamide intake was evaluated using repeated 24h dietary records (n= 5.5 [SD 3.0]), linked to a comprehensive food composition database. Associations between acrylamide intake and breast cancer risk (overall, premenopausal and post-menopausal) were assessed by Cox hazard models adjusted for known risk factors. Results: The mean (SD) dietary acrylamide intake was 30.1 (21.9) µg/d (main contributors: coffee, potato fries and chips, pastries and cakes, and bread). During follow-up, 1016 first incident breast cancer cases were diagnosed (431 premenopausal, 585 postmenopausal). A borderline significant positive association was observed between acrylamide intake and breast cancer risk overall (HRQ4 vs Q1= 1.21 [95% CI: 1.00-1.47]) and a positive association was observed with premenopausal cancer (HRQ4 vs Q1= 1.40 [95% CI: 1.04-1.88]). Restricted cubic spline analyses suggested evidence for non-linearity of these associations, with higher HR for intermediate (Q2) and high (Q4) exposures. Receptor-specific analyses revealed a positive association with estrogen receptor-positive breast cancer, which represented 86% of total cancer cases. Acrylamide intake was not associated with post-menopausal breast cancer. Conclusions: Results from this large prospective cohort study suggest the potential deleterious role of dietary acrylamide in breast cancer etiology, especially in premenopausal women, and provide new insights that should encourage further mitigation strategies to reduce the content of acrylamide in food.
Citation Format: Alice Bellicha, Gaëlle Wendeu-Foyet, Xavier Coumoul, Meriem Koual, Fabrice Pierre, Françoise Guéraud, Laurent Zelek, Charlotte Debras, Bernard Srour, Laury Sellem, Emmanuelle Kesse-Guyot, Chantal Julia, Pilar Galan, Serge Hercberg, Mélanie Deschasaux-Tanguy, Mathilde Touvier. Dietary exposure to acrylamide and breast cancer risk: results from the NutriNet-Santé cohort [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P2-06-03.
... Acrylamide, which is produced during roasting coffee beans at high temperatures, may be the mechanism causing this outcome [44]. High acrylamide intake may be scienti cally conceivable as a potential risk factor for OC [45]. ...
Objective: Currently, the association between smoking, alcohol, and coffee intake and the risk of ovarian cancer (OC) remains conflicting. In this study, we used a two-sample mendelian randomization (MR) method to evaluate the association of smoking, drinking and coffee consumption with the risk of OC and prognosis.
Methods: Five risk factors related to lifestyles (cigarettes per day, smoking initiation, smoking cessation, alcohol consumption and coffee consumption) were chosen from the Genome-Wide Association Study, and 28, 105, 10, 36 and 36 single-nucleotide polymorphisms (SNPs) were obtained as instrumental variables (IVs). Outcome variables were achieved from the Ovarian Cancer Association Consortium. Inverse-variance-weighted method was mainly used to compute odds ratios (OR) and 95% confidence intervals (Cl).
Results: The two-sample MR analysis supported the causal association of genetically predicted smoking initiation (OR: 1.15 per SD, 95%CI: 1.02-1.29, P=0.027) and coffee consumption (OR: 1.40 per 50% increase, 95%CI: 1.02-1.93, P=0.040) with the risk of OC, but not cigarettes per day, smoking cessation, and alcohol consumption. Subgroup analysis based on histological subtypes revealed a positive genetical predictive association between coffee consumption and endometrioid OC (OR: 3.01, 95%CI: 1.50-6.04, P=0.002). Several smoking initiation-related SNPs (rs7585579, rs7929518, rs2378662, rs10001365, rs11078713, rs7929518, and rs62098013), and coffee consumption-related SNPs (rs4410790, and rs1057868) were all associated with overall survival and cancer-specific survival in OC.
Conclusion: Our findings provide the evidence for a favorable causal association of genetically predicted smoking initiation and coffee consumption with OC risk, and coffee consumption is linked to a greater risk of endometrioid OC.
... However, to date, epidemiologic evidence remains scarce. One recent systematic review of cohort studies reported a positive association between dietary acrylamide and the risk of ovarian cancer (11), but most reviews detected no association with the risk of cancer at other sites (12)(13)(14)(15). In particular, to our knowledge, only 5 prospective cohort studies (16)(17)(18)(19)(20) and 1 case-cohort study (whose findings were reported in 2 studies) (21,22) have investigated the associations between dietary acrylamide and risk of breast cancer, which is the most frequent female cancer worldwide (23). ...
Background
Acrylamide is classified as a probable human carcinogen by the International Agency for Research on Cancer but epidemiologic evidence on the carcinogenicity of acrylamide from dietary sources is limited.
Objectives
This study aimed to investigate the associations between dietary acrylamide and breast cancer risk in the NutriNet-Santé cohort, accounting for menopausal and hormone receptor status.
Methods
This prospective cohort study included 80,597 French females (mean ± SD age at baseline: 40.8 ± 14 y) during a mean ± SD follow-up of 8.8 ± 2.3 y. Acrylamide intake was evaluated using repeated 24-h dietary records (n ± SD = 5.5 ± 3.0), linked to a comprehensive food composition database. Associations between acrylamide intake and breast cancer risk (overall, premenopausal, and postmenopausal) were assessed by Cox hazard models adjusted for known risk factors (sociodemographic, anthropometric, lifestyle, medical history, and nutritional factors).
Results
The mean ± SD dietary acrylamide intake was 30.1 ± 21.9 µg/d (main contributors: coffee, potato fries and chips, pastries, cakes, bread). During follow-up, 1016 first incident breast cancer cases were diagnosed (431 premenopausal, 585 postmenopausal). A borderline significant positive association was observed between dietary acrylamide exposure and breast cancer risk overall (HR for quartile 4 compared with 1: 1.21; 95% CI: 1.00, 1.47) and a positive association was observed with premenopausal cancer (HRQ4vs.Q1: 1.40; 95% CI: 1.04, 1.88). Restricted cubic spline analyses suggested evidence for nonlinearity of these associations, with higher HRs for intermediate (quartile 2) and high (quartile 4) exposures. Receptor-specific analyses revealed positive associations with estrogen receptor–positive breast cancer (total and premenopausal). Acrylamide intake was not associated with postmenopausal breast cancer.
Conclusions
Results from this large prospective cohort study suggest a positive association between dietary acrylamide and breast cancer risk, especially in premenopausal females, and provide new insights that support continued mitigation strategies to reduce the content of acrylamide in food.
This trial was registered at clinicaltrials.gov as NCT03335644.
... Coffee contains a complex mixture of chemicals that have been shown to elicit antimutagenic, anticarcinogenic, and antioxidant properties in experimental studies (8). In contrast, coffee (and other dietary components) also contains acrylamide, which is considered to be a carcinogen; however, results on the association between acrylamide and EC risk are inconsistent (9). Previous studies have reported an inverse association between coffee consumption and circulating concentrations of estrogen and C-peptide, a marker of insulin secretion, both of which are involved in endometrial carcinogenesis (10)(11)(12). ...
Background
Epidemiological studies suggest that coffee consumption may be inversely associated with risk of endometrial cancer (EC), the most common gynecological malignancy in developed countries. Furthermore, coffee consumption may lower circulating levels of estrogen and insulin, hormones implicated in endometrial carcinogenesis. Antioxidants and other chemopreventive compounds in coffee may have anticarcinogenic effects. Based on available meta-analyses, the World Cancer Research Fund concluded that consumption of coffee probably protects against EC.
Objective
Our main aim was to examine the association between coffee consumption and EC risk by combining individual-level data in a pooled analysis. We also sought to evaluate potential effect modification by other risk factors of EC.
Patients and Methods
We combined individual-level data from 19 epidemiologic studies (6 cohort, 13 case-control) of 12,159 endometrial cancer cases and 27,479 controls from the Epidemiology of Endometrial Cancer Consortium (E2C2). Logistic regression was used to calculate odds ratios (OR) and their corresponding 95% confidence intervals (CI). All models were adjusted for potential confounders including age, race, body mass index, smoking status, diabetes status, study design and study site.
Results
Coffee drinkers had a lower risk of EC compared to non-coffee drinkers (multi-adjusted OR = 0.87, 95% CI = 0.79,0.95). There was a dose-response relationship between higher coffee consumption and lower risk of EC: compared to non-coffee drinkers, the adjusted pooled ORs for those who drank 1, 2–3 and more than 4 cups/day were 0.90 (95% CI = 0.82,1.00), 0.86 (95% CI = 0.78,0.95), and 0.76 (95% CI = 0.66,0.87), respectively (p for trend < 0.001). The inverse association between coffee consumption and EC risk was stronger in participants with body mass index (BMI) over 25 kg/m2.
Conclusion
The results of the largest analysis to date pooling individual-level data further support the potentially beneficial health effects of coffee consumption in relation to EC, especially among females with higher BMI.
... Proces ten nie jest jednak bez znaczenia dla zdrowia człowieka, gdyż właśnie w ten sposób w produktach żywnościowych, które są poddawane obróbce termicznej w wysokiej temperaturze, wytwarza się akryloamid [37,38]. Wysokie temperatury smażenia, powyżej 120°C, przyczyniają się do wytwarzania związku toksycznego -AA, który jest dla ludzi prawdopodobnie kancerogenny, a spożycie takiej żywości z dużym prawdopodobieństwem przyczynia się do zachorowania na raka [19,39,40]. Codzienne spożycie produktów wysokoprzetworzonych (takich jak krakersy, chipsy, słodycze czy żywność typu fast food) dostarcza do organizmu cłowieka ogromne ilości energii, która niekoniecznie zostaje wydatkowana w ciągu dnia. ...
