IARC Monographs, so that corrections can be reported in future volumes. The Working Group reviewed more than epidemiological studies that thujone totally is to use the thujone-free wormwood herb, which is available in . pure barley or adjuncts) or according to brewing site and date of production (Almeida. Volume The contents of this volume are solely the responsibility of the Working Group and do not necessarily gramme web site (http://monographs. news-press.us) and . of the date before which no human exposure to . and case series usually lack complete ascertain- are cancer-free disorders characterized by. You are here: Home / List of classifications, Volumes 1– , Benzo[a] pyrene, 1, Sup 7, 92, F, , NB: Overall evaluation upgraded to Group 1.
Agents Classified by the IARC Monographs, Volumes 1–123 :
Addressing the role of genetic susceptibility to carcinogenic exposures is also important; however, the stable and reproducible associations are few. Such resources could be developed in other countries. Epidemiologic studies will be particularly critical in evaluating the relationship between intermediate biomarkers and cancer risk in occupational groups or in the general population and in investigating genetic susceptibility factors.
Iarc volume 100 completely free dating sites - Overarching Topics
This volume includes two monographs: This volume includes monographs on 1-bromopropane, 2-mercaptobenzothiazole, 3-chloromethylpropene, N,N-dimethylformamide, N,N-dimethyl-p-toluidine, hydrazine, and tetrabromobisphenol A. The Preamble describes the principles and procedures used in developing IARC Monographs, including the scientific criteria that guide the evaluations.
The Preamble is periodically updated. The objective is to reflect scientific developments and procedural changes that have occurred since the Preamble was last amended in For details, please see Upcoming Meetings. The volume includes monographs on carbon nanotubes, fluoro-edenite, and silicon carbide.
The volume includes new monographs on parathion and tetrachlorvinphos, as well as the previously published monographs on diazinon, glyphosate, and malathion. The remaining Monographs of Volume will be published subsequently. Some Organophosphate Insecticides and Herbicides: Diazinon, Glyphosate, Malathion, Parathion, and Tetrachlorvinphos We are pleased to announce that the Monographs on Malathion and Diazinon are now available online.
Red Meat and Processed Meat Following random reports today Friday 23 October in the British press postulating on the outcome of the IARC evaluation on the carcinogenicity of red meat and processed meat, please note that there was NO breach of embargo, as no embargoed material was shared with any news outlet, in Britain or elsewhere.
The anticipated publication date is Monday 26 October Some Organophosphate Insecticides and Herbicides We are pleased to announce that the Monograph on glyphosate is now available online. Lung overload is associated with persistent pulmonary inflammation, ROS, cell injury and proliferation, and fibrosis in rats and mice; and with gene mutation and lung tumors in rats. Qualitatively similar lung responses, including reduced lung clearance, pulmonary inflammation, and fibrosis, have been observed in workers in dusty jobs, although elevated lung tumors have not been observed in epidemiologic studies of TiO2 workers Baan et al.
Recent subchronic studies in rats confirm earlier findings that particle size as well as crystal structure and coatings can influence pulmonary responses inflammation, cytotoxicity, and cell proliferation to TiO2 Sager et al. The observation of inhaled discrete nanoscale TiO2 particles inside rat alveolar epithelial cell organelles, including the nucleus Geiser et al. Epidemiologic studies with well-characterized exposures and adequate follow-up are needed, especially for workers producing or using nanoscale TiO2.
Possible cohorts include workers in industries using nanoscale TiO2, such as the cosmetic industry. Given increasing applications of nano-TiO2 in consumer products, there is a need to develop better techniques to detect TiO2 in tissues and to examine possible carcinogenicity of nano-TiO2 by other routes of exposure e. Diesel engine exhaust Two meta-analyses estimated the summary risk for lung cancer and diesel engine exhaust DE exposure to range from 1.
Two studies nearing completion will provide information on quantitative exposure—response data based on historical exposure estimates. These include a cohort and nested case—control study of lung cancer in U. If the research demonstrates exposure response, it will be important to identify the underlying mechanisms of DE-induced carcinogenesis and identify the components of DE that are most biologically active in humans.
