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Advisory Group recommendations on priorities for the IARC Monographs
... However, the WHO International Agency for Research on Cancer (IARC) Monographs programme, which identifies potential carcinogenic hazards, has not evaluated aspartame to date. A recent report of the IARC priorities advisory group [2,3] notes that while previous epidemiologic studies did not typically find an association between aspartame intake and cancer risk, some new studies have suggested the possibility of a link. Among them, a prospective study of hematologic malignancies found a positive association with multiple myeloma and non-Hodgkin lymphoma in men [4]. ...
... Mechanistic studies relevant to the key characteristics of carcinogens have also been carried out (e.g., [9][10][11]). For these reasons, the IARC priorities advisory group recommended aspartame as a high priority for evaluation [2,3]. In addition to IARC, JECFA has also recommended aspartame as a high-priority substance for re-evaluation [12]. ...
Citation: Schorb, S.; Gleiss, K.; Wedekind, R.; Suonio, E.; Kull, A.-K.; Kuntz, M.; Walch, S.G.; Lachenmeier, D.W. Assessment of Aspartame (E951) Occurrence in Selected Foods and Abstract: This study examines the occurrence of the artificial sweetener aspartame (E951) in foods and beverages sampled by food control authorities in Germany between 2000 and 2022. The dataset was obtained through the Consumer Information Act. Out of 53,116 samples analyzed, aspartame was present in 7331 samples (14%), of which 5703 samples (11%) in nine major food groups were further evaluated. The results showed that aspartame was most commonly found in powdered drink bases (84%), flavored milk drinks (78%), chewing gum (77%), and diet soft drinks (72%). In the solid food groups, the highest mean aspartame content was detected in chewing gum (1543 mg/kg, n = 241), followed by sports foods (1453 mg/kg, n = 125), fiber supplements (1248 mg/kg, n = 11), powdered drink bases (1068 mg/kg, n = 162), and candies (437 mg/kg, n = 339). Liquid products generally had the highest aspartame content in diet soft drinks (91 mg/L, n = 2021), followed by regular soft drinks (59 mg/L, n = 574), flavored milk drinks (48 mg/kg, n = 207), and mixed beer drinks (24 mg/L, n = 40). These results suggest that aspartame is commonly used in some foods and beverages in Germany. The levels of aspartame found were generally within the legal limits set by the European Union. These findings provide the first comprehensive overview of aspartame in the German food market and may be particularly useful in informing the forthcoming working groups of the WHO International Agency for Research on Cancer (IARC) and the WHO/FAO Joint Expert Committee on Food Additives (JECFA), which are in the process of evaluating the human health hazards and risks associated with the consumption of aspartame.
... Although their use has been progressively limited and banned in Europe during the 90 s, due to their resistance to degradation, PBDE and PBB are widespread in the environment [1]. The long-term toxic effects of PBDE and PBB in humans are not completely elucidated, but they are known to have endocrine disrupting properties and in 2019 PBDE have been included in the high-priority list of agents not previously evaluated by the International Agency for Research on Cancer (IARC) Monographs based on relevant bioassay and mechanistic studies [2,3]. ...
... PFAS are characterized by long half-lives in the biota and humans and biomonitoring studies have suggested that PFOA and PFOS, the two main PFAS representatives, are ubiquitously present in the blood of humans worldwide [5]. PFAS are strongly suspected to act as endocrine disrupting chemicals (EDCs), and PFOA has been classified by the IARC as "possibly carcinogenic to humans" (Group 2B) [3,6]. ...
Background
Brominated flame retardants (BFR) and per- and polyfluorinated alkylated substances (PFAS) are two groups of substances suspected to act as endocrine disruptors. Such substances could therefore be implicated in the occurrence of breast cancer, nevertheless, previous studies have led to inconstant results. Due to the large correlation between these substances, and the possibly non-linear effects they exert, evaluating their joint impact as mixtures on health remains challenging.
This exploratory study aimed to generate hypotheses on the relationship between circulating levels of 7 BFR (6 polybrominated diphenyl ethers and 1 polybrominated biphenyls) and 11 PFAS and the risk of breast cancer in a case–control study nested in the E3N French prospective cohort by performing two methods: Principal Component Regression (PCR) models, and Bayesian Kernel Machine Regression (BKMR) models.
Methods
194 post-menopausal breast cancer cases and 194 controls were included in the present study. Circulating levels of BFR and PFAS were measured by gas chromatography coupled to high-resolution mass spectrometry and liquid chromatography coupled to tandem mass spectrometry, respectively. The first statistical approach was based on Principal Component Analysis (PCA) followed by logistic regression models that included the identified principal components as main exposure variables. The second approach used BKMR models with hierarchical variable selection, this latter being suitable for highly correlated exposures. Both approaches were also run separately for Estrogen Receptor positive (ER +) and Estrogen Receptor negative (ER-) breast cancer cases.
Results
PCA identified four principal components accounting for 67% of the total variance. Component 3 showed a marginal association with ER + breast cancer risk. No clear association between BFR and PFAS mixtures and breast cancer was identified using BKMR models, and the credible intervals obtained were very wide. Finally, the BKMR models suggested a negative cumulative effect of BFR and PFAS on ER- breast cancer risk, and a positive cumulative effect on ER + breast cancer risk.
Conclusion
Although globally no clear association was identified, both approaches suggested a differential effect of BFR and PFAS mixtures on ER + and ER- breast cancer risk. However, the results for ER- breast cancer should be interpreted carefully due to the small number of ER- cases included in the study. Further studies evaluating mixtures of substances on larger study populations are needed.
... Aflatoxins such as AFB1, AFB2, AFG1, AFG2, and AFM1 are characterized as Group 1 carcinogens [85,86]. According to the IARC report, aflatoxins are annotated as mediumpriority agents with possible consideration for future evaluation regarding additional sites of cancer [176]. Several studies have confirmed the link between aflatoxins and increased risk of hepatic cancer. ...
... A bioassay in rats reported FB1 hepatotoxicity and hepato-carcinogenicity [187]. There is a recommendation for a high evaluation priority for FB1 due to substantial emerging information after the previous evaluation by the IARC Monographs [176]. There is evidence for ceramide synthase inhibition in individuals who consumed corn-based foods high in FB1 [188]. ...
Mycotoxins are well established toxic metabolic entities produced when fungi invade agricultural/farm produce, and this happens especially when the conditions are favourable. Exposure to mycotoxins can directly take place via the consumption of infected foods and feeds; humans can also be indirectly exposed from consuming animals fed with infected feeds. Among the hundreds of mycotoxins known to humans, around a handful have drawn the most concern because of their occurrence in food and severe effects on human health. The increasing public health importance of mycotoxins across human and livestock environments mandates the continued review of the relevant literature, especially with regard to understanding their toxicological mechanisms. In particular, our analysis of recently conducted reviews showed that the toxicological mechanisms of mycotoxins deserve additional attention to help provide enhanced understanding regarding this subject matter. For this reason, this current work reviewed the mycotoxins’ toxicological mechanisms involving humans, livestock, and their associated health concerns. In particular, we have deepened our understanding about how the mycotoxins’ toxicological mechanisms impact on the human cellular genome. Along with the significance of mycotoxin toxicities and their toxicological mechanisms, there are associated health concerns arising from exposures to these toxins, including DNA damage, kidney damage, DNA/RNA mutations, growth impairment in children, gene modifications, and immune impairment. More needs to be done to enhance the understanding regards the mechanisms underscoring the environmental implications of mycotoxins, which can be actualized via risk assessment studies into the conditions/factors facilitating mycotoxins’ toxicities.
... Every five years an international, Interdisciplinary Advisory Group recommends agents (i.e., chemical, physical, or biological entity or exposure circumstance) for review by the Monographs program. Cobalt and antimony compounds were listed as high and medium priority, respectively, by the Advisory Group on the Monograph priorities for 2020-2024 for further evaluation and were evaluated in 2022 (IARC, 2019a;Marques et al., 2019). Other agents of relevance to this chapter, such as welding fumes and indium tin oxide, were evaluated in 2017 (IARC, 2018). ...
Metals and their compounds are persistent in the environment and originate from multiple sources. Some metals are essential for the human body while others, such as cadmium and arsenic, are known carcinogens. Health effects associated with the acute or chronic inhalation of airborne metals remains an area of intense research interest, especially for mixtures. Inhalation is a primary route of exposure to metals and occurs in the workplace and in the environment. This chapter provides public health officials, physicians, toxicologists, and others with an overview of the major components involved in the respiratory toxicology of airborne metals. General health effects associated with metal inhalation, risk factors associated with environmental and occupational exposures, and pulmonary deposition and handling will be discussed.
... A working group has identified industrial agents considered high priority for evaluation by the IARC Monographs Program (Marques et al., 2019). Guided by these priorities, the study aimed to investigate the associations between childhood cancer and maternal residential exposure in pregnancy to three solvents (i.e., 1,1,1-TCA, PCE, carbon disulfide (CS 2 )) tracked in California by the Environmental Protection Agency's Toxics Release Inventory (TRI) program. ...
Background
Maternal solvent exposure has been suspected to increase offspring cancer risk. The study aimed to evaluate the associations between maternal residential exposure to solvents from industrial pollution during pregnancy and childhood cancer.