Introduction and objective
Food is a basis for proper functioning of the human body. Inadequate quality of consumed food products may have a negative impact on mhuman health. Acrylamide (AA) is a dangerous and harmful chemical compound contained in food products. The aim of the study was to identify and analyze data from literature concerning the risk to consumer health associated with the consumption of highly processed foods containing acrylamide, and to estimate the size of this risk.
Material and methods
Analysis of the size of consumer health risk related to exposure to AA in food was performed by
reviewing the available literature data published over 11 years (from 2011–2021). Data on the consumption of particular food products by an average Pole was obtained from the Central
Statistical Office. Adult exposure was calculated to assess the health risks to consumers from consuming individual foods containing AA. The health risk was estimated in accordance with US EPA guidelines.
Results
The analysis of the size of health risk to an average Pole performed based on three scenarios that assumed the consumption of selected food products containing minimum, medium and high amounts of acrylamide did not show any significant exposure in any groups of products
Conclusions
The estimated health risk resulting from exposure to acrylamide contained in food did not show any
significant exposure, however, considering that a person consumes food containing AA throughout the whole life the content of this toxic compound in food products is important.
... Acrylamide, a highly chemical reactive substance obtained as a by-product of the cooking process during the Maillard reaction, is considered by the International Agency for Research on Cancer as a probable class 2A human carcinogen [1,2]. Studies have shown that exposure to acrylamide increases the risk of kidney, endometrial, and ovarian cancer [3]. The mechanism involved in acrylamideinduced cancer is still unclear, but genotoxic and non-genotoxic pathways have been suggested [4]. ...
Lepidium meyenii Walp (red maca) is a high Andean plant cultivated since the Incas and has innumerable therapeutic properties. The study aims to identify its phytochemical composition using UHPLC-ESI-MS/MS, and evaluate its effects on acrylamide-induced oxidative stress. The lyophilized aqueous extract of red maca (LAqE-RM) was orally administered in doses of 1 and 2 g/kg body weight for 4 weeks. Malondialdehyde (MDA) levels in erythrocytes, brain, and liver, as well as hepatic levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. Administration of acrylamide for 2 and 4 weeks significantly increased (p < 0.001) MDA levels in erythrocytes, brain, and liver. However, LAqE-RM prevented (p < 0.001) an increase in MDA levels in all tissues studied. Likewise, the groups treated with LAqE-RM presented significantly (p < 0.001) lower levels of ALT and AST compared to the control. Treatment with LAqE-RM ameliorated the acrylamide-induced oxidative stress by reducing MDA levels in erythrocytes, brain, and liver and by lowering liver levels of ALT and AST in a dose-dependent manner. Twenty-five secondary metabolites were identified and characterized from LAqE-RM based on UHPLC mass
... Acrylamide, a highly chemical reactive substance obtained as a by-product of the cooking process during the Maillard reaction, is considered by the International Agency for Research on Cancer as a probable class 2A human carcinogen [1,2]. Studies have shown that exposure to acrylamide increases the risk of kidney, endometrial, and ovarian cancer [3]. The mechanism involved in acrylamideinduced cancer is still unclear, but genotoxic and non-genotoxic pathways have been suggested [4]. ...
Lepidium meyenii Walp (red maca) is a high Andean plant cultivated since the time of the Incas, and has innumerable therapeutic properties. The study aims to identify its phytochemical composition using UHPLC–Q/Orbitrap/MS/MS, and to evaluate its effects on acrylamide-induced oxidative stress. The lyophilized aqueous extract of red maca (LAqE-RM) was orally administered in doses of 1 and 2 g/kg body weight for 4 weeks. Malondialdehyde (MDA) levels in erythrocytes, brain and liver, as well as hepatic levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. Administration of acrylamide for 2 weeks and 4 weeks significantly increased (p <0.001) MDA levels in erythrocytes, brain, and liver. However, LAqE-RM was able to prevent (p <0.001) an increase in MDA levels in all tissues studied. Likewise, the groups treated with LAqE-RM presented significantly (p <0.001) lower levels of ALT and AST compared to the control. Treatment with LAqE-RM ameliorated the acrylamide-induced oxidative stress by reducing MDA levels in erythrocytes, brain, and liver, and by reducing liver levels of ALT and AST in a dose dependent manner. Twenty-five secondary metabolites were identified and characterized from LAqE-RM based on UHPLC mass spectrophotometry, these include; carbolines, alkamides, fatty acids and macamides, which are probably involved in their antioxidant protective role.
This preprint has not undergone peer review or any post-submission improvements or corrections. The Version of Record of this article is published in Plant Foods for Human Nutrition, and is available online at https://doi.org/10.1007/s11130-022-01000-2
... Experimental studies on animals have revealed that acrylamide has a genotoxic and neurotoxic effect and causes cancer in multiple organs and tissues (Anonymous, 2005(Anonymous, , 2015Rice, 2005;Park et al., 2021). Studies on humans have reported that dietary acrylamide exposure is associated with some types of cancer (Hirvonen et al., 2010;Pelucchi et al., 2015;Liu et al., 2017;Adani et al., 2020), negatively affects fetal development during pregnancy, such as low birth weight (Duarte-Salles et al., 2013), and also leads to neurological effects such as tingling, pain, and numbness in the hands, arms, legs (Goffeng et al., 2011;Kopanska et al., 2018). The Joint Food and Agriculture Organization/World Health Organization (FAO/WHO) Expert Committee on Food Additives defined neurotoxic No Observed Adverse Effect Level (NOAEL) for acrylamide as 0.2 mg kg -1 bw/day (Anonymous, 2011). ...
The aim of this study was to determine the acrylamide level of fried potatoes, peppers, eggplant and zucchini, and to examine the effect different order of vegetables on the acrylamide level of other vegetables in consecutive frying sessions. In this study, in which four different types of vegetables were fried separately and together with sunflower oil, 52 frying sessions were performed in 13 separate frying groups, analyzing a total of 208 samples in LC-MS/MS. The study was carried out at the Eastern Anatolia High Technology Application and Research Center (Erzurum, Turkey) between 20 January and 15 February 2021. Potatoes, peppers, eggplants, and zucchinis were fried consecutively and mean acrylamide levels of they were determined as 1042, 502, 167, and 553 μg kg-1, respectively. Statistically significant results between consecutive frying sessions of all vegetables and acrylamide levels were obtained. The acrylamide levels obtained for all types of vegetables indicate that oil should not be used sequentially. However, there was no difference between the change in the order of vegetables and their acrylamide levels in frying. The results show that the fried foods do not cause an additional load of acrylamide in the oil. More research should be conducted on the effect of consumers' culinary practices on acrylamide levels in foods.
... The European Commission classified it as acrylamide carcinogen and mutagen in Category 1B, and as a reproductive toxicant in Category 2 (European Commission, 2008). It has been reported in various studies that acrylamide increases the risk of developing some types of cancer, adversely affects the reproductive and nervous systems, and causes eye and skin irritations (Duarte-Salles et al., 2013;Pelucchi et al., 2015;Kopanska et al., 2018;Adani et al., 2020). The Joint FAO/WHO Expert Committee on Food Additives (JECFA) defined neurotoxic No Observed Adverse Effect Level (NOAEL) value for acrylamide as 0.2 mg/kg bw/day (Joint FAO/WHO Expert Committee on Food Additives (JECFA, 2011). ...
Bread is a food of global importance for nutrition. Therefore, contaminants from the heat treatment of bread may be considered a potential health issue. In this study, 5-hydroxymethyl-2-furfural (5-HMF) and acrylamide levels were determined using HPLC and GC/MS, respectively, in 26 bread types (n = 52) widely consumed in Turkey. Then, the exposure of individuals with different demographic characteristics to 5-HMF and acrylamide was calculated, and risk assessments were performed. The 5-HMF and acrylamide levels in the samples ranged from 3.50 to 120 mg/kg and from 60.7 to 130 µg/kg, respectively. The highest levels of 5-HMF and acrylamide were measured in the white and semi-industrial/traditional bread groups. Statistically significant differences were found between bread groups (p < 0.05). The exposure levels of 5-HMF and acrylamide in males and females between the ages of 15–18 were higher than in other age groups. The target hazard quotient (non-carcinogenic) values calculated for acrylamide exposure showed no health problem, while the carcinogenic risk values indicated potential and high levels of risk. The exposure to 5-HMF was relatively high. The results can serve as a guide for reducing exposure to 5-HMF and acrylamide through bread consumption.
Background
Previous research has found associations between various non-genetic factors and breast cancer (BrCa) risk. This study summarises and appraises the credibility of the available evidence on the association between non-genetic factors and BrCa risk.
Methods
We conducted an umbrella review of meta-analyses. Medline, Scopus, and the Cochrane databases were systematically searched for meta-analyses examining non-genetic factors and BrCa incidence or mortality. The strength of the evidence was graded in four categories (i.e., weak, suggestive, highly suggestive, convincing).