These and other biomarkers could be incorporated in cross-sectional epidemiologic studies of DE exposure and biomarkers of inflammation, genotoxicity, and other relevant early biological effects. Refractory ceramic fibers Refractory ceramic fibers RCF , which have replaced asbestos as high-temperature insulation, induce benign and malignant lung tumors in rats Mast et al. Only one small U. A European study found an exposure-related excess of pleural plaques after controlling for past asbestos exposure Cowie et al.
Identification and follow-up of new and established U. Animal research has not been conducted on the combined effects of RCF and granular, low-biosoluble particles such as TiO2, which can aggravate effects of inhaled fibers.
The impact of fiber length on carcinogenicity should also be investigated. The validity of negative dose—response data in rats after inhalation exposure to RCF is questionable because there are indications that the sensitivity of the rat inhalation model with man-made fibers is relatively low Muhle and Pott ; Wardenbach et al.
Future research in developing a sensitive rat inhalation model for RCF is needed. Carbon black Sorahan and Harrington reported elevated lung cancer in an update of the U. Several recent subchronic studies in rats and mice Duffin et al. Research needs include updating epidemiology cohorts with data on work histories and exposures in relation to particle size and surface area, and recruitment of additional carbon black facilities.
The relationship between occupational exposure to carbon black and validated biomarkers of oxidative stress should be examined and exposure—response relationships in humans and rodents quantified, including the role of particle size. Styrene and styrene-7,8-oxide In , a U. National Toxicology Program NTP expert panel reviewed styrene, finding limited evidence in humans but sufficient evidence of animal carcinogenicity from multiple studies in mice by multiple routes Styrene Expert Panel Epidemiologic studies of styrene in the styrene—butadiene rubber industry have been limited by multiple exposures, a limitation partially addressed by retrospective exposure assessment Sathiakumar et al.
Studies in the fiberglass boat— building industry have been limited by small size and short duration of exposure Ruder et al. Interpretation of the epidemiologic evidence is complicated by findings of higher risk in less-exposed cohorts, variation in high-LHC sites in different studies, and inconsistency in findings for pancreatic cancer.
At least 70 publications released since the styrene monograph IARC explore various mechanistic aspects of potential carcinogenicity in humans and rodents. Recommendations for new research include pooled analyses of human studies on chromosome aberrations and other genotoxic effects and updating the existing epidemiologic studies with particular attention to the accurate diagnosis and classification of LHCs.
Recent exposure and biomarker studies have shown that PO forms chemically stable hemoglobin and DNA adducts and that concentrations of these adducts are related linearly to air concentrations of PO Boogaard et al. Potential cohorts for future epidemiologic studies exist in a number of industries and countries; occupational study cohorts should include women, if possible, because PO might be a mammary carcinogen Rudel et al.
Formaldehyde Formaldehyde has been classified by IARC as a Group 1 carcinogen based on sufficient evidence for nasopharyngeal cancer in humans Baan et al. Both IARC and the NTP scientific review panel have recently supported a causal relation between formaldehyde and acute myeloid leukemia based on new research findings Baan et al. Mechanisms through which inhaled formaldehyde may cause leukemia should be explored further, including exposure to circulating blood or stem cells in the nose and pathways by which inhaled formaldehyde or formaldehyde-derived intermediates can reach bone marrow or lymphatic tissue.
Follow-up of existing occupational cohorts should continue, with registry linkage to identify incident cancers and attention to appropriate classification and grouping of LHCs. Additional studies of the genotoxic and hematologic effects of formaldehyde exposure in occupational cohorts and in experimental animals would be useful, and such studies should incorporate sensitive biological markers of internal dose. Acetaldehyde Acetaldehyde is the first metabolite of ethanol oxidation.
These studies strongly suggest that acetaldehyde derived from the metabolism of ethanol contributes to upper digestive tract cancers. The accumulated scientific evidence warrants a new evaluation of acetaldehyde by IARC. Exposures to acetaldehyde in occupational settings should be characterized and the potential for conducting epidemiologic studies explored.
These studies should consider all potential sources of exposure to acetaldehyde and the extent to which genetic polymorphisms influence carcinogenic risks. Studies in the flavoring industry may be of particular interest. Meta-analyses would be useful because individual studies have limited statistical power for these relatively uncommon cancer sites. Additional studies of cancer incidence and mortality in new cohorts without multiple solvent exposures e.