Methods
The present study included 15,744 cancer cases (aged 0–19 years at diagnosis) identified from California Cancer Registry and 283,141 controls randomly selected from California Birth Registry (20:1 frequency-matched by birth year: 1998–2016). We examined industrial releases of tetrachloroethylene and 1,1,1-trichloroethane within 3 km of the birth address, while we used a 5 km buffer for carbon disulfide. We calculated the total exposure from all linked Toxic Release Inventory sites during each index pregnancy and assigned “ever/never” and “high/low exposed/unexposed” exposure, using median values. We performed quadratic decay models to estimate cancer risks associated with maternal solvent exposure in pregnancy.
Results
1,1,1-Trichloroethane was associated with rhabdomyosarcoma (adjusted Odds Ratio (aOR): 1.96; 95% Confidence Interval (CI): 1.16, 3.32) in the “ever exposed” group. Ever exposure to carbon disulfide was associated with increased risks of medulloblastoma (OR = 1.85, 95% CI 1.01, 3.40) and ependymoma (OR = 1.63 95% CI 0.97, 2.74).
Conclusions
Overall, our findings suggested maternal residential exposure to solvents from industrial sources might be associated with elevated childhood cancer risks.
... IARC periodically convenes such advisory groups to ensure that the agents evaluated in the Monographs are selected on the basis of the latest scientific evidence relevant to carcinogenicity. 1 A detailed report of the Advisory Group recommendations will be published in due course. 2 The Advisory Group assessed the response to a public call for nominations and considered more than 200 candidate agents, including the recommended priority agents remaining from a similar Advisory Group meeting convened in 2019. 3 The Advisory Group comprised scientists with expertise across the spectrum of topics relevant to carcinogenicity. In drawing ...
In March, 2024, an Advisory Group of 28 independent scientists from 22 countries met in Lyon, France to recommend priorities for
carcinogenicity evaluations by the International Agency for Research on Cancer (IARC) Monographs programme during 2025–29. IARC periodically convenes such advisory groups to ensure that the agents evaluated in the Monographs are selected on the basis of the latest scientific evidence relevant to carcinogenicity.1 A detailed report of the Advisory Group recommendations will be published in due course.2 The Advisory Group assessed the response to a public call for nominations and considered more than 200 candidate agents, including
the recommended priority agents remaining from a similar Advisory Group meeting convened in 2019.3 The Advisory Group comprised scientists with expertise across the spectrum of topics relevant to carcinogenicity. In drawing heir conclusions, the members appraised, for each nominated agent, the evidence regarding human exposure, cancer in humans, cancer in
experimental animals, and carcinogen mechanisms according to precepts described in the Preamble to the IARC Monographs.1 Systematic literature searches were complemented by a text mining and database fusion approach to identify relevant studies, document the relative abundance of literature for the different evidence streams, and map chemical similarity4 in support of decisions on prioritisation for individual agents and groups of agents.
... Additionally, in this study, non-shared environmental factors accounted for 71% of the variation in susceptibility to nervous system tumors. These findings are in line with the general notion that nervous system tumors, similar to most neoplasms, are predominantly attributable to environmental factors and somatic aberrations (17,18). ...
Background
The contribution of genetic and environmental factors to susceptibility to nervous system tumors remains unclear. We performed a quantitative genetic study using a sibling design to estimate the heritability of nervous system tumors, as well as the proportion of the risk of these tumors, which is attributable to environmental factors.
Methods
We conducted a population-based cohort study using Swedish National Register data. All individuals born in Sweden during 1950–2010 with available information on both biological parents were included. A Multi-Generation Register was used to identify family clusters, including both full- and half-siblings. Initially, one index person was randomly selected from each cluster containing only full siblings and one sibling was randomly assigned to this index person. Subsequently, within each of the remaining clusters of full- and half-siblings, an index person was randomly selected, and a half-sibling was randomly assigned to this index person. Among the randomly selected siblings, cases of nervous system tumors were identified using the cancer registry. Quantitative genetic models were used to estimate the proportion of the variance in nervous system tumors attributable to additive genetic factors, shared environment, and individual-specific environment.
Results
The heritability of nervous system tumors was estimated to be 29% (95% confidence interval (CI) = 19%–39%), while the contribution of the non-shared environment to the variance of nervous system tumors was estimated to be 71% (95% CI = 61%–81%). The shared environmental parameter was estimated as zero in the full model.
Conclusion
The variation in susceptibility to nervous system tumors is predominantly attributable to non-shared environmental factors, followed by genetic factors.
... In addition, the working group discussed glyphosate (Group 2 A, probably carcinogenic to humans) [95]. Glyphosate is widely used in the region [96] and the subject of major debate; however, the IARC Advisory Group in 2019 indicated that there were no new studies of cancer in humans to conduct a new review of this pesticide [97]. Moving forward, it is essential to establish surveillance and monitoring systems for diseases associated with pesticide exposure in order to identify the magnitude of the problem and define evidence-based prevention policies and interventions [94]. ...
... Although a growing number of studies have investigated the relationship between PBDEs and cancer development, limited evidence exists to elucidate carcinogenic effects of most PBDEs both in animal and in human case-control epidemiological studies, except for decaBDE, for which the U.S. Environmental Protection Agency indicated "suggestive evidence of carcinogenic potential" in 2008. Recently, the PBDEs were included in the highpriority list of agents not previously evaluated by the International Agency for Research on Cancer (IARC) Monographs [96]. ...
Simple Summary
Endocrine disruptors are chemicals that can interfere and interact with the endocrine system, resulting in altered hormonal signaling and function. PBDEs are common endocrine disruptors that have been commonly used in industrial products, and their environmental accumulation has become a rising concern. Human exposure to PBDEs has been shown to influence glucose metabolism, thyroid and ovarian function and potentially affect cancer risk. Evidence, however, is often conflicting. This narrative review provides a comprehensive overview of the potential role of PBDEs in human health, with a particular focus on glucose metabolism, endocrine diseases and cancer. A deeper understanding of the complex interplay between exposure to endocrine disruptors, on one side, and obesity, diabetes, related metabolic disturbances and cancer, on the other side, can help guide public health interventions, in order to reduce the burden of these major social threats.
Abstract
There is increasing evidence of the role of endocrine disruptors (EDs) derived from commonly employed compounds for manufacturing and processing in altering hormonal signaling and function. Due to their prolonged half-life and persistence, EDs can usually be found not only in industrial products but also in households and in the environment, creating the premises for long-lasting exposure. Polybrominated diphenyl ethers (PBDEs) are common EDs used in industrial products such as flame retardants, and recent studies are increasingly showing that they may interfere with both metabolic and oncogenic pathways. In this article, a multidisciplinary panel of experts of the Italian Association of Medical Diabetologists (AMD), the Italian Society of Diabetology (SID), the Italian Association of Medical Oncology (AIOM), the Italian Society of Endocrinology (SIE) and the Italian Society of Pharmacology (SIF) provides a review on the potential role of PBDEs in human health and disease, exploring both molecular and clinical aspects and focusing on metabolic and oncogenic pathways.
... Such mycotoxins include an array of secondary metabolites such as deoxynivalenol (DON), fumonisins, T-2 toxin, zearalenone, aflatoxins, ochratoxins, and patulin etc. [2]. Their accumulation in agricultural crops, grain stores, and the environment more broadly remain associated with adverse health effect to animals as well as humans upon consumption or inhalation [3,4], most recently including links to cancer [5]. ...
Mycotoxins, derived from toxigenic fungi such as Fusarium, Aspergillus, and Penicillium species have impacted the human food chain for thousands of years. Deoxynivalenol (DON), is a tetracyclic sesquiterpenoid type B trichothecene mycotoxin predominantly produced by F. culmorum and F. graminearum during the infection of corn, wheat, oats, barley, and rice. Glycosylation of DON is a protective detoxification mechanism employed by plants. More recently, DON glycosylating activity has also been detected in fungal microparasitic (biocontrol) fungal organisms. Here we follow up on the reported conversion of 15-acetyl-DON (15-ADON) into 15-ADON-3-O-glycoside (15-ADON-3G) in Clonostachys rosea. Based on the hypothesis that the reaction is likely being carried out by a uridine diphosphate glycosyl transferase (UDP-GTase), we applied a protein structural comparison strategy, leveraging the availability of the crystal structure of rice Os70 to identify a subset of potential C. rosea UDP-GTases that might have activity against 15-ADON. Using CRISPR/Cas9 technology, we knocked out several of the selected UDP-GTases in the C. rosea strain ACM941. Evaluation of the impact of knockouts on the production of 15-ADON-3G in confrontation assays with F. graminearum revealed multiple UDP-GTase enzymes, each contributing partial activities. The relationship between these positive hits and other UDP-GTases in fungal and plant species is discussed.
... [12][13][14] On the basis of these cancer bioassays, an IARC advisory group recommended to give aspartame high priority for the International Agency for Research on Cancer (IARC) Monographs programme during 2020-2024. 15 In humans, a meta-analysis commissioned by the World Health Organisation (WHO) showed that overall, there was no association between AS intake and cancer incidence or mortality. 16 Results from this review (from 26 pooled case-control studies) indicate that high intake of AS, mostly coming from saccharin, might be linked to bladder cancer, although with high heterogeneity between studies. ...