Results
A total of 781 meta-analyses from 280 publications were evaluated and graded. We included exposures related to anthropometric measurements, biomarkers, breast characteristics and diseases, diet and supplements, environment, exogenous hormones, lifestyle and social factors, medical history, medication, reproductive history, and pregnancy. The largest number of examined associations was found for the category of diet and supplements and for exposures such as aspirin use and active smoking. The statistically significant (P-value < 0.05) meta-analyses were 382 (49%), of which 204 (53.4%) reported factors associated with increased BrCa risk. Most of the statistically significant evidence (n = 224, 58.6%) was graded as weak. Convincing harmful associations with heightened BrCa risk were found for increased body mass index (BMI), BMI and weight gain in postmenopausal women, oral contraceptive use in premenopausal women, increased androstenedione, estradiol, estrone, and testosterone concentrations, high Breast Imaging Reporting and Data System (BIRADS) classification, and increased breast density. Convincing protective factors associated with lower BrCa risk included high fiber intake and high sex hormone binding globulin (SHBG) levels while highly suggestive protective factors included high 25 hydroxy vitamin D [25(OH)D] levels, adherence to healthy lifestyle, and moderate-vigorous physical activity.
Conclusions
Our findings suggest some highly modifiable factors that protect from BrCa. Interestingly, while diet was the most studied exposure category, the related associations failed to reach higher levels of evidence, indicating the methodological limitations in the field. To improve the validity of these associations, future research should utilise more robust study designs and better exposure assessment techniques. Overall, our study provides knowledge that supports the development of evidence-based BrCa prevention recommendations and guidance, both at an individual level and for public health initiatives.
Trial registration
PROSPERO CRD42022370675.
Background
Acrylamide (AA) is a toxic substance formed when cooking starch-based foods at high temperatures. Studies have shown that AA can cause neurotoxicity, reproductive toxicity and so on. However, there remains limited understanding of the potential skeletal toxicity of AA.
Objective
The aim of this study was to investigate the potential skeletal toxicity of AA, as well as the potential bone protective effects of Resveratrol (RVT).
Methods
Based on the daily intake of adult women, adult female mice was treated with AA at 0, 0.01, 0.1, 1 mg/kg/d or AA/RVT (1 mg/kg/d AA +10 mg/kg/d RVT) for 8 weeks, and skeletal toxicity were evaluated by RT-qPCR and histopathological techniques.
Results
The results found that exposure to AA (0.1 or 1 mg/kg/d) after 8 weeks, osteogenesis exhibited pathological damage characteristics such as inhibition of growth plate function, and reduction of fibrous tissue, and cartilage exhibited pathological damage characteristics such as irregular cell morphology and arrangement, and damage to the tidal line. The results of cellular functional gene testing showed a decrease in the expression of functional genes in osteoblasts and chondrocytes. Meanwhile, after further co-treatment with AA (1 mg/kg/d) and resveratrol (RVT) (10 mg/kg/d), we found that RVT restored AA-induced damage to osteogenesis and cartilage, and reduced the high apoptosis and oxidative stress levels in osteogenesis/cartilage after AA exposure.
Conclusion
In summary, this study confirmed the skeletal toxicity of AA on female adult mice, and further clarified the antioxidant protective effect of RVT on this toxicity.
Kızartma yöntemi, bilinen en eski pişirme yöntemlerinden biridir. Kızartılmış besinler lezzet, renk, doku ve görünüm gibi organoleptik ve duyusal özellikleri sayesinde tüketiciler tarafından sıklıkla tercih edilmektedir. Kızartmada kullanılan yağın türü, yağ asidi bileşimi ve niteliği oldukça önemlidir. Çünkü kızartma süresince sıcaklık, nem ve oksijene bağlı olarak birçok kimyasal reaksiyon meydana gelmektedir. Bu reaksiyonların ilerlemesi ile ısıl proses kirleticileri olarak adlandırılan ve kanser başta olmak üzere obezite, kardiyovasküler hastalıklar gibi birçok sağlık problemi ile ilişkilendirilen; akrilamid, 3-kloropropan-1,2-diol (3-MCPD), glisidil esterleri (GE), polisiklik aromatik hidrokarbonlar (PAH), trans yağ asitleri (TYA) ve furan oluşmaktadır. Bu çalışmanın amacı, güncel araştırmalar doğrultusunda kızartmada kullanılan yağları incelemek ve kızartma işlemi sonucunda oluşan ısıl proses kirleticilerinin sağlık üzerindeki etkilerini değerlendirmektir.
Thermal processing is one of the important techniques for most of the plant-based food and herb medicines before consumption and application in order to meet the specific requirement. The plant and herbs are rich in amino acids and reducing sugars, and thermal processing may lead to Maillard reaction, resulting as a high risk of acrylamide pollution. Acrylamide, an organic pollutant that can be absorbed by the body through the respiratory tract, digestive tract, skin and mucous membranes, has potential carcinogenicity, neurological, genetic, reproductive and developmental toxicity. Therefore, it is significant to conduct pollution determination and risk assessment for quality assurance and security of medication. This review demonstrates state-of-the-art research of acrylamide focusing on the toxicity, formation, contamination, determination, and mitigation in taking food and herb medicine, to provide reference for scientific processing and ensure the security of consumers.
Acrylamide, identified by the International Cancer Research Center as a possible carcinogenic compound to humans, is a contaminant formed as a result of the thermal process in many foods, such as coffee, French fries, biscuits and bread, which are frequently consumed by individuals in their daily lives. The biggest concern about acrylamide is that the health risks have not yet been fully elucidated. For this reason, many studies have been carried out on acrylamide in the food, nutrition and health equation. This study focused on epidemiological studies examining the associations between dietary acrylamide exposure and cancer risk. For this purpose, articles published in PubMed, Isı Web of Knowledge, Scopus and Science Direct databases between January 2002 and April 2022 were systematically examined using various keywords, and a total of 63 articles were included in the study. Although some studies on reproductive, urinary, gastrointestinal, respiratory and other systems and organs stated that there is a positive relationship between dietary acrylamide exposure and cancer risk, many publications did not disclose a relationship in this direction. Studies examining the relationship between dietary acrylamide exposure and cancer should be planned to include more people and foods in order to obtain more reliable results. Making research plans in this way is very important in terms of guiding health policies to be formed in the future.
Purpose
Acrylamide (AA) is a potential carcinogen that mainly comes from fried, baked and roasted foods, and Hb adducts of AA (HbAA) and its metabolite glycidamide (HbGA) are the biomarkers of its exposure. Increasing evidence suggests that AA is associated with various hormone-related cancers. This study aims to explore the association of HbAA and HbGA with female serum sex hormone concentrations.Methods
942 women from the National Health and Nutrition Examination Survey cycles (2013–2016) were included in this cross-sectional study. The associations between HbAA or HbGA or HbGA/HbAA and sex hormones were assessed by the multiple linear regression. Further stratified analyses were conducted to figure out the effects of menopausal status, BMI and smoking status on sex hormone levels.ResultsAmong all participants, 597 were premenopausal and 345 were postmenopausal. HbAA was positively associated with both two androgen indicators. Specifically, a ln-unit increase in HbAA was associated with 0.41 ng/dL higher ln(total testosterone, TT) (95% CI 0.00, 0.27) and 0.14 ng/dL higher ln(free testosterone) (95%CI 0.00, 0.28), respectively. However, HbGA concentrations had no association with sex hormones in the overall population. Additionally, HbGA/HbAA was negatively associated with TT and SHBG in the overall population as well as postmenopausal women. In stratified analysis, higher HbAA was associated with rising TT in postmenopausal women (β = 0.29, 95%CI 0.04, 0.53) and underweight/normal-weight women (β = 0.18, 95%CI 0.03, 0.33). Other indicators had no significant association detected in estradiol and sex hormone-binding globulin.Conclusion
Our results revealed that HbAA was positively associated with androgen concentrations, especially in postmenopausal and BMI < 25 women.
Background:
Increasing evidence have been provided that the exposure to environment pollutants was associated obesity, while whether the exposure to volatile organic chemicals (VOC) was associated with obesity or abdominal obesity is yet to be clarified.
Method:
A cross-sectional study using data from the 6 survey cycles (2005-2006, 2011-2018, 2017-2020) of NHANES program was performed. Obesity and abdominal obesity were identified as a BMI >30 and a waist circumference >102 cm for men or >88 cm for women respectively. The quantile logistic regression method was used to analyze the association between VOC metabolites (VOCs) in urine and obesity, and the quantile regression method was used for the association analysis between VOCs in urine and BMI, as well as waist circumference.
Results:
A total of 17 524 participants (4965 obesity, 7317 abdominal obesity) were included, and participants in the obesity or abdominal obesity groups showed higher VOCs in urine than that in the control group. The CEMA was identified as the risk factor for obesity and abdominal obesity in all the 4 models, and its detected OR for obesity in the Q2 to Q4 of model 3 was 1.169 (Q2, p < 0.05), 1.306 (Q3, p < 0.001) and 1.217 (Q4, p < 0.01) respectively. And its OR for abdominal obesity in the Q2 to Q4 of model 3 was 1.222 (Q2, p < 0.01), 1.448 (Q3, p < 0.001) and 1.208 (Q4, p < 0.05) respectively. A significantly positive association between CEMA and BMI, as well as waist circumference, was also detected.
Conclusion:
In this study, we found that the exposure to VOC (Acrolein, Acrylamide, Acrylonitrile, 1,3-Butadiene, Crotonaldehyde, Cyanide, N,N-Dimethylformamide, Ethylbenzene, styrene, Propylene oxide, Toluene and Xylene) was significantly associated with obesity or abdominal obesity. And also, more prospective studies and related experimental researches should be carried out to further demonstrate the conclusion of this study.
Background:
Acrylamide (AA) is classified as "probably carcinogenic to humans (Class 2A)" by the International Agency for Research on Cancer. AA causes cancer owing to its mutagenic and genotoxic metabolite, glycidamide (GA), and its effects on sex hormones. Both AA and GA can interact with hemoglobin to hemoglobin adducts (HbAA and HbGA, respectively), which are considered appropriate biomarkers of internal exposure of AA. However, few epidemiological studies reported an association of HbAA and HbGA with breast cancer (BC).
