Evidence Of Carcinogenicity In Humans Research Articles

SAT565 Is Firefighting An Occupational Risk For Papillary Thyroid Cancer? A Case Report

Abstract Disclosure: S.A. Diamond-Rossi: None. P. Lee: None. C. Thomas: None. R. Stanislawski: None. J. Kim: None. Background: Papillary thyroid cancer (PTC) is the most prevalent histologic type of thyroid cancer. The toxic exposures associated with firefighting from both protective gear and combustion products have brought to question whether this population is at an increased risk of developing certain malignancies, including thyroid cancer. The objective of this case report is to raise awareness of the possible association between firefighting and thyroid cancer. Case Presentation: A 46-year-old asymptomatic male career firefighter presented to our clinic following a mobile screening thyroid ultrasound which revealed bilateral suspicious nodules. FNAs of a 1.0 cm right nodule and 1.2 cm left nodule were consistent with papillary thyroid cancer. Lymph node mapping revealed bilateral suspicious lymph nodes in levels 3 and 4 with FNAs confirming metastatic PTC. He underwent total thyroidectomy with bilateral central and lateral lymph node dissections confirming multifocal disease, which included numerous submillimeter foci of PTC. 21 of 68 lymph nodes had metastatic disease. He is now scheduled for adjuvant radioactive iodine therapy. Discussion: Compared to the general population, firefighters have a higher incidence of thyroid cancer. In 2022, the International Agency for Research on Cancer (IARC) announced that occupational exposure as a firefighter would be considered a Group 1 carcinogen, designating this exposure as having sufficient evidence for carcinogenicity in humans. In recognition of this risk, our local fire department, the Fairfax County Fire & Rescue, has implemented a cancer screening protocol offered to firefighters which includes a mobile thyroid ultrasound. Our patient had extensive disease with bilateral lymph node involvement requiring radioactive iodine after surgical resection. Without a screening ultrasound, it can be presumed that our patient would have presented later and perhaps with even more advanced disease. Firefighters are exposed to carcinogens and possible endocrine disrupting chemicals as part of their work, either via their protective equipment or products of the fire itself. More research is needed to determine if the higher incidence of thyroid cancer can be attributed to this occupational exposure versus surveillance bias due to increased screening of this population in recent years. Presentation: Saturday, June 17, 2023

Effects of radiofrequency electromagnetic fields (RF EMF) on cancer in laboratory animal studies.

The carcinogenicity of radiofrequency electromagnetic fields (RF EMF) has been evaluated by the International Agency for Research on Cancer (IARC) in 2011. Based on limited evidence of carcinogenicity in humans and in animals, RF EMF were classified as possibly carcinogenic to humans (Group 2B). In 2018, based on a survey amongst RF experts, WHO prioritized six major topics of potential RF EMF related human health effects for systematic reviews. In the current manuscript, we present the protocol for the systematic review of experimental laboratory animal studies (cancer bioassays) on exposure to RF fields on the outcome of cancer in laboratory animals. In the framework of WHO's Radiation Program, the aim of this work is to systematically evaluate effects of RF EMF exposure on cancer in laboratory animals. WHO's Handbook (2014) for guideline development will be followed with appropriate adaptation. The selection of eligible studies will be based on Population, Exposures, Comparators, and Outcomes (PECO) criteria. We will include peer-reviewed articles and publicly available reports from government agencies reporting original data about animal cancer bioassays on exposure to RF EMF. The studies are identified by searching the following databases: MEDLINE (PubMed), Science Citation Index Expanded and Emerging Sources Citation Indes (Web of Science), Scopus, and the EMF Portal. No language or year-of-publication restrictions are applied. The methods and results of eligible studies will be presented in accordance with the PRISMA 2020 guidelines. Study evaluation of individual studies will be assessed using a risk of bias (RoB) tool developed by the Office of Health Assessment and Translation (OHAT) with appropriate considerations including sensitivity for evaluating RF EMF exposure in animal cancer bioassays. The final evaluation on the certainty of the evidence on a carcinogenic risk of RF EMF exposure in experimental animals will be performed using the OHAT Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach with appropriate considerations. The protocol has been registered in an open-source repository (PROSPERO). The study is partly financially supported by the World Health Organization. No additional funding was provided outside author salaries through their places of employment.