Research is needed to determine which TCE metabolites are the agents of carcinogenesis for specific sites. Studies of effects of TCE exposure on cell-signaling pathways and epigenetic changes induced by TCE and its metabolites would help in determining potential mechanisms of carcinogenicity. TCE is metabolized by the cytochrome P CYP pathway to oxidative metabolites and by the glutathione GSH conjugation pathway to genotoxic metabolites; incorporation of data on genetic polymorphisms in glutathione S-transferase and CYP2E1 would be useful in this regard.
Further studies in this industry could be facilitated by using exhaled-breath specimens for study inclusion and exposure assessment McKernan et al. A major research gap is that mechanisms of carcinogenicity are not characterized sufficiently or tested; studies are needed that evaluate the genotoxic and oxidative potential of alternative metabolic pathways.
Last, adequate physiologically based pharmacokinetic PBPK models should be developed that allow for prediction of metabolism and difference in metabolism between species for a number of key metabolites to aid in the identification of sensitive subpopulations and target organs for a carcinogenic response.
Epidemiologic case—control and cohort studies have found positive, but inconsistent, associations for cancers of a number of sites. Based on animal and epidemiologic studies to date, sites of particular interest for future studies include brain, breast, and the lymphohematopoietic system. Available epidemiologic studies of DCM are limited by small numbers of exposed cases, few women enrolled, and poor exposure assessments.
The major research need is the identification of new large cohorts with adequate numbers of women and robust exposure assessment using current and retrospective department-specific exposure or biological markers. In addition to identifying larger cohorts of film and textile workers, some potential new occupations include workers in furniture stripping or automobile body repair shops.
Urinary DCM has been shown to correlate with air measurements Imbriani and Ghittori , and studies are needed to develop and evaluate urinary DCM measurements for use in exposure assessment. Recent mechanistic studies have questioned the role of the GSH pathway in toxicity Landi et al.
Clearly, research is needed with regard to the metabolites involved and the mechanism of carcinogenicity of DCM-induced rodent tumors, especially in the context of informing human risk. Before accurate PBPK models can be developed, the metabolism and metabolites responsible for toxicity at specific targets should be investigated. Chloroform trichloromethane Chloroform causes cancer in rats and mice, most likely through a mechanism involving cytotoxicity Schoeny et al.
Exposure to chloroform is primarily through drinking water and swimming pool water; thus, the epidemiology is based on exposure to this complex mixture and not to chloroform per se. Since the last IARC evaluation IARC a , several epidemiologic studies have been published on the association between exposure to chloroform in disinfection by-products DBPs and risk of bladder cancer, including a pooled analysis of previous case—control studies Villanueva et al. Exposures to chloroform and other DBPs may be higher from showering, bathing, or swimming than from oral exposure to drinking water.
Epidemiologic case—control studies should incorporate information on route of exposure and detailed DBP exposure assessment, as well as pooling information from multiple studies and countries, where feasible. There should also be follow-up of cohorts of medical personnel exposed to chloroform when chloroform was used as an anesthetic gas. Moreover, mixtures of PCBs associated with occupational and environmental exposure have changed over time and vary across the occupational and population groups studied.
In addition, environmental and metabolic processes substantially alter the composition of PCB mixtures in the environment and in the body. As a result, residual PCBs in the environment involve altered mixtures differing in composition—and possibly more toxic and persistent—than the mixtures that were used commercially Cogliano Among most occupational cohorts, dermal and airborne exposures predominate, whereas among the general population, dietary exposures are generally most significant.
Although most studies of highly exposed occupational cohorts find cancer excesses for specific cancer sites, the sites involved have been quite variable. Associations between NHL and levels of certain PCB congeners in serum have been reported in several cohort and case—control studies Engel et al.
More research is needed on these mechanisms and on cell proliferation, which could also play an important role in the induction of mutations and subsequent carcinogenicity. Di 2-ethylhexyl phthalate DEHP Although extensive human exposure to DEHP occurs through its use as a plasticizer of polyvinyl chloride PVC , definitive epidemiologic studies are not available because of the difficulty in identifying highly exposed workers in retrospective cohort or case—control studies.