Methods:
We conducted a nested case-control study within the Japan Public Health Center-based Prospective Study cohort (125 cases and 250 controls). Cases and controls were categorized into tertiles (Lowest, Middle, and Highest) using the distribution of HbAA or HbGA levels in the control group and estimated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression, adjusting for potential confounders.
Results:
No association was observed between HbAA (ORHighest vs. Lowest, 1.34, 95% CI, 0.69-2.59), HbGA (ORHighest vs. Lowest, 1.46, 95% CI, 0.79-2.69), their sum HbAA+HbGA (ORHighest vs. Lowest, 1.36, 95% CI, 0.72-2.58) and BC; however, some evidence of positive association was observed between their ratio, HbGA/HbAA, and BC (ORHighest vs. Lowest, 2.19, 95% CI, 1.11-4.31).
Conclusions:
There was no association between biomarkers of AA and BC.
Impact:
It is unlikely that AA increases BC risk; however, the association of AA with BC may need to be evaluated, with a focus not only on the absolute amount of HbAA or HbGA but also on HbGA/HbAA and the activity of metabolic genes.
Commonly consumed foods and beverages can contain chemicals with reported carcinogenic activity in rodent models. Moreover, exposures to some of these substances have been associated with increased cancer risks in humans. Food-borne carcinogens span a range of chemical classes and can arise from natural or anthropogenic sources, as well as form endogenously. Important considerations include the mechanism(s) of action (MoA), their relevance to human biology, and the level of exposure in diet. The MoAs of carcinogens have been classified as either DNA-reactive (genotoxic), involving covalent reaction with nuclear DNA, or epigenetic, involving molecular and cellular effects other than DNA reactivity. Carcinogens are generally present in food at low levels, resulting in low daily intakes, although there are some exceptions. Carcinogens of the DNA-reactive type produce effects at lower dosages than epigenetic carcinogens. Several food-related DNA-reactive carcinogens, including aflatoxins, aristolochic acid, benzene, benzo[a]pyrene and ethylene oxide, are recognized by the International Agency for Research on Cancer (IARC) as causes of human cancer. Of the epigenetic type, the only carcinogen considered to be associated with increased cancer in humans, although not from low-level food exposure, is dioxin (TCDD). Thus, DNA-reactive carcinogens in food represent a much greater risk than epigenetic carcinogens.
Several non-genetic factors have been associated with ovarian cancer incidence or mortality. To evaluate the strength and validity of the evidence we conducted an umbrella review of the literature that included systematic reviews/meta-analyses that evaluated the link between non-genetic risk factors and ovarian cancer incidence and mortality. We searched PubMed, EMBASE, Cochrane Database of Systematic Reviews and performed a manual screening of references. Evidence was graded into strong, highly suggestive, suggestive or weak based on statistical significance of the random effects summary estimate and the largest study in a meta-analysis, the number of cases, between-study heterogeneity, 95% prediction intervals, small study effects, and presence of excess significance bias. We identified 212 meta-analyses, investigating 55 non-genetic risk factors for ovarian cancer. Risk factors were grouped in eight broad categories: anthropometric indices, dietary intake, physical activity, pre-existing medical conditions, past drug history, biochemical markers, past gynaecological history and smoking. Of the 174 meta-analyses of cohort studies assessing 44 factors, six associations were graded with strong evidence. Greater height (RR per 10 cm 1.16, 95% confidence interval (CI) 1.11–1.20), body mass index (BMI) (RR ≥ 30 kg/m2 versus normal 1.27, 95% CI 1.17–1.38) and three exposures of varying preparations and usage related to hormone replacement therapy (HRT) use increased the risk of developing ovarian cancer. Use of oral contraceptive pill reduced the risk (RR 0.74, 95% CI 0.69–0.80). Refining the significance of genuine risk factors for the development of ovarian cancer may potentially increase awareness in women at risk, aid prevention and early detection.
Characterising the change in the risk of a health‐related outcome according to the levels of an exposure is increasingly popular in systematic reviews. We provide an introduction to the statistical methods currently used to perform linear and non‐linear dose‐response analysis based on aggregated data from multiple studies. We explain how dose‐response associations are estimated within a study and summarised across studies. A re‐analysis of observational studies about coffee consumption and mortality is used to illustrate how to move beyond a linear dose‐response trend, and the complexity of making inference on relative risks when using restricted cubic splines.
Background
Acrylamide is widely found in food as a side-product of high-temperature heating of starch-rich food. It has attracted much attention because of its neurotoxicity and carcinogenicity. However, the cancer risk and disease burden of dietary acrylamide exposure have not been quantified in China.
Objective
To estimate the cancer risk and the disease burden attributable to dietary acrylamide exposure and quantify its health hazards.
Method
We first performed an exposure assessment of acrylamide in food, based on which the incremental excess lifetime cancer risk (ELCR) was calculated for cancer risk assessment. The DisMod Ⅱ software and the DALY calculator in R were used to calculate the disease burden due to dietary acrylamide exposure.
Results
Average dietary acrylamide exposure in males was 0.1531 μg·kg⁻¹·d⁻¹ and that in females was 0.1554 μg·kg⁻¹·d⁻¹, resulting in an ELCR of 7.81 × 10⁻⁵ for males and 7.92 × 10⁻⁵ for females in China. The dietary acrylamide exposure resulted in about 23,688.09 DALYs of cancers among the Chinese population in 2016, including 1331.93 DALYs of breast cancer, 243.32 DALYs of endometrial cancer, 248.91 DALYs of ovarian cancer, and 176.28 DALYs of kidney cancer, respectively.
Conclusion
The health hazards of dietary acrylamide exposure deserve attention. The burden of disease assessment could quantify the health hazards of food contaminants for prioritizing policies.
Fried starchy foods have the conditions to produce harmful compounds, such as acrylamide and malondialdehyde (MDA). One of these popular and commonly consumed foods among Iranians is Tah-Dig. This study aimed to evaluate the factors that affect their production and also levels in Tah-Dig. In this cross-sectional study, the information about the cooking pattern and consumption of Tah-Dig was randomly obtained from 611 households in Kermanshah through a dietary pattern questionnaire. Samples were provided by the households were classified according to type (potato, rice and bread) and color (golden, light brown and dark brown). Acrylamide levels were measured by a LC–mass spectrometer, and MDA levels were measured using a barbituric acid kit. More than 77.7% of participants consumed Tah-Dig at least 5 times a week. Potato Tah-Dig had the highest amount of acrylamide (1096 ± 637 ng/g). By changing the color value from golden to dark brown, the amount of acrylamide in all types of Tah-Dig increased significantly (P-value < 0.001). The highest amount of MDA was ascribed to canola oil (1527.89 ± 519.20 ng/L) and the lowest to ghee (546.12 ± 213.43 ng/L), after the Tah-Dig was cooked. No correlation was found between the type of oil and the amount of acrylamide. Tah-Dig is considered a harmful food among Iranian households due to its high consumption frequency and the abundance of acrylamide and MDA. Food and nutrition policymakers should consider teaching the proper cooking ways of such foods to the people.
Background
Evidence associating diet with the incidence of renal cell carcinoma (RCC) is inconclusive. We aimed to summarize evidence associating dietary factors with RCC incidence and assess the strength and validity of this evidence.
Methods
We conducted an umbrella review of systematic reviews or meta-analyses (SRoMAs) that assessed the association between diet and RCC incidence. Through April 2021, PubMed, Web of Science, Embase, The Cochrane Library, Scopus, and WCRF were searched. Two independent reviewers selected studies, extracted data, and appraised the quality of SRoMAs. According to credibility assessment criteria, evidence can be divided into five categories: convincing (class I), highly suggestive (class II), suggestive (class III), weak (class IV), and nonsignificant (class V).
Results
Twenty-nine meta-analyses were obtained after screening. After excluding 7 overlapping meta-analyses, 22 meta-analyses including 502 individual studies and 64 summary hazard ratios for RCC incidence were included: dietary patterns or dietary quality indices (n = 6), foods (n = 13), beverages (n = 4), alcohol (n = 7), macronutrients (n =15), and micronutrients (n =19). No meta-analyses had high methodological quality. Five meta-analyses exhibited small study effects; one meta-analysis showed evidence of excess significance bias. No dietary factors showed convincing or highly suggestive evidence of association with RCC in the overall analysis. Two protective factors had suggestive evidence (vegetables (0.74, 95% confidence interval 0.63 to 0.86) and vitamin C (0.77, 0.66 to 0.90)) in overall analysis. One protective factor had convincing evidence (moderate drinking (0.77, 0.70 to 0.84)) in Europe and North America and one protective factor had highly suggestive evidence (cruciferous vegetables (0.78, 0.70 to 0.86)) in North America.
Conclusions
Although many meta-analyses have assessed associations between dietary factors and RCC, no high-quality evidence exists (classes I and II) in the overall analysis. Increased intake of vegetables and vitamin C is negatively associated with RCC risk. Moderate drinking might be beneficial for Europeans and North Americans, and cruciferous vegetables might be beneficial to North Americans, but the results should be interpreted with caution. More researches are needed in the future.