REMOVAL OF BERYLLIUM (Be2+) FROM WATER SAMPLES BY SORPTION PROCESS: A REVIEW

Beryllium (Be2+) is an important industrial metal because of its unusual material properties: it is lighter than aluminium and six times stronger than steel. Beryllium is a strategic metal due to its low density combined with its strength, low neutron absorption, high melting point and high modulus of elasticity. Beryllium is often alloyed with other metals such as copper and is an important component of materials used in the aerospace, automotive, energy, defense, medical, and electronics industries. However, beryllium and its compounds are very toxic, especially to the lungs, skin, and eyes. Beryllium compounds are known carcinogens based on sufficient evidence of carcinogenicity in humans from human studies. Toxic effects of beryllium include immunotoxic, allergic, mutagenic, and carcinogenic effects. Mammalian tissues do not excrete it, so the effects are cumulative and can lead to death at high concentrations. Therefore, removal of Be2+ is important. In this review, the removal of Be2+ from water samples by sorption processes using different sorbents was summarized. The effects of process parameters on the removal of Be2+ have been summarized. The work discussed showed that ion exchange resins, various modified biosorbents metal oxides can be used for the removal of Be2+. The results showed that the pH of the solution has an important effect on the removal rate. Sorption kinetics vary from 3 minutes to 48h. When the functional groups are on the surface of the sorbent, the sorption process is rapid. However, if the surface of the sorbent is covered with oxides such as magnetite, it takes longer to reach equilibrium. Published work shows that more than 99 % of Be2+ can be removed from solution.

2,2’-dichloro-4,4’-methylenedianiline – inhalable fraction and vapours. Documentation of proposed values of occupational exposure limits (OELs)

2,2’-dichloro-4,4’-methylenedianiline – inhalable fraction and vapours. Documentation of proposed values of occupational exposure limits (OELs)

Extremely low-frequency magnetic fields and risk of childhood leukemia: A risk assessment by the ARIMMORA consortium.

Exposure to extremely low-frequency magnetic fields (ELF-MF) was evaluated in an International Agency for Research on Cancer (IARC) Monographs as "possibly carcinogenic to humans" in 2001, based on increased childhood leukemia risk observed in epidemiological studies. We conducted a hazard assessment using available scientific evidence published before March 2015, with inclusion of new research findings from the Advanced Research on Interaction Mechanisms of electroMagnetic exposures with Organisms for Risk Assessment (ARIMMORA) project. The IARC Monograph evaluation scheme was applied to hazard identification. In ARIMMORA for the first time, a transgenic mouse model was used to mimic the most common childhood leukemia: new pathogenic mechanisms were indicated, but more data are needed to draw definitive conclusions. Although experiments in different animal strains showed exposure-related decreases of CD8+ T-cells, a role in carcinogenesis must be further established. No direct damage of DNA by exposure was observed. Overall in the literature, there is limited evidence of carcinogenicity in humans and inadequate evidence of carcinogenicity in experimental animals, with only weak supporting evidence from mechanistic studies. New exposure data from ARIMMORA confirmed that if the association is nevertheless causal, up to 2% of childhood leukemias in Europe, as previously estimated, may be attributable to ELF-MF. In summary, ARIMMORA concludes that the relationship between ELF-MF and childhood leukemia remains consistent with possible carcinogenicity in humans. While this scientific uncertainty is dissatisfactory for science and public health, new mechanistic insight from ARIMMORA experiments points to future research that could provide a step-change in future assessments. Bioelectromagnetics. 37:183-189, 2016. © 2016 Wiley Periodicals, Inc.

Historical review of the causes of cancer.