Use of artificial sweeteners (AS) such as aspartame, cyclamate, saccharin and sucralose is widespread. We evaluated the association of use of aspartame and other AS with cancer. In total 1881 colorectal, 1510 breast, 972 prostate and 351 stomach cancer and 109 chronic lymphocytic leukaemia (CLL) cases and 3629 population controls from the Spanish Multicase‐Control (MCC‐Spain) study were recruited (2008‐2013). The consumption of AS, from table‐top sweeteners and artificially sweetened beverages, was assessed through a self‐administered and validated food frequency questionnaire (FFQ). Sex‐specific quartiles among controls were determined to compare moderate consumers (<third quartile) and high consumers (≥ third quartile) vs non consumers (reference category), distinguishing aspartame‐containing products and other AS. Unconditional logistic regression models were used to estimate adjusted OR and 95%CI, and results were stratified by diabetes status. Overall, we found no associations between the consumption of aspartame or other AS and cancer. Among participants with diabetes, high consumption of other AS was associated with colorectal cancer (OR = 1.58, 95% CI 1.05‐2.41, P trend = .03) and stomach cancer (OR = 2.27 [0.99‐5.44], P trend = .06). High consumption of aspartame, was associated with stomach cancer (OR = 2.04 [0.7‐5.4], P trend = .05), while a lower risk was observed for breast cancer (OR = 0.28 [0.08‐0.83], P trend = .03). In some cancers, the number of cases in participants with diabetes were small and results should be interpreted cautiously. We did not find associations between use of AS and cancer, but found associations between high consumption of aspartame and other AS and different cancer types among participants with diabetes.
... Consensus-building efforts have recently led to the publication of a set of "Recommendations for the conduct of systematic reviews in toxicology and environmental health research (COSTER)" [22]. Several SRs of cancer hazards from exposure to RF-EMF are in progress, promoted by the WHO [23] and other entities [24], including a planned re-evaluation of the carcinogenicity of RF-EMF by the IARC [25]. However, no epidemiological study has investigated cancer risks and how they relate to individual integrated exposure from multiple RF-EMF sources. ...
The evolution of emerging technologies that use Radio Frequency Electromagnetic Field (RF-EMF) has increased the interest of the scientific community and society regarding the possible adverse effects on human health and the environment. This article provides NextGEM’s vision to assure safety for EU citizens when employing existing and future EMF-based telecommunication technologies. This is accomplished by generating relevant knowledge that ascertains appropriate prevention and control/actuation actions regarding RF-EMF exposure in residential, public, and occupational settings. Fulfilling this vision, NextGEM commits to the need for a healthy living and working environment under safe RF-EMF exposure conditions that can be trusted by people and be in line with the regulations and laws developed by public authorities. NextGEM provides a framework for generating health-relevant scientific knowledge and data on new scenarios of exposure to RF-EMF in multiple frequency bands and developing and validating tools for evidence-based risk assessment. Finally, NextGEM’s Innovation and Knowledge Hub (NIKH) will offer a standardized way for European regulatory authorities and the scientific community to store and assess project outcomes and provide access to findable, accessible, interoperable, and reusable (FAIR) data.
... Although studies have revealed an elevated risk of SCEC in PD patients, they have significant limitations, including insufficient sample sizes and correction for potential confounders. Poor oral health, as demonstrated by PD and tooth loss/decay, is a potentially significant and controllable risk factor for changes in the oral microbiome, which may support the development of esophageal cancer (Marques et al., 2019). Numerous epidemiological studies have examined oral health as measured by tooth loss, DMFT score, periodontal health, and oral hygiene practices, including brushing, as risk factors for SCEC (Abnet et al., 2001;Brandilyn et al., 2017;Fitzpatrick and Katz, 2010;Lee et al., 2014). ...
Aim
The potential links between periodontal disease and various cancers have drawn more and more attention in recent years. The objective of the current study was to investigate any potential associations between parameters of periodontal disease, the number of teeth lost, and the risk of developing squamous cell esophageal cancer in a representative adult sample.
Materials and Methods
The study sample included 178 healthy individuals with matched age and socioeconomic status as controls and 60 patients with the primary histological type of esophageal cancer, Squamous Cell Esophageal Cancer. Data were collected from cases and controls on epidemiological factors like age, gender, smoking status, alcohol intake, socio-economic status, level of education, and prior medical/dental history. The clinical data on periodontal health status was obtained through a clinical examination. This data concerned Probing Pocket Depth (PPD), Clinical Attachment Loss (CAL), the number of teeth lost, and the common risk factors for Squamous Cell Esophageal Carcinoma. Additionally, univariate, and logistic regression models that were modified for potential confounders were used to estimate unadjacent and adjacent odds ratios (ORs) and 95% confidence intervals (CIs).
Results
Lower socioeconomic status (p = 0.048) (OR = 1.882, 95% CI = 0.987–3.591), smoking (p = 0.052) (OR = 1.768, 95% CI = 0.931–3.359), moderate and heavy alcohol abuse (p = 0.035) (OR = 1.880, 95% CI = 0.987 3.579), and irregular tooth brushing frequency (p = 0.001) (OR = 0.326, 95% CI = 0.171–0.619) were indeed discovered to be significantly linked.
Conclusion
Individuals with lower socio-economic status, smoking, moderate and heavy alcohol consumption, and irregular tooth brushing frequency were significantly associated with Periodontal diseases and Squamous Cell Esophageal Cancer.
... 1 These toxic secondary metabolites produced by filamentous fungi, such as Fusarium, Aspergillus, and Penicillium species, 2 have been documented to cause a range of adverse effects on human health, including genotoxicity and carcinogenicity. 3,4 Although mycotoxin regulation has been harshly established for agricultural products by most European countries, 5,6 there are still numerous kinds of marketed contaminated commodities that exceed the permitted limits for mycotoxins. 7 The phenomenon of mycotoxin contamination significantly impacts the economy and trade as a result of rejections of contaminated commodities. ...
Exposure to mycotoxins can pose a variety of adverse health effects to mammals. Despite dozens of mycotoxin decontamination strategies applied from pre- to postharvest stages, it is always challenging to guarantee a safe level of these natural toxic compounds in food and feedstuffs. In the context of the increased occurrence of drug-resistance strains of mycotoxin-producing fungi driven by the overuse of fungicides, the search for new natural-product-based solutions is a top priority. This review aims to shed a light on the promising potential of stilbenoids extracted from renewable agricultural wastes (e.g., grape canes and forestry byproducts) as antimycotoxin agents. Deeper insights into the mode of actions underlying the bioactivity of stilbenoid molecules against fungal pathogens, together with their roles in plant defense responses, are provided. Safety aspects of these natural compounds on humans and ecology are discussed. Perspectives on the development of stilbenoid-based formulations using encapsulation technology, which allows the bypassing of the limitations related to stilbenoids, particularly low aqueous solubility, are addressed. Optimistically, the knowledge gathered in the present review supports the use of currently underrated agricultural byproducts to produce stilbenoid-abundant extracts with a high efficiency in the mitigation of mycotoxins in food and feedstuffs.
... In 2019 an expert advisory group recommended the reclassification of RF by IARC (with high priority), based on newly available animal and mechanistic evidence [9]. RF-EMFs include the part of the electromagnetic spectrum comprising the frequency range from 100 kHz to 300 GHz and are used in medical diagnostics and therapy, in industry, domestic appliances, security and navigation, and especially in telecommunications [10]. ...
Low-frequency electromagnetic fields have grown exponentially in recent years due to technological development and modernization. The World Health Organization (WHO)/International Agency for Research on Cancer (IARC) has classified radiofrequency electromagnetic fields (RF-EMFs) as possibly carcinogenic to humans (Group 2B), and recent studies have investigated the association between exposure to electromagnetic fields in parents and possible health effects in children, especially the development of tumours of the central nervous system (CNS). The objective of this systematic review was to collate all evidence on the relationship between parental occupational exposure to electromagnetic fields and the development of CNS cancer in children and to evaluate this association. This review was prepared according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, Embase, and Web of Science were searched from January 1990 to April 2021. The search was conducted using the following search string: “occupational” AND “child” AND “electromagnetic” AND “cancer”. Seventeen articles met our inclusion criteria: 13 case-control studies, two cohort studies, and 2 meta-analyses. Most of the studies showed several methodological weaknesses that limited their results. Due to a lack of consistency regarding the outcome as well as the heterogeneity in the reviewed studies, the body of evidence for the effects of parental exposure to electromagnetic fields is not clear. Methodological heterogeneity in the way that studies were conducted could be responsible for the lack of consistency in the findings. Overall, the body of evidence allows no conclusion on the relationship between parental exposure to electromagnetic fields and the occurrence of CNS tumours in children.
... Since then, at least 3 systematic reviews have been published demonstrating a positive association between HPV and OAC together with a few studies addressing molecular and genomic signatures characteristic of these virally driven BD and OAC [26,34,35,40]. Unfortunately, the Advisory Group recommendations on priorities for the IARC Monographs during 2020-2024 place HPV as a low priority for evaluation, though virologists worldwide will be making submissions for upgrading this assessment [104]. ...
Simple Summary
Esophageal cancer is not an uncommon malignancy in the world with a relatively high mortality. There has been a dramatic upward trajectory (approximately 400%) in the number of patients diagnosed with the glandular form of esophageal cancer (adenocarcinoma) since the 1970’s. It has been thought that this condition is related to chronic heartburn causing Barrett’s esophagus (a pre-cancerous condition), smoking and obesity. Nevertheless, this excess number of esophageal cancers is not entirely explained by these known risk factors despite improved screening, detection and treatment strategies. The discovery of high-risk type human papillomavirus (with an increased cancer potential) being strongly associated with this glandular form of tumor of the esophagus in a subset of patients (approximately 25%) may partially explain this anomaly. This discovery will aid improved detection rates of those with a greater risk of progressing to malignancy and modified treatment strategies including vaccination in the hope of reduced mortality.