Trial registration
PROSPERO CRD42021246619
Acrylamide forms in many commonly consumed foods. In animals, acrylamide causes tumors, neurotoxicity, developmental and reproductive effects. Acrylamide crosses the placenta and has been associated with restriction of intrauterine growth and certain cancers. The impact on human health is poorly understood and it is impossible to say what level of dietary exposure to acrylamide can be deemed safe as the assessment of exposure is uncertain. The determination of hemoglobin (Hb) adducts from acrylamide is increasingly being used to improve the exposure assessment of acrylamide. We aim to outline the literature on Hb adduct levels from acrylamide in humans and discuss methodological issues and research gaps. A total of 86 studies of 27,966 individuals from 19 countries were reviewed. Adduct levels were highest in occupationally exposed individuals and smokers. Levels ranged widely from 3 to 210 pmol/g Hb in non-smokers and this wide range suggests that dietary exposure to acrylamide varies largely. Non-smokers from the US and Canada had slightly higher levels as compared with non-smokers from elsewhere, but differences within studies were larger than between studies. Large studies with exposure assessment of acrylamide and related adduct forming compounds from diet during early-life are encouraged for the evaluation of health effects.
Acrylamide (AA) is a neurotoxic, genotoxic, and carcinogenic compound developed during heating at high temperatures. Foods such as potatoes, biscuits, bread and coffee are the main foodstuffs containing AA. Cigarette smoke may be a significant additional source of exposure. However, AA content may vary among different types of cigarettes. The study aimed to evaluate the AA content in conventional cigarettes (CC) and heated tobacco products (HTP) and its resulting exposure through their use. AA levels from the two types of cigarettes were determined by GC-MS and the daily exposure to AA was also ascertained. The margin of exposure (MOE) was calculated for neurotoxic and carcinogenic risk based on benchmark dose lower confidence limit for a 10% response (BMDL10) of 0.43 and 0.17, 0.30, and 1.13 mg/kgbw/day. AA level in CC ranged from 235 to 897 ng/cigarette, whereas HTP reported AA levels in the range of 99–187 ng/cigarette. The data showed a low neurotoxic risk for either CC or HTP, whereas a carcinogenic risk emerged through the smoking of CC based on different Benchmark doses. The carcinogenic risk for CC based on the highest Benchmark dose that was considered showed unsafe levels, as little as 10 CC cigarettes/day, whereas it was almost always of low concern for HTP. Another approach based upon the incremental lifetime cancer risk (ILCR) analysis led to similar results, exceeding, in some cases, the safety value of 10−4, as far as CC are concerned. Overall, the results confirmed that CC are a significant source of AA, and its levels were five times higher than in HTP.
Rationale:
Acrylamide is classified as a probable human carcinogen that is metabolised to glycidamide, which can covalently bind to DNA. The aim of this study was to investigate the formation of N7-glycidamide-guanine (N7-GA-Gua) adducts in human blood DNA following exposure to acrylamide present in carbohydrate rich foods as part of the normal human diet.
Methods:
Lymphocyte DNA was extracted from blood samples obtained from healthy human volunteers. Following thermal depurination of the DNA samples, N7-GA-Gua adducts were quantified using a validated LC-MS/MS method incorporating a stable isotope-labelled internal standard. Estimated dietary acrylamide intake was recorded by completion of food frequency questionnaires for the 24 hours prior to volunteer blood donation.
Results:
A LC-MS/MS method was validated with a limit of detection of 0.25 fmol and a lower limit of quantitation of 0.50 fmol on column. N7-GA-Gua adducts were detected in human blood DNA with the levels ranging between 0.3 to 6.3 adducts per 108 nucleotides. The acrylamide intake was calculated from the food frequency questionnaires ranging between 20.0 and 78.6 μg.
Conclusions:
Identification and quantification of N7-GA-Gua adducts in the blood DNA of healthy volunteers suggests that dietary acrylamide exposure may lead to the formation of DNA adducts. This important finding warrants further investigation to ascertain a correlation between environmental/dietary acrylamide exposure and levels of DNA adducts.
Background:
Three prospective studies have evaluated the association between dietary acrylamide intake and endometrial cancer (EC) risk with inconsistent results. The objective of this study was to evaluate the association between acrylamide intake and EC risk: for overall EC, for type-I EC, and in never smokers and never users of oral contraceptives (OCs). Smoking is a source of acrylamide, and OC use is a protective factor for EC risk.
Methods:
Cox regression was used to estimate hazard ratios (HRs) for the association between acrylamide intake and EC risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Acrylamide intake was estimated from the EU acrylamide monitoring database, which was matched with EPIC questionnaire-based food consumption data. Acrylamide intake was energy adjusted using the residual method.
Results:
No associations were observed between acrylamide intake and overall EC (n=1382) or type-I EC risk (n=627). We observed increasing relative risks for type-I EC with increasing acrylamide intake among women who both never smoked and were non-users of OCs (HRQ5vsQ1: 1.97, 95% CI: 1.08-3.62; likelihood ratio test (LRT) P-value: 0.01, n=203).
Conclusions:
Dietary intake of acrylamide was not associated with overall or type-I EC risk; however, positive associations with type I were observed in women who were both non-users of OCs and never smokers.
The relation between dietary acrylamide intake and esophageal cancer (EC) risk, including esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC), has not been consistent. We evaluated the association between dietary acrylamide intake and EAC, ESCC, and overall EC in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.
Multivariate Cox proportional hazards models were used to estimate the HR and 95 % confidence interval (95 % CI). Since nonlinear relations were observed, HRs were displayed for quartiles of acrylamide intake in μg per day.
After a mean follow-up of 11 years, 341 EC were identified, 142 of which were EAC, 176 ESCC, and 23 other histological types or not specified. An increase in EC risk was observed in the second and third quartiles (HRQ2vsQ1 1.75, 95 % CI 1.12-2.74; HRQ3vsQ1 1.66, 95 % CI 1.05-2.61), but not in the fourth quartile, and there was no evidence for a linear dose-response trend. HRs were similarly elevated but not statistically significant when ESCC and EAC were analyzed separately, due to the small number of cases observed. No associations were observed when quartiles were based on energy-adjusted acrylamide intake.
In the EPIC cohort, an association between estimated dietary acrylamide intake and an increased risk of developing EC was observed in the middle quartiles but not in the highest quartile; however, results from other larger cohorts or consortia, and results from biomarker studies, might add to the evidence provided by this analysis, suggesting that acrylamide is not an important risk factor for EC.
Acrylamide, a probable human carcinogen, is present in heat-treated carbohydrate-rich foods. Epidemiological studies have not shown a clear association between acrylamide intake and colorectal cancer risk. This may be due to the molecular heterogeneity in colorectal tumors, which was not taken into consideration before. Since the acrylamide metabolite glycidamide induces specific DNA mutations in rodents, we investigated whether acrylamide is associated with colorectal cancer risk characterized by mutations in KRAS and APC; key genes in colorectal carcinogenesis. This case-cohort analysis, within the Netherlands Cohort Study on diet and cancer, was based on 7.3 years of follow-up. Acrylamide intake was assessed with a food frequency questionnaire. Mutation analysis of codons 1286-1520 in exon 15 in APC and codons 12 and 13 in exon 1 in KRAS was performed on tumor tissue of 733 cases. Hazard ratios were calculated using Cox proportional hazards analysis. Among men, acrylamide intake was statistically significantly associated with an increased risk of particularly tumors with an activating KRAS mutation (HR 4(th) quartile vs. 1(st): 2.12 (95% CI: 1.16-3.87), p-trend: 0.01). Among women, acrylamide intake was statistically significantly associated with a decreased risk of particularly tumors with a truncating APC mutation (4(th) quartile vs. 1(st): 0.47 (95% CI: 0.23-0.94), p-trend: 0.02), but only in the highest quartile of intake. This is the first study to show that acrylamide might be associated with colorectal cancer with specific somatic mutations, differentially in men and women. More research is needed to corroborate or refute these findings.
In 1994, acrylamide (AA) was classified as a probable human carcinogen by the International Agency for Research on Cancer. In 2002, AA was discovered at relatively high concentrations in some starchy, plant-based foods cooked at high temperatures.
A prospective analysis was conducted to evaluate the association between the dietary intake of AA and ductal adenocarcinoma of the exocrine pancreatic cancer (PC) risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort using Cox regression modeling. EPIC includes >500 000 men and women aged 35-75 at enrollment from 10 European countries. AA intake was estimated for each participant by combining questionnaire-based food consumption data with a harmonized AA database derived from the EU monitoring database of AA levels in foods, and evaluated in quintiles and continuously.
After a mean follow-up of 11 years, 865 first incident adenocarcinomas of the exocrine pancreas were observed and included in the present analysis. At baseline, the mean dietary AA intake in EPIC was 26.22 µg/day. No overall association was found between continuous or quintiles of dietary AA intake and PC risk in EPIC (HR:0.95, 95%CI:0.89-1.01 per 10 µg/day). There was no effect measure modification by smoking status, sex, diabetes, alcohol intake or geographic region. However, there was an inverse association (HR: 0.73, 95% CI: 0.61-0.88 per 10 µg/day) between AA intake and PC risk in obese persons as defined using the body mass index (BMI, ≥30 kg/m(2)), but not when body fatness was defined using waist and hip circumference or their ratio.
Dietary intake of AA was not associated with an increased risk of PC in the EPIC cohort.
Because of the pressure for timely, informed decisions in public health and clinical practice and the explosion of information in the scientific literature, research results must be synthesized. Meta-analyses are increasingly used to address this problem, and they often evaluate observational studies. A workshop was held in Atlanta, Ga, in April 1997, to examine the reporting of meta-analyses of observational studies and to make recommendations to aid authors, reviewers, editors, and readers.