Animal studies have also suggested additional target organs in rats [pancreatic acinar-cell adenoma David et al. Further characterization of DEHP exposures in industry is needed and could be carried out in established cohorts in PVC-processing factories using monoethylhexyl phthalate and mono 2-ethylcarboxypentyl phthalate as sensitive and specific biomarkers of DEHP exposure. Atrazine Schoeny et al. Although the mechanism by which atrazine causes mammary tumors in Sprague-Dawley rats may not be relevant to humans Schoeny et al.
For example, does atrazine interfere with the hypothalamic—pituitary—ovarian axis or alter the secretion of luteinizing hormone and prolactin in humans?
More extensive microarray and proteomic studies in rodents and humans would help to characterize the pathways disrupted by atrazine. Studies should also investigate the ability of atrazine to alter immune function and aromatase in species relevant to humans, as well as in human molecular epidemiology studies.
Several studies have found nonsignificant associations between atrazine exposure and NHL; for example, a study of 36, atrazine-exposed pesticide applicators in the U. Follow-up of the AHS cohort through is now under way and, along with analysis of biomarkers among corn farmers and similar studies in atrazine-exposed women Bakke et al. Shift work Excess incidence of breast cancer has been observed consistently in studies of women with prolonged exposure to shift work involving exposure to light at night Kolstad ; Stevens Research needs in this area include a a better definition of what is meant by shift work and related exposure metrics; b studies of markers of circadian disruption in non—day workers; c better descriptions of controls and their exposure to light at night; and d investigation of the effect of variations in expression of circadian genes on cancer in shift workers.
An emerging area of interest is the relative toxicity of occupational chemical exposure depending on time of day of that exposure. The marked circadian variations in cell division and DNA repair during the daily cycle are controlled by the circadian genes Haus and Smolensky ; Stevens et al.
Therefore, non—day workers may have very different susceptibility to occupational exposures compared with day workers. Studies are also needed to determine if shift work is associated with other cancers, especially hormonally related cancers, and prostate cancer in particular. If further experimental and epidemiologic evidence confirms a causal association between exposure to light at night and breast cancer, it will be important to develop interventions to reduce the risk. Conclusions Research gaps and opportunities have been identified that can help to resolve uncertainties regarding the carcinogenicity in humans of a number of important IARC-classified agents.
We hope that this process will lead to well-planned epidemiologic and mechanistic studies for these agents, as well as renewed interest and funding for studies of agents for which there are substantial or widespread occupational and environmental exposures. Several important scientific developments are likely to increase the challenges and complexities of carcinogen testing and evaluation in the future.
Use of omics techniques will accelerate the understanding of the cellular and molecular basis for biological responses to environmental and occupational exposures, and high-throughput technologies will increase the number of agents that can be tested. The important role of organ and organism-level responses such as inflammation, immunomodulation, and hormonal influences, as well as interindividual variation in susceptibility and genetic repair in the carcinogenic process, are increasingly understood.
Therefore, the science of carcinogen testing and evaluation must be increasingly multidisciplinary, examining biologic responses from the molecular to the organism, and using test systems and approaches that capture multiple mechanisms and end points. Most carcinogenic mechanisms are not simple, and evidence is often too limited to conclude lack of relevance to humans.
When evidence regarding mechanism is considered in the upgrading or downgrading of carcinogens, it should be evaluated with the same rigor as traditional epidemiologic and bioassay data [see, for example, the IARC preamble IARC e with regard to epidemiologic studies, including types of studies to be considered, quality of studies, role of meta- and pooled analyses, and criteria for causality].
Epidemiologic studies will be particularly critical in evaluating the relationship between intermediate biomarkers and cancer risk in occupational groups or in the general population and in investigating genetic susceptibility factors. In the rush to embrace new biotechnologies in epidemiology, we must not lose sight of the tremendous gains in knowledge that have accrued from conventional epidemiologic occupational cohort and case—control studies.
We encourage investigators to continue to search for study populations in which the linkage of work history information and mortality or cancer incidence data can be informative about the cancer risks of workers with different job or industry titles or different exposure histories. We also encourage release in deidentified form of completed epidemiologic studies for reanalysis, as is commonly done with government-funded studies in the United States.