Abstract
Esophageal cancer is a relatively common malignancy worldwide with a high mortality (5-year survival of <15%). Despite screening, surveillance, improved imaging and treatment, the exponential rise in OAC continues. The strongest risk factors for OAC are chronic heartburn and metaplastic transformation of the lower third of the esophagus (Barrett’s esophagus). The risk profile includes Caucasian race, male gender older age, obesity and smoking. Although the tumor risk in BO has been progressively revised downwards, the exponential rise in OAC remains unchecked. This paradox points to an unidentified missing link. Relatively recently, we provided the world’s initial data for a strong association of biologically relevant hr-HPV with BD and OAC. Since then, systematic reviews and meta-analysis have documented HPV DNA prevalence rates in OAC of between 13 to 35%. In this review, we provide some evidence for a probable causal relationship between hr-HPV and OAC. This is challenging given the multifactorial etiology and long latency. Increasingly, high-risk HPV (hr-HPV) is regarded as a risk factor for OAC. This discovery will aid identification of a sub-group of high-risk progressors to esophageal cancer by surveillance and the development of effective preventive strategies including vaccination.
... The International Association for Research on Cancer (IARC) acknowledged the exposure risks of firefighting and classified the occupation of firefighting as Group 1, carcinogenic to humans, based on evidence available in 2022 [8,10,11]. PAH exposure is an important factor that was considered by the IARC monograph working group in 2010 and again in 2022 [11,12]. Not all PAHs have similar toxicity and therefore it is important to evaluate toxicity equivalencies (TEQ) using methods such as the model created by Nisbet and LaGoy [5]. ...
Chronic health risks associated with firefighting continue to be documented and studied, however, the complexity of occupational exposures and the relationship between occupational exposure and contaminated personal protective equipment (PPE) remains unknown. Recent work has revealed that common PPE cleaning practices, which are becoming increasingly more common in the fire service, are not effective in removing certain contaminants, such as polycyclic aromatic hydrocarbons (PAHs), from PPE. To better understand the relationship between contaminated firefighter PPE and potential exposure to PAHs, and to gain further understanding of the efficacy of cleaning practices, we used a standardized fire exposure simulator that created repeatable conditions and measured PPE surface contamination levels via wipe sampling and filters attached to firefighter gear worn by standing mannequins. This study examined the effects of repeated (40 cycles) PPE cleaning (laundering and on-scene preliminary exposure reduction (PER) techniques) and repeated exposures on PAH concentration on different surfaces. Further exploration included examination of contamination breakthrough of turnout jackets (comparing outer shell and interior liner) and evaluation of off-gassing PAHs from used gear after different cleaning treatments. When compared by jacket closure type (zipper and hook and dee), total PAH concentration wiped from gear after exposure and cleanings showed no significant differences. Regression analysis indicated that there was no effect of repeated exposures on PAH contamination levels (all sampling sites combined; before fire 10, 20, and 40; after fire 1, 10, 20, and 40; p-value > 0.05). Both laundering and on-scene PER significantly reduced contamination levels on the exterior pants and helmets and were effective at reducing PAH contamination. The jacket outer shell had significantly higher PAH contamination than the jacket liner. Both laundering and wet soap PER methods (post-fire) are effective in reducing surface contamination and appear to prevent accumulation of contamination after repeated exposures. Semi-volatile PAHs deep within the fibers of bulky PPE are not effectively reduced via PER or machine laundering, therefore, permitting continued off-gassing of these compounds. Further research is needed to identify the most effective laundering methods for firefighter turnout gear that considers the broad spectrum of common contaminants.
... Данные по категории «новообразования» в возрастной группе 15-17 лет приведены на рис. 4 одновременно с данными роста абонентской базы, что предполагает увеличение суммарной экспозиции ЭМП ИКТ: примерно до 2010 г. экспозиция формируется за счёт абонентских терминалов, а после этого времени также и за счёт сетевой инфраструктуры ИКТ. По данным Росстата (2020 г.), в группе-индикаторе заболеваемость новообразованиями всех этиологий выросла к настоящему времени в 4,2 раза по сравнению с «домобиль- [27,28]. При этом, согласно отчёту IARC, есть ясность в механизме возникновения злокачественных опухолей при воздействии радиочастот сотовой связи, однако вероятность развития злокачественных новообразований и условия их возникновения не ясны. ...
There was carried out the analysis of information and computer technologies (ICT), which are the main hygienically significant sources of non-ionizing electromagnetic radiation for children and adolescents. Early forecasts (before 2008) about the adverse impact of the ICT electromagnetic field on the health of children and adolescents, the fundamental scientific basis for forecasts and data on their feasibility to date are considered. According to state statistics, forecasts of an increase in morbidity due to EMF exposure to children and adolescents are likely to come true. For the period 1995-2019, 15-17 years children, a steady trend was identified for the gain in cerebral malignant neoplasms, diseases of the nervous system, blood, hematopoietic organs, and individual disorders involving the immune mechanism. The number of recorded malignant neoplasms of the brain in the adolescent contingent allows performing for the first time “case-control” analysis. Uncertainties in assessing the conditionality of the increase in the incidence in children under the influence of non-ionizing ICT electromagnetic radiation are associated with difficulties in determining personal doses. The limits of EMF exposure of the user’s head by a mobile device, which were developed in 1994, are now outdated and it is necessary to change the limits, as the devices and parameters of exposure to non-ionizing electromagnetic radiation of ICT have changed. It is necessary to confirm the reliability of the hygienic safety factor of EMF remote control in relation to children’s contingents in the conditions of modern and promising information and computer technologies, including taking into account possible synergy under the action of radio frequency EMF, optical screen radiation, sound effects and functional load. Obviously, today what is required is an integrated approach to ensuring the health of children “hygiene in the digital environment”. The article substantiates the foreign standards to affect the design and equipment for information and communication technologies of the educational environment in the Russian Federation, which is one of the important reasons for the deterioration of children’s health.
... The IARC has announced that acrylamide is high on its list of chemicals to be reevaluated in terms of the classification of carcinogenicity in humans (10). As opposed to the limited data from 1994, there is now a fair amount of epidemiological data for the agency to consider. ...
... 23 No human data were available at the time of this IARC evaluation in 1991, and a recent IARC Monograph working group recommended that some pyrethroids (including permethrin) should be a high priority for reevaluation. 24 The NHANES study did not find associations with overall cancer mortality and was limited due to a few cancer deaths. 15 Two prior investigations have reported associations between permethrin and multiple myeloma incidence in AHS applicators. ...
Objectives:
Pyrethroid insecticides have been linked with multiple health outcomes. One study reported an association with increased all-cause and cardiovascular mortality. Given the widespread use of pyrethroids, these findings warrant confirmation. We explored associations of permethrin/pyrethroid use with overall and cause-specific mortality among 50 665 licensed pesticide applicators in the Agricultural Health Study.
Methods:
At enrolment (1993-1997), participants self-reported information on permethrin/pyrethroid use. Information on causes of death came from linkage with death registries through 2016. We used Cox proportional hazards models to estimate HRs and 95% CIs with adjustment for potential confounders.
Results:
Over an average 21 years of follow-up, 19.6% (9,955) of the cohort died. We found no clear evidence that ever-use of permethrin/pyrethroid was associated with elevated overall mortality or with mortality from most causes examined. There was suggestive evidence, based on a small number of deaths among those exposed, for elevated pyrethroid-associated mortality from some neurological, respiratory and genitourinary diseases in the overall sample and from lung cancer among never-smokers.
Conclusion:
Although based on mortality, which is also affected by survival, rather than incidence, these findings are biologically plausible, and future investigations in other populations may be warranted.
... In 2012, AFB 1 was classified as the Group 1 carcinogen (carcinogenic to humans) by the International Agency for Research on Cancer (IARC) (Haque et al., 2020). Further studies and conclusions by IARC and World Cancer Research Fund (WCRF) strongly supported the linkage of AFB 1 to liver cancer and other types of cancer risks (Marques et al., 2019;Claeys et al., 2020). In China, the risks of exposure to aflatoxin B 1 in foodstuffs or feeds still needed long-term supervision and control . ...
Aflatoxins are naturally occurring high-toxic secondary metabolites, which cause worldwide environmental contaminations and wastes of food and feed resources and severely threaten human health. Thus, the highly efficient methods and technologies for detoxification of aflatoxins are urgently needed in a long term. In this work, we report the construction of recombinant Kluyveromyces lactis strains GG799(pKLAC1-Phs mnp ), GG799(pKLAC1-Plo mnp ), GG799(pKLAC1-Phc mnp ), and then the food-grade expression of the three manganese peroxidases in these strains, followed by the degradation of aflatoxin B 1 (AFB 1 ) using the fermentation supernatants. The expression of the manganese peroxidases was achieved in a food-grade manner since Kluyveromyces lactis is food-safe and suitable for application in food or feed industries. The inducible expression process of the optimal recombinant strain GG799(pKLAC1-Phc mnp ) and the aflatoxin B 1 degradation process were both optimized in detail. After optimization, the degradation ratio reached 75.71%, which was an increase of 49.86% compared to the unoptimized results. The degradation product was analyzed and determined to be AFB 1 -8,9-dihydrodiol. The recombinant strain GG799(pKLAC1-Phc mnp ) supernatants degraded more than 90% of AFB 1 in the peanut samples after twice treatments. The structural computational analysis for further mutagenesis of the enzyme PhcMnp was also conducted in this work. The food-grade recombinant yeast strain and the enzyme PhcMnp have potential to be applied in food or feed industries.