Twenty-seven participants were selected by a steering committee, based on expertise in clinical practice, trials, statistics, epidemiology, social sciences, and biomedical editing. Deliberations of the workshop were open to other interested scientists. Funding for this activity was provided by the Centers for Disease Control and Prevention.
We conducted a systematic review of the published literature on the conduct and reporting of meta-analyses in observational studies using MEDLINE, Educational Research Information Center (ERIC), PsycLIT, and the Current Index to Statistics. We also examined reference lists of the 32 studies retrieved and contacted experts in the field. Participants were assigned to small-group discussions on the subjects of bias, searching and abstracting, heterogeneity, study categorization, and statistical methods.
From the material presented at the workshop, the authors developed a checklist summarizing recommendations for reporting meta-analyses of observational studies. The checklist and supporting evidence were circulated to all conference attendees and additional experts. All suggestions for revisions were addressed.
The proposed checklist contains specifications for reporting of meta-analyses of observational studies in epidemiology, including background, search strategy, methods, results, discussion, and conclusion. Use of the checklist should improve the usefulness of meta-analyses for authors, reviewers, editors, readers, and decision makers. An evaluation plan is suggested and research areas are explored.
Background:
Acrylamide is a probable human carcinogen formed during cooking of starchy foods. Two large prospective cohort studies of dietary acrylamide intake and ovarian cancer risk observed a positive association, although two other studies reported no association.
Methods:
We measured acrylamide exposure using red blood cell acrylamide and glycidamide hemoglobin adducts among women in two large prospective cohorts: the Nurses' Health Study and Nurses' Health Study II. Between blood collection and 2010, we identified 263 incident cases of epithelial ovarian cancer, matching two controls per case. We used logistic regression models to examine the association between acrylamide exposure and ovarian cancer risk, adjusting for matching factors, family history of ovarian cancer, tubal ligation, oral contraceptive use, body mass index, parity, alcohol intake, smoking, physical activity, and caffeine intake.
Results:
The multivariate-adjusted relative risk (RR) of ovarian cancer comparing the highest versus lowest tertile of total acrylamide adducts was 0.79 (95% CI, 0.50-1.24, P trend = 0.08). The comparable RR of ovarian cancer among non-smokers at blood draw was 0.85 (95% CI, 0.57-1.27, P trend = 0.14). The association did not differ by tumor histology (serous invasive versus not), P for heterogeneity = 0.86. Individual adduct types (acrylamide or glycidamide) were not associated with risk.
Conclusions:
We observed no evidence that acrylamide exposure as measured by adducts to hemoglobin is associated with an increased risk of ovarian cancer.
Impact:
Our finding indicates that acrylamide intake may not increase risk of ovarian cancer.
Acrylamide, a probable human carcinogen, is present in many everyday foods. Since the finding of its presence in foods in 2002, epidemiological studies have found some suggestive associations between dietary acrylamide exposure and the risk of various cancers. The aim of this prospective study is to investigate for the first time the association between dietary acrylamide intake and the risk of several histological subtypes of lymphatic malignancies.
The Netherlands Cohort Study on diet and cancer includes 120,852 men and women followed-up since September 1986. The number of person years at risk was estimated by using a random sample of participants from the total cohort that was chosen at baseline (n =5,000). Acrylamide intake was estimated from a food frequency questionnaire combined with acrylamide data for Dutch foods. Hazard ratios (HRs) were calculated for acrylamide intake as a continuous variable as well as in categories (quintiles and tertiles), for men and women separately and for never-smokers, using multivariable-adjusted Cox proportional hazards models.
After 16.3 years of follow-up, 1,233 microscopically confirmed cases of lymphatic malignancies were available for multivariable-adjusted analysis. For multiple myeloma and follicular lymphoma, HRs for men were 1.14 (95% CI: 1.01, 1.27) and 1.28 (95% CI: 1.03, 1.61) per 10 µg acrylamide/day increment, respectively. For never-smoking men, the HR for multiple myeloma was 1.98 (95% CI: 1.38, 2.85). No associations were observed for women.
We found indications that acrylamide may increase the risk of multiple myeloma and follicular lymphoma in men. This is the first epidemiological study to investigate the association between dietary acrylamide intake and the risk of lymphatic malignancies, and more research into these observed associations is warranted.
Conjectured associations between dietary acrylamide intake and cancer have been evaluated in more than 15 epidemiologic studies examining almost every major cancer site. We have critically reviewed the epidemiologic studies of estimated dietary acrylamide exposure and cancer. As substantially greater acrylamide exposure occurs through tobacco smoke than dietary exposure, we present the results separately for never smokers or adjusted statistically for smoking status, where possible. After an extensive examination of the published literature, we found no consistent or credible evidence that dietary acrylamide increases the risk of any type of cancer in humans, either overall or among nonsmokers. In particular, the collective evidence suggests that a high level of dietary acrylamide intake is not a risk factor for breast, endometrial, or ovarian cancers, which have generated particular interest because of a conjectured hormonal mechanism of acrylamide. Moreover, the absence of a positive association between smoking and ovarian and endometrial cancers suggests that any association of these cancers with the much lower, more sporadic dietary acrylamide intake is unlikely. In conclusion, epidemiologic studies of dietary acrylamide intake have failed to demonstrate an increased risk of cancer. In fact, the sporadically and slightly increased and decreased risk ratios reported in more than two dozen papers examined in this review strongly suggest the pattern one would expect to find for a true null association over the course of a series of trials. Therefore, continued epidemiologic investigation of acrylamide and cancer risk appears to be a misguided research priority.
Information on the relation between acrylamide exposure and risk of pancreatic cancer is scanty and inconsistent.
We investigated the issue in a case-control study conducted from 1991 to 2008 in Northern Italy. Cases were 326 patients with incident pancreatic cancer, admitted to major teaching and general hospitals. Controls were 652 subjects admitted to the same hospitals with acute non-neoplastic conditions. Acrylamide mean content of various food items was derived from international databases and Italian sources. Odds ratios (ORs) and 95% confidence intervals (CIs) of pancreatic cancer were derived using conditional logistic regression adjusted for several covariates, including energy intake.
The ORs of pancreatic cancer for subsequent quintiles of acrylamide intake, as compared with the lowest one, were 1.48 (95% CI 0.88-2.50), 1.57 (95% CI 0.91-2.69), 1.70 (95% CI 0.98-2.96) and 1.49 (95% CI 0.83-2.70), with no trend in risk (P value 0.21). The OR for an increase in acrylamide intake of 10 μg/day was 1.01 (95% CI 0.92-1.10). No meaningful difference between ORs was found in strata of smoking habit, alcohol drinking, body mass index and other selected covariates.
This study found no association between dietary acrylamide and pancreatic cancer in an Italian population.
Acrylamide has been associated to cancer risk in rodents, but data on humans are inconclusive. We thus carried out a critical review and meta-analysis of studies of exposure to acrylamide and cancer.
We identified 586 publications, 25 presented relevant results. We conducted meta-analyses of studies of dietary intake based on random-effects models by calculating pooled relative risks (RR) and the corresponding 95% confidence intervals (CI). We combined results of occupational studies according to a fixed-effect model.
The summary RRs for an increase of 10 μg/day of acrylamide intake were close to unity for all the cancers considered, ranging from 0.98 for esophageal cancer to 1.01 for colon, endometrial, ovarian and kidney cancer. None of the estimates was significant. Exclusion of one case-control study from Sweden resulted in a summary RR of kidney cancer of 1.04 (95% CI 1.00-1.08). The combined standardized mortality ratios for high occupational exposure were 1.67 (95% CI 0.83-2.99) for pancreatic cancer and 2.22 (95% CI 0.81-4.84) for kidney cancer.
Available studies consistently suggest a lack of an increased risk of most types of cancer from exposure to acrylamide. The main association that requires further monitoring involves kidney cancer.
No studies to date have demonstrated a clear association with breast cancer risk and dietary exposure to acrylamide.Methods:A 217-item food frequency questionnaire was used to estimate dietary acrylamide intake in 33,731 women aged 35-69 years from the UK Women's Cohort Study followed up for a median of 11 years.
In all, 1084 incident breast cancers occurred during follow-up. There was no evidence of an overall association between acrylamide intake and breast cancer (hazard ratio=1.08 per 10 μg day(-1), 95% CI: 0.98-1.18, P(trend)=0.1). There was a suggestion of a possible weak positive association between dietary acrylamide intake and premenopausal breast cancer after adjustment for potential confounders (hazard ratio=1.2, 95% CI: 1.0-1.3, P(trend)=0.008). There was no suggestion of any association for postmenopausal breast cancer (hazard ratio=1.0, 95% CI: 0.9-1.1, P(trend)=0.99).
There is no evidence of an association between dietary acrylamide intake and breast cancer. A weak association may exist with premenopausal breast cancer, but requires further investigation.
The BJC is owned by Cancer Research UK, a charity dedicated to understanding the causes, prevention and treatment of cancer and to making sure that the best new treatments reach patients in the clinic as quickly as possible. The journal reflects these aims. It was founded more than fifty years ago and, from the start, its far-sighted mission was to encourage communication of the very best cancer research from laboratories and clinics in all countries. The breadth of its coverage, its editorial independence and it consistent high standards, have made BJC one of the world's premier general cancer journals. Its increasing popularity is reflected by a steadily rising impact factor.
To assess the association between dietary acrylamide intake and the risk of cancer among male smokers.
The study consisted of 27,111 male smokers, aged 50-69 years, without history of cancer. They were participants of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study in Finland. The men completed a validated dietary questionnaire and a questionnaire on general background characteristics (including smoking habits) at baseline. Incident cases of cancer were identified through the national Finnish Cancer Registry.
During an average 10.2 year follow-up, 1,703 lung cancers, 799 prostate cancers, 365 urothelial cancers, 316 colorectal cancers, 224 stomach cancers, 192 pancreatic cancers, 184 renal cell cancers, and 175 lymphomas were diagnosed. Dietary acrylamide intake was positively associated with the risk of lung cancer; relative risk (RR) in the highest versus the lowest quintile in the multivariable-adjusted model was 1.18 ((95% confidence interval (CI) 1.01-1.38, p for trend 0.11). Other cancers were not associated with acrylamide intake.
High acrylamide intake is associated with increased risk of lung cancer but not with other cancers in male smokers.
Acrylamide is a probable human carcinogen formed during cooking of many common foods. Epidemiologic studies on acrylamide and breast cancer risk have been null; however, positive associations with ovarian and endometrial cancers have been reported. We studied acrylamide intake and risk for breast, endometrial, and ovarian cancers in a prospective cohort study.
We assessed acrylamide intake among 88,672 women in the Nurses' Health Study using food frequency questionnaires administered every 4 years. Between 1980 and 2006, we identified 6,301 cases of invasive breast cancer, 484 cases of invasive endometrial adenocarcinoma, and 416 cases of epithelial ovarian cancer. We used Cox proportional hazards models to study the association between acrylamide and cancer risk.
We found no association between acrylamide intake and breast cancer overall or according to estrogen and progesterone receptor status. We found an increased risk for endometrial cancer among high acrylamide consumers (adjusted relative risk for highest versus lowest quintile = 1.41; 95% CI, 1.01-1.97; P for trend = 0.03). We observed a nonsignificant suggestion of increased risk for ovarian cancer overall (relative risk, 1.25; 95% CI, 0.88-1.77; P trend = 0.12), with a significantly increased risk for serous tumors (relative risk, 1.58; 95% CI, 0.99-2.52; P trend = 0.04). Associations did not differ by smoking status.
We observed no association between acrylamide and breast cancer. Risk for endometrial cancer and possibly ovarian cancer was greater among high acrylamide consumers.
This is the second prospective study to report positive associations with endometrial and ovarian cancers. These associations should be further evaluated to inform public health policy.
Acrylamide, a potential human carcinogen, has been discovered in a variety of heat-treated carbohydrate-rich food products. Previously, dietary acrylamide intake was shown to be associated with endocrine-related cancers in humans. We assessed the association between dietary acrylamide intake and risk of postmenopausal breast cancer stratified by estrogen and progesterone receptor status. This study was embedded within the Netherlands Cohort Study on diet and cancer, which was initiated in 1986 enrolling 62,573 women aged 55–69 years at baseline. After 13.3 years of follow-up, 2225 incident breast cancer cases were ascertained, with hormone receptor status information for 43%. Cox proportional hazards analysis was applied to determine hazard ratios in quintiles of dietary acrylamide intake stratifying on estrogen receptor (ER) and progesterone receptor (PR) and smoking status. No association was observed for overall breast cancer or receptor-negative breast cancer risk, irrespective of smoking status. A statistically non-significantly increased risk of ER positive, PR positive and joint receptor-positive breast cancer was found in never-smoking women. The multivariable-adjusted hazard ratios were 1.31 (95% CI: 0.87–1.97, P
trend = 0.26) for ER+, 1.47 (0.86–2.51, P
trend = 0.14) for PR+, and 1.43 (0.83–2.46, P
trend = 0.16) for ER+PR+, when comparing women in the highest quintile of acrylamide intake (median 36.8 μg/day) to women in the lowest (median 9.5 μg/day). This study showed some indications of a positive association between dietary acrylamide intake and receptor-positive breast cancer risk in postmenopausal never-smoking women. Further studies are needed to confirm or refute our observations.
Acrylamide exposure has been related to an increased incidence of oral and thyroid tumors in animal studies. In 1986, 120,852 persons (aged 55-69 years) were included in the Netherlands Cohort Study. Dietary acrylamide intake was assessed with a food frequency questionnaire and was based on chemical analysis of all relevant Dutch foods. Hazard ratios were adjusted for smoking and other confounders. After 16.3 years of follow-up, there were 101, 83, 180, and 66 cases of oral cavity, oro-hypopharynx, larynx, and thyroid cancer, respectively. Average daily dietary acrylamide intake was 21.8 microg (standard deviation, 12.1). Dietary acrylamide intake was not associated with increased risk of oral cavity (hazard ratio (HR) per 10-microg intake/day = 0.90, 95% confidence interval (CI): 0.73, 1.10), oro-hypopharynx (HR = 0.74, 95% CI: 0.53, 1.03), larynx (HR = 1.05, 95% CI: 0.91, 1.21), or thyroid (HR = 1.03, 95% CI: 0.82, 1.27) cancer. For nonsmokers, hazard ratios were not increased either. Dietary acrylamide was statistically significantly associated with increased risk of oral cavity cancer in female nonsmokers, but case numbers were small. Dietary acrylamide intake was not positively associated with risk of head-neck and thyroid cancer, except with oral cavity cancer risk for female nonsmokers. A negative association for males was indicated.
Acrylamide is a probable human carcinogen that is present in several heat-treated foods. In epidemiological studies, positive associations between dietary acrylamide intake and the risks of endometrial, ovarian, estrogen receptor-positive breast, and renal cell cancers have been observed. The association between dietary acrylamide intake and lung cancer risk is not known.
We conducted a case-cohort study among 58 279 men and 62 573 women (aged 55-69 years) in the Netherlands Cohort Study on Diet and Cancer. Intakes of acrylamide-containing foods and risk factors for cancer were assessed with a self-administered questionnaire at baseline in 1986 and combined with acrylamide levels in relevant Dutch foods to assess total dietary acrylamide intake. The number of person-years at risk was estimated by using a random sample of participants from the total cohort that was chosen at baseline (n = 5000). Incident lung cancer cases in the total cohort were detected by computerized record linkages to the Netherlands Cancer Registry and the Netherlands Pathology Registry. Hazard ratios and 95% confidence intervals (CIs) for the risk of lung cancer associated with acrylamide intakes were estimated using Cox proportional hazards models that controlled for smoking (status, quantity, and duration) and other lung cancer risk factors. All statistical tests were two-sided.
After 13.3 years of follow-up (September 17, 1986 up to January 1, 2000) there were 2649 cases of primary, histologically verified lung cancer (International Classification of Diseases for Oncology-3 code: C34) when cases with prevalent cancer at baseline (other than skin cancer) were excluded. The multivariable-adjusted hazard ratio of lung cancer for a 10-microg/d increment of acrylamide intake was 1.03 (95% CI = 0.96 to 1.11) for men and 0.82 (95% CI = 0.69 to 0.96) for women. The hazard ratio of lung cancer for the highest (median intake [microg/d]: men = 37.6 and women = 36.8) vs the lowest (median intake [microg/d]: men = 10.8 and women = 9.5) quintile of acrylamide intake was 1.03 (95% CI = 0.77 to 1.39, P(trend) = .85) for men and 0.45 (95% CI = 0.27 to 0.76, P(trend) = .01) for women. The inverse association in women was strongest for adenocarcinoma (hazard ratio for highest vs lowest tertile of intake = 0.40, 95% CI = 0.21 to 0.78; P(trend) = .01).
Acrylamide intake was not associated with lung cancer risk in men but was inversely associated in women, most strongly for adenocarcinoma. This finding suggests that acrylamide is involved in human carcinogenesis through pathways other than genotoxicity.
Acrylamide is a probable human carcinogen, which is present in several heat-treated foods. In epidemiologic studies, positive associations with endometrial, ovarian, and renal cell cancer risk have been observed. The incidence of central nervous system tumors was increased upon acrylamide administration in drinking water to rats. In the current study, the association between dietary acrylamide intake and human brain cancer risk was investigated for the first time.
In 1986, 120,852 persons (ages 55-69 years) were included in the Netherlands Cohort Study on diet and cancer. At baseline, a random subcohort of 5,000 participants was randomly selected from the total cohort for a case-cohort approach. Acrylamide intake was assessed with a food frequency questionnaire at baseline and based on acrylamide analyses in relevant Dutch foods. Hazard ratios (HR) were calculated using Cox proportional hazards analysis. Subgroup analyses were done for microscopically verified brain cancer, astrocytic gliomas, high-grade astrocytic gliomas, and never-smokers. The acrylamide risk estimates were adjusted for possible brain cancer risk factors.
After 16.3 years of follow-up, 216 brain cancer cases were available for analysis. The multivariable-adjusted HR per 10 microg/d increment of acrylamide intake was 1.02 (95% confidence interval, 0.89-1.16). HRs were not significantly increased either when dietary acrylamide intake was analyzed as a categorical variable. Also, there was no association in the subgroups based on histology and smoking.
In this prospective cohort study, acrylamide intake was not associated with brain cancer risk.