... fumonisin B 1 (FB 1 ), FB 2 and FB 3 ), resulting in low yield and grain quality as a consequence of the FER disease [6]. From a toxicological standpoint, FB 1 is classified into group 2B as being possibly carcinogenic to humans [7]. The chemical structure of FB 1 is similar to sphingoid bases such as sphinganine and sphingosine. ...
Fusarium ear rot (FER) caused by Fusarium verticillioides is one of the main fungal diseases in maize worldwide. To develop a pathogen-tailored FER resistant maize line for local implementation, insights into the virulence variability of a residing F. verticillioides population are crucial for developing customized maize varieties, but remain unexplored. Moreover, little information is currently available on the involvement of the archetypal defense pathways in the F. verticillioides–maize interaction using local isolates and germplasm, respectively. Therefore, this study aims to fill these knowledge gaps. We used a collection of 12 F. verticillioides isolates randomly gathered from diseased maize fields in the Vietnamese central highlands. To assess the plant’s defense responses against the pathogens, two of the most important maize hybrid genotypes grown in this agro-ecological zone, lines CP888 and Bt/GT NK7328, were used. Based on two assays, a germination and an in-planta assay, we found that line CP888 was more susceptible to the F. verticillioides isolates when compared to line Bt/GT NK7328. Using the most aggressive isolate, we monitored disease severity and gene expression profiles related to biosynthesis pathways of salicylic acid (SA), jasmonic acid (JA), abscisic acid (ABA), benzoxazinoids (BXs), and pathogenesis-related proteins (PRs). As a result, a stronger induction of SA, JA, ABA, BXs, and PRs synthesizing genes might be linked to the higher resistance of line Bt/GT NK7328 compared to the susceptible line CP888. All these findings could supply valuable knowledge in the selection of suitable FER resistant lines against the local F. verticllioides population and in the development of new FER resistant germplasms.
... 22,23 Uranium at elevated concentrations in groundwater is a concern for its potential chemical toxicity, rather than its radiotoxicity. Although uranium has not yet been proven to be carcinogenic, 24 it is known to accumulate in and cause toxicity to kidneys, liver, and bones. 25 The World Health Organization prescribes drinking water limit of uranium as 30 μg L −1 . ...
... The need for a structured updated appraisal of this body of evidence is widely recognised. Non-ionising radiation (radiofrequency) is among the agents recommended with high priority for re-evaluation by the Advisory Group for the IARC Monographs during 2020-2024 (Marques et al. 2019). Two registered systematic reviews of epidemiological studies on RF-EMF and cancer are underway, focusing on exposures experienced by the general population (Farhat et al. 2020) and workers (Modenese et al. 2020). ...
Background
The World Health Organization (WHO) has an ongoing project to assess potential health effects of exposure to radiofrequency electromagnetic fields (RF-EMF) in the general and working population. Here we present the protocol for a systematic review of the scientific literature on cancer hazards from exposure to RF-EMF in humans, commissioned by the WHO as part of that project.
Objective
To assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to RF-EMF and risk of neoplastic diseases.
Eligibility criteria
We will include cohort and case-control studies investigating neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of handheld transceivers or RF-emitting equipment in the workplace (SR-C). While no restriction on tumour type will be applied, we will focus on selected neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C).
Information sources
Eligible studies will be identified through Medline, Embase, and EMF-Portal.
Risk-of-bias assessment
We will use a tailored version of the OHAT's tool to evaluate the study's internal validity.
Data synthesis
We will consider separately studies on different tumours, neoplasm-specific risks from different exposure sources, and a given exposure-outcome pair in adults and children. When a quantitative synthesis of findings can be envisaged, the main aims of the meta-analysis will be to assess the strength of association and the shape of the exposure–response relationship; to quantify the degree of heterogeneity across studies; and explore the sources of inconsistency (if any). When a meta-analysis is judged inappropriate, we will perform a narrative synthesis, complemented by a structured tabulation of results and appropriate visual displays.
Evidence assessment
Confidence in evidence will be assessed in line with the GRADE approach.
Funding
This project is supported by the World Health Organization. Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; ARPANSA as a WHO Collaborating Centre for Radiation Protection.
Registration
PROSPERO CRD42021236798.
Проанализирована сбываемость радиобиологических прогнозов о возможном росте заболеваемости, обусловленной воздействием электромагнитного поля оборудования сотовой связи. Прогнозы были даны на основе фундаментальных исследований медико-биологических эффектов электромагнетизма, основываясь на принципиальном изменении условий облучения населения и недостаточности научных данных о последствиях облучения головного мозга в неконтролируемых условиях во всех группах населения, включая детей. Показано, что Росстат фиксирует рост заболеваемости за 25 лет по прогнозным группам болезней в популяции подростков 15-17 лет (злокачественные опухоли, болезни нервной системы, нарушение иммунного статуса, болезни органа слуха и зрения). Оценка вклада сотовой связи в рост заболеваемости, выполненная на основе методологии IARC, показывает, что обусловленность роста заболеваемости вредным влиянием электромагнитного поля скорее достоверно существует, чем является случайным совпадением. Однако непосредственное определение риска затруднено в связи с неопределенностью данных дозиметрии, отсутствием современных групп сравнения и неразработанностью концепции приемлемого риска для массовой технологии сотовой связи.
We analyzed the feasibility of radiobiological predictions about a possible increase in the morbidity, which is due to the influence of the electromagnetic field of wireless cellular communication. These predictions were made before 2008 and based on fundamental data research on the biomedical effects of electromag-netism. The principal reasons for the predictions were changes in the conditions of exposure of the general population, insufficient scientific data on the EMF exposure of brain for the general population, including children. 25 years Rosstat's health data has shown an increase of diseases that were in the predictions for aged 15-17 years (malignant tumors, diseases of the nervous system, impaired immune status, diseases of the organ of hearing and vision). We adopted and used the IARC methodology for performed an assess-ment of the contribution of wireless cellular communication to the morbidity. This assessment showed that the conditionality of the increase in the incidence of the harmful effects of the electromagnetic field rather exists reliably than is a coincidence. However, the direct determination of risk is difficult due to the uncer-tainty of dosimetry data, the lack of modern comparison groups and the undeveloped concept of accepta-ble risk for mass cellular communication technology.
Background:
Mycotoxins, fungal metabolites prevalent in many foods, are recognized for their role in carcinogenesis, especially when interacting with oncogenic viruses.
Objectives:
This scoping review synthesizes current evidence on the human cancer risk associated with mycotoxin exposure and oncogenic virus infections.
Methods:
Searches were conducted on PubMed, Embase, and Web of Science. Studies were selected based on the PECOS framework. Data extraction involved narrative and qualitative presentation of findings, with meta-analysis where feasible. Risk of bias and outcome quality were assessed using the OHAT tool and GRADE approach.
Results:
From 25 included studies, 18 focused on aflatoxins and hepatitis viruses in hepatocellular carcinoma (HCC). Four studies examined aflatoxin B1 (AFB1) and human papilloma virus (HPV) in cervical cancer, while three investigated AFB1 with Epstein-Barr virus (EBV) in lymphomagenesis. The review highlights a significant synergistic effect between AFB1 and hepatitis B and C viruses in HCC development. Significant interactions between AFB1 and HPV, as well as AFB1 and EBV, were observed, but further research is needed.
Conclusions:
The synergistic impact of mycotoxins and oncogenic viruses is a critical public health concern. Future research, especially prospective cohort studies and investigations into molecular mechanisms, is essential to address this complex issue.
Objective
The study investigated maternal exposure to heavy metals from industrial sources during pregnancy as potential risk factors for childhood cancer.
Methods
Cases ages 0-19 were identified from California Cancer Registry. Controls (20:1 ratio) were randomly selected from California Birth Registry, frequency-matched by birth year (1998-2016). We estimated maternal exposure to lead, nickel and cobalt in ambient air from the Toxic Release Inventory. We examined “ever/never”, and “high/low” exposures, categorized by median exposure. Models were adjusted for maternal age, race/ethnicity, method of payment for prenatal care, neighborhood socioeconomic status, and urban/rural residence.
Results
Among highly-exposed persons, lead was associated with an increased teratoma risk (aOR: 1.52; 95% CI: 0.97, 2.37), while nickel was associated with an increased rhabdomyosarcoma risk (aOR: 1.45; 95% CI: 1.03, 2.04). Cobalt was associated with an increased glioma risk (aOR: 2.25, 95% CI 1.39, 3.65) among ever-exposed persons. Inverse associations were found between Wilms tumor and nickel among the ever exposed and highly exposed (ever: aOR: 0.75; 95% CI: 0.59, 0.96; high: aOR: 0.64; 95% CI: 0.45, 0.93).
Conclusions
Findings suggest air pollution from heavy metals released by industrial sources may elevate childhood cancer risk.
Human Papillomaviruses (HPV) are a diverse family of non-enveloped dsDNA viruses that infect the skin and mucosal epithelia. Persistent HPV infections can lead to cancer frequently involving integration of the virus into the host genome, leading to sustained oncogene expression and loss of capsid and genome maintenance proteins. Microhomology-mediated double-strand break repair, a DNA double-stranded breaks repair pathway present in many organisms, was initially thought to be a backup but it's now seen as vital, especially in homologous recombination-deficient contexts. Increasing evidence has identified microhomology (MH) near HPV integration junctions, suggesting MH-mediated repair pathways drive integration. In this comprehensive review, we present a detailed summary of both the mechanisms underlying MH-mediated repair and the evidence for its involvement in HPV integration in cancer. Lastly, we highlight the involvement of these processes in the integration of other DNA viruses and the broader implications on virus lifecycles and host innate immune response.
The performance targets for 6G are driven by a vision of the future with Tbs data rates, microsecond latency and increased connection density that cannot be delivered by 5G systems. It is expected that 6G will use a combination of low frequencies for coverage and high frequency bands for extreme data rates at short ranges. New 6G spectrum bands could extend beyond 100 GHz and up to 3 THz but there are technical challenges. International human exposure limits and compliance assessment methods are available up to 300 GHz. It is important that these are extended to the potential new frequency ranges. The consensus of the scientific community is that there are no established health hazards for radio technologies (2G, 3G, 4G, 5G or 6G and beyond) that comply with these technology independent guidelines. Typical environmental radio signal levels have not changed by very much over the last 20 years and remain a small fraction of exposure limits. Similarly, mobile devices typically operate far below their maximum transmit power. The WHO health risk assessment for RF-EMF needs to be future looking in order to provide reassurance about the safety of not yet deployed RF technologies, including 6G, technology complies with the international guidelines. Stakeholders should ensure that information on real-world 6G RF-EMF levels and specific statements on 6G safety from trusted agencies are available when 6G launches in the 2030s.
The Senate Commission on Food Safety (SKLM) of the German Research Foundation (DFG) has reviewed the currently available data in order to assess the health risks associated with the use of acetaldehyde as a flavoring substance in foods. Acetaldehyde is genotoxic in vitro. Following oral intake of ethanol or inhalation exposure to acetaldehyde, systemic genotoxic effects of acetaldehyde in vivo cannot be ruled out (induction of DNA adducts and micronuclei). At present, the key question of whether acetaldehyde is genotoxic and mutagenic in vivo after oral exposure cannot be answered conclusively. There is also insufficient data on human exposure. Consequently, it is currently not possible to reliably assess the health risk associated with the use of acetaldehyde as a flavoring substance. However, considering the genotoxic potential of acetaldehyde as well as numerous data gaps that need to be filled to allow a comprehensive risk assessment, the SKLM considers that the use of acetaldehyde as a flavoring may pose a safety concern. For reasons of precautionary consumer protection, the SKLM recommends that the scientific base for approval of the intentional addition of acetaldehyde to foods as a flavoring substance should be reassessed.
Background:
The International Agency for Research on Cancer (IARC) Monographs program assembles expert working groups who publish a critical review and evaluation of data on agents of interest. These comprehensive reviews provide a unique opportunity to identify research needs to address classification uncertainties. A multidisciplinary expert review and workshop held in 2009 identified research gaps and needs for 20 priority occupational chemicals, metals, dusts, and physical agents, with the goal of stimulating advances in epidemiological studies of cancer and carcinogen mechanisms. Overarching issues were also described.
Objectives:
In this commentary we review the current status of the evidence for the 20 priority agents identified in 2009. We examine whether identified Research Recommendations for each agent were addressed and their potential impact on resolving classification uncertainties.
Methods:
We reviewed the IARC classifications of each of the 20 priority agents and identified major new epidemiological and human mechanistic studies published since the last evaluation. Information sources were either the published Monograph for agents that have been reevaluated or, for agents not yet reevaluated, Advisory Group reports and literature searches. Findings are described in view of recent methodological developments in Monographs evidence evaluation processes.
Discussion:
The majority of the 20 priority agents were reevaluated by IARC since 2009. The overall carcinogen classifications of 9 agents advanced, and new cancer sites with either "sufficient" or "limited" evidence of carcinogenicity were also identified for 9 agents. Examination of published findings revealed whether evidence gaps and Research Recommendations have been addressed and highlighted remaining uncertainties. During the past decade, new research addressed a range of the 2009 recommendations and supported updated classifications for priority agents. This supports future efforts to systematically apply findings of Monograph reviews to identify research gaps and priorities relevant to evaluation criteria established in the updated IARC Monograph Preamble. https://doi.org/10.1289/EHP12547.
Recent evidence has shown that the human microbiome is associated with various diseases, including cancer. The salivary microbiome, fecal microbiome, and circulating microbial DNA in blood plasma have all been used experimentally as diagnostic biomarkers for many types of cancer. The microbiomes present within local tissue, other regions, and tumors themselves have been shown to promote and restrict the development and progression of cancer, most often by affecting cancer cells or the host immune system. These microbes have also been shown to impact the efficacy of various cancer therapies, including radiation, chemotherapy, and immunotherapy. Here, we review the research advances focused on how microbes impact these different facets and why they are important to the clinical care of cancer. It is only by better understanding the roles these microbes play in the diagnosis, development, progression, and treatment of cancer, that we will be able to catch and treat cancer early.
Arecoline is a critical bioactive component in areca nuts with toxicity and pharmacological activities. However, its effects on body health remain unclear. Here, we investigated the effects of arecoline on physiologic and biochemical parameters in mouse serum, liver, brain, and intestine. The effect of arecoline on gut microbiota was investigated based on shotgun metagenomic sequencing. The results showed that arecoline promoted lipid metabolism in mice, manifested as significantly reduced serum TC and TG and liver TC levels and a reduction in abdominal fat accumulation. Arecoline intake significantly modulated the neurotransmitters 5-HT and NE levels in the brain. Notably, arecoline intervention significantly increased serum IL-6 and LPS levels, leading to inflammation in the body. High-dose arecoline significantly reduced liver GSH levels and increased MDA levels, which led to oxidative stress in the liver. Arecoline intake promoted the release of intestinal IL-6 and IL-1β, causing intestinal injury. In addition, we observed a significant response of gut microbiota to arecoline intake, reflecting significant changes in diversity and function of the gut microbes. Further mechanistic exploration suggested that arecoline intake can regulate gut microbes and ultimately affect the host's health. This study provided technical help for the pharmacochemical application and toxicity control of arecoline.
Obesity and obesity-related disorders such as cancer, type 2 diabetes, and fatty liver have become a global health problem. It is well known that the primary cause of obesity is positive energy balance. In addition, obesity is the consequence of complex gene and environment interactions that result in excess calorie intake being stored as fat. However, it has been revealed that there are other factors contributing to the worsening of obesity. The presence of nontraditional risk factors, such as environmental endocrine-disrupting chemicals, has recently been associated with obesity and comorbidities caused by obesity. The aim of this review was to examine the evidence and potential mechanisms for acrylamide having endocrine-disrupting properties contributing to obesity and obesity-related comorbidities. Recent studies have suggested that exposure to environmental endocrine-disrupting obesogens may be a risk factor contributing to the current obesity epidemic, and that one of these obesogens is acrylamide, an environmental and industrial compound produced by food processing, particularly the processing of foods such as potato chips, and coffee. In addition to the known harmful effects of acrylamide in humans and experimental animals, such as neurotoxicity, genotoxicity, and carcinogenicity, acrylamide also has an obesogenic effect. It has been shown in the literature to a limited extent that acrylamide may disrupt energy metabolism, lipid metabolism, adipogenesis, adipocyte differentiation, and various signaling pathways, and may exacerbate the disturbances in metabolic and biochemical parameters observed as a result of obesity. Acrylamide exerts its main potential obesogenic effects through body weight increase, worsening of the levels of obesity-related blood biomarkers, and induction of adipocyte differentiation and adipogenesis. Additional mechanisms may be discovered. Further experimental studies and prospective cohorts are needed, both to supplement existing knowledge about acrylamide and its effects, and to clarify its established relationship with obesity and its comorbidities.
Exposure to certain chemicals in the environment may contribute to the risk of developing cancer. Although cancer risk from environmental chemical exposure among general populations is considered low compared to that in occupational settings, many people may nevertheless be chronically exposed to relatively low levels of environmental chemicals which vary by such various factors as residential area, lifestyle, and dietary habits. It is therefore necessary to assess population-specific exposure levels and examine their association with cancer risk. Here, we reviewed epidemiological evidence on cancer risk and exposure to dichlorodiphenyltrichloroethane (DDT), hexachlorocyclohexane (HCH), polychlorinated biphenyls (PCBs), per- and polyfluoroalkyl substances (PFASs), cadmium, arsenic, and acrylamide. Japanese are widely exposed to these chemicals, mainly through the diet, and an association with increased cancer risk is suspected. Epidemiological evidence from Japanese studies to date does not support a positive association between blood concentrations of DDT, HCH, PCBs, and PFASs and risk of breast or prostate cancer. We established assessment methods for dietary intake of cadmium, arsenic, and acrylamide using a food frequency questionnaire. Overall, dietary intakes of cadmium, arsenic, and acrylamide were not significantly associated with increased risk of total cancer and major cancer sites in the Japan Public Health Center-based Prospective Study. However, statistically significant positive associations were observed between dietary cadmium intake and risk of estrogen receptor-positive breast cancer among postmenopausal women, and dietary arsenic intake and risk of lung cancer among male smokers. In addition, studies using biomarkers as exposure assessment revealed statistically significant positive associations between urinary cadmium concentration and risk of breast cancer, and between ratio of hemoglobin adducts of acrylamide and glycidamide and risk of breast cancer. Epidemiological studies of general populations in Japan are limited and further evidence is required. In particular, studies of the association of organochlorine and organofluorine compounds with risk of cancer sites other than breast and prostate cancer are warranted, as are large prospective studies of the association between biomarkers of exposure and risk of cancer.