Acrylamide, a probable human carcinogen, is formed during high-temperature cooking of many commonly consumed foods. It is widespread; approximately 30% of calories consumed in the United States are from foods containing acrylamide. In animal studies, acrylamide causes mammary tumors, but it is unknown whether the level of acrylamide in foods affects human breast cancer risk. The authors studied the association between acrylamide intake and breast cancer risk among 90,628 premenopausal women in the Nurses' Health Study II. They calculated acrylamide intake from food frequency questionnaires in 1991, 1995, 1999, and 2003. From 1991 through 2005, they documented 1,179 cases of invasive breast cancer. They used Cox proportional hazards models to assess the association between acrylamide and breast cancer risk. The multivariable-adjusted relative risk of premenopausal breast cancer was 0.92 (95% confidence interval: 0.76, 1.11) for the highest versus the lowest quintile of acrylamide intake (P(trend) = 0.61). Results were similar regardless of smoking status or estrogen and progesterone receptor status of the tumors. The authors found no associations between intakes of foods high in acrylamide, including French fries, coffee, cereal, potato chips, potatoes, and baked goods, and breast cancer risk. They found no evidence that acrylamide intake, within the range of US diets, is associated with increased risk of premenopausal breast cancer.
The association between dietary acrylamide intake and the incidence of invasive breast cancer was examined among 61,433 Swedish women who were cancer free and completed a food frequency questionnaire in 1987-1990 and again in 1997. During a mean follow-up of 17.4 years, a total of 2,952 incident cases of breast cancer were diagnosed in the cohort. In multivariate analyses controlling for breast cancer risk factors, no statistically significant association was observed between long-term acrylamide intake (assessed at baseline and in 1997) and the risk of breast cancer, overall or by estrogen receptor (ER) and progesterone receptor (PR) status. The multivariate rate ratios comparing extreme quartiles of acrylamide intake were 0.91 (95% confidence interval (CI): 0.80, 1.02) for overall breast cancer, 0.89 (95% CI: 0.74, 1.08) for ER+PR+ tumors, 1.17 (95% CI: 0.84, 1.64) for ER+PR- tumors, and 0.91 (95% CI: 0.61, 1.38) for ER-PR- tumors. The association between acrylamide intake and breast cancer risk did not differ by smoking status. These findings for Swedish women do not support the hypothesis that dietary acrylamide is positively associated with risk of breast cancer, at least not within the ranges of acrylamide consumed by this population.
Acrylamide is a probable human carcinogen that was detected in several heat-treated foods, such as French fries and crisps, in 2002. Prospective studies are needed on acrylamide and human cancer risk. We prospectively investigated the association between acrylamide and gastrointestinal cancer risk. In 1986, 120,852 men and women (aged 55-69 y) were included in the Netherlands Cohort Study on diet and cancer. At baseline, a random subcohort of 5000 participants was selected for a case-cohort approach. Acrylamide intake was assessed with a FFQ at baseline and was based on acrylamide analyses in relevant Dutch foods. After 13.3 y of follow-up, 2190, 563, 349, and 216 cases of colorectal, gastric, pancreatic, and esophageal cancer, respectively, were available for analysis. The daily acrylamide intake of the subcohort was (mean +/- SD) 21.7 +/- 12.1 microg. A 10-microg/d increment of acrylamide intake was associated with multivariable-adjusted Cox proportional hazard rate ratios (HR) (95% CI) of 1.00 (0.96-1.06), 1.02 (0.94-1.10), 1.06 (0.96-1.17), and 0.96 (0.85-1.09) for colorectal, gastric, pancreatic, and esophageal cancer, respectively. For former or never-smokers, the corresponding HR were: 1.03 (0.94-1.12), 1.09 (0.98-1.22), 1.07 (0.93-1.24), and 0.92 (0.76-1.11). There were some significantly increased risks within subgroups stratified by obesity, nonoccupational physical activity, and age, factors that were a priori selected based on their capacity to modify cytochrome P4502E1 activity. Overall, acrylamide intake was not associated with colorectal, gastric, pancreatic, and esophageal cancer risk, but some subgroups deserve further attention.
Male and female Fischer 344 rats were maintained on treated drinking water providing dosages of 0 (controls), 0.01, 0.1, 0.5, or 2.0 mg acrylamide/kg body wt/day for 2 years to assess the chronic toxicity and oncogenic potential of the chemical. The mean body weights of male and female rats receiving 2.0 mg/kg/day and of male rats receiving 0.5 mg/kg/day were minimally decreased when compared with controls. During the last 4 months of the study, there was an increase in mortality among male and female rats receiving 2.0 mg/kg/day. A target organ effect, characterized by degeneration of peripheral nerves, was observed in rats receiving 2.0 mg/kg/day. The incidence of several tumor types was increased in the rats receiving 2.0 mg/kg/day when compared with controls. In females, increased tumor incidences were observed in the mammary gland, central nervous system, thyroid gland-follicular epithelium, oral tissues, uterus, and clitoral gland. In males the incidence of tumors of the thyroid gland-follicular epithelium and scrotal mesothelium was increased. Male rats receiving 2.0 mg/kg/day also had increased incidence of central nervous system tumors when compared to historical controls but not when compared to concurrent controls. The only tumor incidence which was significantly increased at the 0.5 mg/kg/day level was scrotal mesothelioma. There was no statistically significant increase of any tumor type at the 0.1 or 0.01 mg/kg/day dose levels. However, the incidence of scrotal mesothelioma at the 0.1 mg/kg/day level was greater than that observed in the control group or historically reported in this laboratory.
Recently, disturbingly high levels of acrylamide were unexpectedly detected in widely consumed food items, notably French fries, potato crisps, and bread. Much international public concern arose since acrylamide has been classified as a probable carcinogen, although based chiefly on laboratory evidence; informative human data are largely lacking. We reanalysed a population-based Swedish case-control study encompassing cases with cancer of the large bowel (N=591), bladder (N=263) and kidney (N=133), and 538 healthy controls, assessing dietary acrylamide by linking extensive food frequency data with acrylamide levels in certain food items recorded by the Swedish National Food Administration. Unconditional logistic regression was used to estimate odds ratios, adjusting for potential confounders. We found consistently a lack of an excess risk, or any convincing trend, of cancer of the bowel, bladder, or kidney in high consumers of 14 different food items with a high (range 300-1200 microg kg(-1)) or moderate (range 30-299 microg kg(-1)) acrylamide content. Likewise, when we analysed quartiles of known dietary acrylamide intake, no association was found with cancer of the bladder or kidney. Unexpectedly, an inverse trend was found for large bowel cancer (P for trend 0.01) with a 40% reduced risk in the highest compared to lowest quartile. We found reassuring evidence that dietary exposure to acrylamide in amounts typically ingested by Swedish adults in certain foods has no measurable impact on risk of three major types of cancer. It should be noted, however, that relation of risk to the acrylamide content of all foods could not be studied.
The BJC is owned by Cancer Research UK, a charity dedicated to understanding the causes, prevention and treatment of cancer and to making sure that the best new treatments reach patients in the clinic as quickly as possible. The journal reflects these aims. It was founded more than fifty years ago and, from the start, its far-sighted mission was to encourage communication of the very best cancer research from laboratories and clinics in all countries. The breadth of its coverage, its editorial independence and it consistent high standards, have made BJC one of the world's premier general cancer journals. Its increasing popularity is reflected by a steadily rising impact factor.
The fact that acrylamide, a proven rodent carcinogen, is present in significant quantities (up to several mg/kg of foodstuff)
in a wide range of commonly consumed human foods is alarming. Attempts to determine a possible involvement of dietary acrylamide
in human cancers have not been conclusive, however. To resolve the carcinogenicity of acrylamide to humans, the as yet unknown
mechanism of action of acrylamide needs to be unraveled. The present review is a synopsis of research on the known and hypothetical
modes of action of acrylamide of relevance for carcinogenesis. Both genotoxic and non-genotoxic modes of action of acrylamide
are discussed with special emphasis on DNA adduct-targeted mutagenesis. Mechanistic data are presented from various experimental
systems including in vitro experiments and in vivo rodent and human studies with special focus on mouse models. Human exposure data, including estimates of daily intake of
dietary acrylamide in different populations and the corresponding cancer risk assessments are provided. The significant gaps
in knowledge, which currently preclude a more definitive evaluation of human cancer risk due to exposure to dietary acrylamide,
are highlighted. Future directions for research on acrylamide and cancer are outlined, and potential challenges are underscored.
The third edition of this book reviews the global burden of cancer, causes of cancer, and current priorities and future directions in cancer epidemiology and prevention research. The book maintains the structure of previous editions with seventy-two chapters organized into five major sections: Basic Concepts; The Magnitude of Cancer; The Causes of Cancer; Cancer by Tissue of Origin, and Cancer Prevention and Control. The introductory chapters under Basic Concepts highlight the advances in genomic and molecular biology that have applications in morphologic classification of malignant tumors, and in the elucidation of critical genetic events that result in malignant transformation and tumor invasion. The section on the Magnitude of Cancer reviews global patterns of cancer incidence and mortality in relation to country of residence, age, gender, race and ethnicity, and socioeconomic status. The section on The Causes of Cancer reviews the spectrum of environmental, lifestyle and genetic risk factors that are associated with the origin of human cancers. Chapters on Cancer by Tissue of Origin review systematically the demographic, environmental, and host factors that impact the origin and progression of cell-and organ-specific neoplasms. The concluding section, Cancer Prevention and Control, addresses methods and applications for translating epidemiologic, laboratory, and clinical research observations into preventive interventions. Special emphasis is provided on measuring the impact of behavioral interventions on health-promoting practices, as well as governmental policies that regulate environmental carcinogens.
This paper presents a command, glst, for trend estimation across different exposure levels for either single or multiple summarized case-control, incidence-rate, and cumulative incidence data. This approach is based on constructing an approximate covariance estimate for the log relative risks and estimating a corrected linear trend using generalized least squares. For trend analysis of multiple studies, glst can estimate fixed- and random-effects metaregression models. Copyright 2006 by StataCorp LP.