Introduction. Lung cancer is the most common type of occupational malignancies. A "case–control" study may allow an initial assessment of the impact of certain factors on the risk of developing malignant neoplasms. The study aims to conduct a "case–control" study by collecting data through a questionnaire and identifying a possible link between the incidence of lung malignancies and professional activity. Materials and methods. Researchers conducted a case-control study in the Rostov region. The authors carried out data collection by the questionnaire method. Results. Specialists received 363 questionnaires for persons from the "cases" group and 599 for persons from the control group. The ratio of lung cancer detection risks in coal industry workers was higher compared to the population control (OR=1,229(0.891–1.696)), was lower compared to humanitarian workers (OR=0.983(0.645–1.500)). The risk ratio of lung cancer detection in smoking men was higher (OR=1.997; CI (0.792–5.036)). Workers who smoke more than one pack per day have a higher risk of lung cancer detection (OR=1,667(0.860–3.231)). Statistically significant risk ratio in the group of construction sector workers compared to humanitarian workers OR=2.275(1.244–4.159), as well as in the group of technical professions OR=0.606(0.404–0.909). Limitations. Insufficient research potential due to the high level of refusal of respondents, administrative and legal restrictions, little information and its inaccuracy. Conclusion. There was a tendency to increase the risk of lung cancer among coal industry workers compared to other professions, as well as a tendency to increase the risk of lung cancer among coal industry workers who smoke more than one pack per day (but without achieving statistically reliable indicators). Further epidemiological studies in this direction are needed based on the use of modern digital databases. Ethics. Protocol No. 4 of April 17, 2019 of the meeting of the Local Ethics Committee of the Izmerov Research Institute of Occupational Health.
Da alcuni anni, nel mondo della politica e dei media, avanza incalzante l’idea
della bioeconomia come nuova frontiera dell’economia ‘verde’, la panacea
capace di coniugare lavoro e ambiente. Ma è davvero così? Cosa sono le
Strategie di bioeconomia europea e italiana? Tali Strategie sono in sintonia
con la teoria bioeconomica di Georgescu Roegen fondata sull’idea di
un’economia compatibile con la vita e le leggi della natura?
Tali Strategie rappresentano un’opportunità o un rischio per le economie
locali? Che effetti produrranno sul paesaggio e i patrimoni territoriali? Sugli
assetti socio-ecologici? Come incideranno sulle dinamiche ad effetto
climatico? Quali impatti produrranno sulle matrici vitali, sulla salute e sulle
comunità territoriali? Quali gli scenari geopolitici connessi?
Research on occupational causes of cancer has identified 47 known (Group 1) agents associated with 23 types of cancer through 2017, an increase from 28 agents in 2004 (1, 2). Occupational agents include chemicals and chemical mixtures; radiation and radionuclides; airborne particles and complex mixtures; and metals and metal compounds. The global burden of cancer due to 14 of the Group 1 agents was estimated to total 349 000 [95% uncertainty interval (UI) 269 000–427 000] deaths in 2016, or 3.9% (95% UI 3.2–4.6%) of all cancer deaths, including 299 998 or 17.6% (95% UI 13.8–21.3%) of lung cancer deaths (3). There are also exposures in various occupations, industries, or processes classified as Group 1 where the causal agent is not necessarily identified. In 2022, occupational exposure as a firefighter was most recently classified in Group 1, with sufficient evidence among humans for mesothelioma and bladder cancer, and limited evidence for other cancers (4). Despite achievements in identifying occupational causes of cancer, a range of research needs remain, including identifying additional cancer sites for Group 1 agents and more definitive studies for exposures where the evidence among humans remains limited or inadequate (1, 5–7). There may be outstanding methodological concerns or findings that are inconsistent or of poor quality or informativeness. Research recommendations to address classification uncertainties for 20 priority occupational agents have been detailed (8). They include conducting new epidemiological studies in highly exposed occupations or populations, improving (quantitative) exposure assessment including through biomarkers of exposure, enhancing statistical power through extended follow-up or pooled studies, and furthering human mechanistic studies. High quality human mechanistic evidence can provide valuable information when epidemiology studies are not available or feasible (5). A 2019 Advisory Group considered 170 different agents in terms of their suitability for (re-)evaluation with a range of chemical, metal, or complex exposures of relevance for occupational settings prioritized based on new human epidemiology, mechanistic and/or cancer bioassay data (9). There have been calls to update existing cohorts when valuable follow-up time has accrued allowing investigation of the full potential impact of exposures on health (10). There is a longstanding need for occupational epidemiological and exposure assessment studies in low- and middle-income countries, where there are often few or no available studies and exposure levels maybe higher (11–14). There may also be differences in working conditions, exposure patterns, and worker protections (15, 16). Research challenges include declines in participation rates, funding, and research infrastructures (1, 17–19). In parallel, epidemiological research has innovated over time to comprise increasingly larger-scale prospective cohort studies and consortia, use of electronic data linkage, causal inference methods and triangulation of evidence, reinforcing the ongoing utility of observational research methods (20). The recent COVID-19 pandemic has reinforced the need for a global perspective in epidemiological research, multidisciplinarity, and broadening perspectives regarding fundamental underlying determinants of health (21, 22). There have also been calls for greater equity and inclusiveness in health research, both in Europe, and worldwide (23, 24). Efforts to stimulate future research and investment in occupation and cancer may benefit from the use of new rapidly evolving research methods, closer alignment with global public health priorities, and strengthening of international partnerships supporting excellence and inclusiveness in research. For example, a range of methodological advancements have emerged from application of exposome concepts in epidemiology. In Europe, birth cohort consortia seeking to characterize the early-life exposome, as well as other efforts, have driven much innovation (25, 26). The exposome concept was proposed in 2005 to stimulate investment to better characterize environmental exposures throughout the lifecourse using novel technologies, offering a complementary perspective to that of the genome (27). Although occupational exposure has previously not been emphasized, research in the internal and external occupational exposome is now beginning to emerge (28). A range of statistical methods for analysis of multiple correlated exposures have advanced (29). Extended Bayesian profile regression mixture (PRM) models have been used to examine multiple highly correlated ionizing radiation exposures for lung cancer risk among miners (30). An exposome-wide association study examined a range of personal and occupational factors in B-cell lymphoma, suggesting that single-factor research approaches maybe suboptimal for new disease insights (31). There are exposome technologies for personal monitoring of workers (28, 32) and other novel research methods including natural language processing and text mining (33, 34), automated network assembly approaches to summarizing literature (35), efforts to combine epidemiological data with those from other evidence streams (36), and new technologies to facilitate secure decentralized pooled analyses of data (37). However, there is an ongoing need for continued efforts to better characterize the occupational and corresponding non-occupational exposome over the lifecourse. Research priorities include establishing new cohort studies with appropriate biosample collection, improved questionnaire and personal monitoring data, increasing multidisciplinary collaboration to utilize innovative data and methods, and integrating genetic data in exposome studies for causal inference (38-40). At the same time, careful consideration of the policy relevance of exposome studies remains of importance (41), as are continued efforts in conventional epidemiological case–control and cohort studies in occupation and cancer (8). Occupational studies examining exposures of relevance for the general population may favor greater investment (42). There are environmental exposure routes for occupational agents, bystander or spousal exposure to occupational agents, and potential transgenerational health effects (43–45). Birth cohorts may represent a typically underused resource for research in occupation and health (46). Principles for safeguarding integrity in environmental and occupational research have also been outlined (47). Research on occupation and cancer may benefit from closer alignment with recent high-profile initiatives on related topics as well as with global public health priorities. The United Nations Sustainable Development Goals note the need for decent work (48). The EU Strategic Framework on Health and Safety at Work describes the elimination of work-related deaths by 2030 and reduced illness through improved data collection, updated rules on hazardous substances, including those of relevance for renewable energy technologies (ie, lead, cobalt) or of asbestos exposure in building renovations for greening, increased health literacy at work, and adapting working conditions for patients (49). A large-scale survey of worker exposure to cancer risk factors is being implemented in Europe to collect standardized data across different European countries (50). The Health Environment Agenda for Europe project defined priority areas for research on rapidly changing work and employment conditions, climate change and worker health, working time and long working hours, ageing workers, and neglected work-related diseases (51). Rapidly changing work conditions were exemplified during the COVID-19 pandemic, with potential direct or indirect effects on health and cancer. Shifts in overall global cancer research focus were also described (52). Increasing unemployment and economic downturns in high- and middle-income countries have been associated with increased cancer mortality for treatable cancers, with less access to healthcare underlying findings (53). There is also increasing interest in precarious employment and potential direct or indirect impacts on health and quality of life (54). Public health efforts directed at catching-up in cancer screening and on improving health systems and public health literacy following the COVID-19 pandemic may offer opportunities to advance cancer control and improved health literacy at work (55, 56). Further, there may greater opportunities for strengthened clinical partnerships for occupational epidemiologists. For example, dramatic gains in survival due to early detection have been demonstrated for lung cancer (57). However, occupational (or environmental) exposures are not systematically incorporated into screening algorithms, and further research and collaboration with clinical partners is warranted (58–61). The potential importance of climate change in cancer, including occupation and cancer, may also not be fully understood (62, 63). Climate change may relate to increasing exposure to environmental or occupational carcinogens, including air pollution, adverse dietary exposures, changes in physical activity levels, ultraviolet radiation, water pollution, infections, and parasites due to extreme weather events, wildfires (4), heat, sea-level rise, and changes in land-use. There may also be disruptions in cancer care. Climate change may further exacerbate existing socioeconomic inequities, and social determinants of cancer. Increasing occupational heat stress is related to acute and chronic health effects as well as reduced productivity (64–66). Studies of occupational heat exposure and cancer risk are beginning to emerge (67). Interventions to jointly address climate change and disease prevention, including cancer, have been proposed (68). There are also new agents rapidly entering the workplace where little is known regarding their carcinogenicity to humans. A planetary health perspective suggests that humanity is outside the safe operating space of the planetary boundary, with increasing production and release of chemical industry production exceeding the ability to conduct safety assessments (69). Lastly, strengthened international partnerships are critical for future advances in occupational cancer research. Efforts in coordination of European birth cohort studies, and later occupational cohort studies, have led to major advancements in research and inclusiveness (25, 26, 70, 71). Network funding initiatives provide valuable support and developed out of a recognized need to increase equitable access to funding and research infrastructures (72). A recent example is the OMEGA-NET COST Action, which sought to improve coordination and harmonization of European occupational cohort studies by connecting researchers through a range of research coordination and capacity building activities, with a particular focus on connecting researchers in traditionally less research-intensive countries (71). Online inventories of occupational cohort studies and exposure assessment tools were developed (73, 74) as were advancements in theoretical frameworks, consensus definitions and recommendations for future research on emerging topics in occupational health (54, 75, 76). The need for occupational epidemiological and exposure monitoring studies in low- and middle-income countries has long been recognized. Priorities for cancer research in low- and middle-income countries have recently been described as separate to those of high-income countries, and highlighted the need to reduce the burden of patients presenting with advanced-stage disease, primary prevention and early detection, and innovative and affordable technology in cancer control (77). Documenting and minimizing exposure to established occupational carcinogens is critical to prioritize interventions and prevent future cancer burden (11, 34, 78). Generating country-specific evidence for effective prevention may be helpful in this regard (77). Research questions on cancers that are of local importance, using appropriate research methods for available infrastructure, and partnerships for mutually rewarding collaborations have been described (77, 79). However, cancer registry and infrastructure challenges have been outlined, including of poor-quality data and an absence of legal frameworks for cancer registration (19). International collaboration has had demonstrated impacts in research and capacity building, though sustained political and financial commitment is needed (16, 80, 81). The occupational epidemiology community has a great opportunity to promote new efforts in occupation and cancer while at the same time reducing inequalities in health and research. Acknowledgements Michelle C Turner is funded by a Ramón y Cajal fellowship (RYC-2017-01892) from the Spanish Ministry of Science, Innovation and Universities and co-funded by the European Social Fund. ISGlobal acknowledges support from the Spanish Ministry of Science and Innovation through the “Centro de Excelencia Severo Ochoa 2019-2023” Program (CEX2018-000806-S), and support from the Generalitat de Catalunya through the CERCA Program. References 1. Loomis D, Guha N, Hall AL, Straif K. Identifying occupational carcinogens: an update from the IARC Monographs. Occup Environ Med 2018;75:593-603. https://doi.org/10.1136/oemed-2017-104944 2. 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Exposure to endocrine-disrupting chemicals, like Polybrominated diphenyl ethers (PBDEs), is suspected of playing a role in the occurrence of breast cancer. Moreover, there is growing evidence that food chemical contaminants, especially lipophilic ones such as PBDEs, could interact with different components of the diet. The objective of the present study was to assess the association between dietary intake of PBDEs and breast cancer risk in the French E3N cohort study, and to investigate the potential modification of this association by vegetable oil consumption.
The study included 67 879 women. Intakes of eight PBDEs were estimated using food consumption data from a validated semi-quantitative food frequency questionnaire, and food contamination levels measured by the French Agency for Food, Environmental and Occupational Health and Safety (ANSES). Cox proportional hazards models were used to estimate Hazard Ratios (HR) and 95% Confidence Intervals (CI) for the association between total PBDEs dietary intake and breast cancer risk. Interaction measures for vegetable oil consumption were estimated on both additive and multiplicative scales.
The women were followed for a maximum of 21.4 years, and 5 686 developed an incident breast cancer. A positive linear trend was highlighted between dietary intake of PBDEs in quintile groups and breast cancer risk, borderline with statistical significance (p-trend=0.06, HRQ5vsQ1 and 95%CI: 1.09 [0.99;1.20]). Interaction measures for vegetable oil consumption were significant in both additive and multiplicative scales. Higher effect sizes of the association were highlighted in high consumers of vegetable oil, i.e. ≥4.6 g/day (HRQ5vsQ1 and 95%CI: 1.23 [1.08; 1.40]), and almost no effect were found in low consumers (HRQ5vsQ1 and 95%CI: 0.97 [0.86; 1.10]).
Highlighting such interactions between nutrients and chemicals is crucial to develop efficient dietary recommendations to limit the negative health effects associated with exposure to food chemical contaminants.
In recent years, it became apparent that cancers either associated with viral infections or aberrantly expressing endogenous retroviral elements (EREs) are more immunogenic, exhibiting an intense intra-tumor immune cell infiltration characterized by a robust cytolytic apparatus. On the other hand, epigenetic regulation of EREs is crucial to maintain steady-state conditions and cell homeostasis. In line with this, epigenetic disruptions within steady-state cells can lead to cancer development and trigger the release of EREs into the cytoplasmic compartment. As such, detection of viral molecules by intracellular innate immune sensors leads to the production of type I and type III interferons that act to induce an antiviral state, thus restraining viral replication. This knowledge has recently gained momentum due to the possibility of triggering intratumoral activation of interferon responses, which could be used as an adjuvant to elicit strong anti-tumor immune responses that ultimately lead to a cascade of cytokine production. Accordingly, several therapeutic approaches are currently being tested using this rationale to improve responses to cancer immunotherapies. In this review, we discuss the immune mechanisms operating in viral infections, show evidence that exogenous viruses and endogenous retroviruses in cancer may enhance tumor immunogenicity, dissect the epigenetic control of EREs, and point to interferon pathway activation in the tumor milieu as a promising molecular predictive marker and immunotherapy target. Finally, we briefly discuss current strategies to modulate these responses within tumor tissues, including the clinical use of innate immune receptor agonists and DNA demethylating agents.
Smallholder farmers are a high-risk group for mycotoxin exposure since they often consume home-grown crops without any quality and safety control. These smallholder farms are often characterized by very typical growing-, harvest- and storage- practices. Moreover, these practices are inherent to their ethnicity. To our knowledge, no prior longitudinal comparative studies have addressed the relationship between traditional pre-, harvest, and post-harvest practices of different smallholder ethnic farmers and the contamination of maize by Fusarium verticillioides and its mycotoxins - fumonisins in different ethnic communities. Therefore, this doctoral dissertation aims to (1) uncover differences in traditional pre-, harvest, and post-harvest maize practices between two ethnic communities Ede and Kinh from the central highlands of Vietnam; (2) analyse the correlation between these traditional practices and the occurrence of F. verticillioides, and fumonisins; (3) evaluate the susceptibility of maize cultivars planted by the ethnic smallholders to F. verticillioides and lastly, (4) seek a biological control strategy against F. verticillioides. This work is timely and important because it is one of the first studies investigating the impact of ethnic customs on mycotoxin presence in the second most important staple food maize after rice in these subsistence farms. The outputs of this doctoral dissertation are a part of the blueprint towards good smallholder maize farms with high productivity, less mycotoxin contamination, and less grain loss. Optimistically, these mycotoxin mitigation strategies could be compatible with maize smallholders from other low and middle-income countries, especially Sub-Saharan Africa.
Fumonisins are one of the most important mycotoxin classes due to their widespread occurrence and potential health threat to humans and animals. Currently, most of the research focuses on the control of fumonisin contamination in the food supply chain. In recent years, significant progress in biochemistry, enzymology, and genetic regulation of fumonisin biosynthesis has been achieved using molecular technology. Furthermore, new insights into the roles of fumonisins in the interaction between fungi and plant hosts have been reported. This review provides an overview of the current understanding of the biosynthesis and regulation of fumonisins. The ecological significance of fumonisins to Fusarium species that produce the toxins is discussed, and the complex regulatory networks of fumonisin synthesis is proposed.
Background:
Identifying cancer hazards is the first step towards cancer prevention. The IARC Monographs Programme, which has evaluated nearly 1000 agents for carcinogenic potential since 1971, typically selects agents for hazard identification on the basis of public nominations, expert advice, published data on carcinogenicity, and public health importance.
Objectives:
Here we present a novel and complementary strategy for identifying agents for hazard evaluation using chemoinformatics, database integration and automated text mining.
Discussion:
To inform selection among a broad range of pesticides nominated for evaluation, we identified and screened nearly 6000 relevant chemical structures, thereafter systematically compiled information on 980 pesticides, creating chemical similarity network maps that allowed cluster visualization by chemical similarity, pesticide class, and publicly available information concerning cancer epidemiology, cancer bioassays, and carcinogenic mechanisms. For the IARC Monograph meetings that took place in March and June 2015, this approach supported high priority evaluation of glyphosate, malathion, parathion, tetrachlorvinphos, diazinon, DDT, lindane, and 2,4-D.
Conclusions:
This systematic approach, accounting for chemical similarity and overlaying multiple data sources, can be used by risk assessors as well as researchers to systematize, inform and increase efficiency in selecting and prioritizing agents for hazard identification, risk assessment, regulation or further investigation. This approach could be extended to an array of outcomes and agents, including occupational carcinogens, drugs, and foods.
International Agency for Research on Cancer
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Sixtieth Session of the IARC Governing Council
International Agency for Research on Cancer.
Sixtieth Session of the IARC Governing Council,
GC/60/13. 2018. http://governance.iarc.fr/GC/
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