In the early 1900s, numerous seminal publications reported that high rates of cancer occurred in certain occupations. During this period, work with infectious agents produced only meager results which seemed irrelevant to humans. Then in the 1980s ground breaking evidence began to emerge that a variety of viruses also cause cancer in humans. There is now sufficient evidence of carcinogenicity in humans for human T-cell lymphotrophic virus, human immunodeficiency virus, hepatitis B virus, hepatitis C virus, human papillomavirus, Epstein-Barr virus, and human herpes virus 8 according to the International Agency for Research on Cancer (IARC). Many other causes of cancer have also been identified by the IARC, which include: Sunlight, tobacco, pharmaceuticals, hormones, alcohol, parasites, fungi, bacteria, salted fish, wood dust, and herbs. The World Cancer Research Fund and the American Institute for Cancer Research have determined additional causes of cancer, which include beta carotene, red meat, processed meats, low fibre diets, not breast feeding, obesity, increased adult height and sedentary lifestyles. In brief, a historical review of the discoveries of the causes of human cancer is presented with extended discussions of the difficulties encountered in identifying viral causes of cancer.

Human Health Effects of Biphenyl: Key Findings and Scientific Issues.

Background:In support of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) has evaluated the human health hazards of biphenyl exposure.Objectives:We review key findings and scientific issues regarding expected human health effects of biphenyl.Methods:Scientific literature from 1926 through September 2012 was critically evaluated to identify potential human health hazards associated with biphenyl exposure. Key issues related to the carcinogenicity and noncancer health hazards of biphenyl were examined based on evidence from experimental animal bioassays and mechanistic studies.Discussion:Systematic consideration of experimental animal studies of oral biphenyl exposure took into account the variety of study designs (e.g., study sizes, exposure levels, and exposure durations) to reconcile differing reported results. The available mechanistic and toxicokinetic evidence supports the hypothesis that male rat urinary bladder tumors arise through urinary bladder calculi formation but is insufficient to hypothesize a mode of action for liver tumors in female mice. Biphenyl and its metabolites may induce genetic damage, but a role for genotoxicity in biphenyl-induced carcinogenicity has not been established.Conclusions:The available health effects data for biphenyl provides suggestive evidence for carcinogenicity in humans, based on increased incidences of male rat urinary bladder tumors at high exposure levels and on female mouse liver tumors. Kidney toxicity is also a potential human health hazard of biphenyl exposure.Citation:Li Z, Hogan KA, Cai C, Rieth S. 2016. Human health effects of biphenyl: key findings and scientific issues. Environ Health Perspect 124:703–712; http://dx.doi.org/10.1289/ehp.1509730

Phenoxy herbicides, soft-tissue sarcoma and non-Hodgkin lymphoma: a systematic review of evidence from cohort and case-control studies.

Phenoxy herbicides have been used widely in agriculture, forestry, parks and domestic gardens. Early studies linked them with soft-tissue sarcoma (STS) and non-Hodgkin lymphoma (NHL), but when last reviewed by the International Agency for Research on Cancer in 1986, the evidence for human carcinogenicity was limited. We searched Medline and Embase, looking for cohort or case-control studies that provided data on risk of STS and/or NHL in relation to phenoxy herbicides, and checked the reference lists of relevant publications for papers that had been missed. The extensive evidence is not entirely consistent, and a hazard of STS or NHL cannot firmly be ruled out. However, if there is a hazard, then absolute risks must be small. Extended follow-up of previously assembled cohorts may be the most efficient way of further reducing uncertainties.

Fast and simple screening for the simultaneous analysis of seven metabolites derived from five volatile organic compounds in human urine using on-line solid-phase extraction coupled with liquid chromatography-tandem mass spectrometry

Recently, the International Agency for Research on cancer classified outdoor air pollution and particulate matter from outdoor air pollution as carcinogenic to humans (IARC Group 1), based on sufficient evidence of carcinogenicity in humans and experimental animals and strong mechanistic evidence. In particular, a wide variety of volatile organic compounds (VOCs) are volatized or released into the atmosphere and can become ubiquitous, as they originate from many different natural and anthropogenic sources, such as paints, pesticides, vehicle exhausts, cooking fumes, and tobacco smoke. Humans may be exposed to VOCs through inhalation, ingestion, or dermal contact, which may increase the risk of leukemia, birth defects, neurocognitive impairment, and cancer. Therefore, the focus of this study was the development of a simple, effective and rapid sample preparation method for the simultaneous determination of seven metabolites (6 mercaptic acids+t,t-muconic acid) derived from five VOCs (acrylamide, 1,3-butadiene, acrylonitrile, benzene, and xylene) in human urine by using automated on-line solid-phase extraction (SPE) coupled with liquid chromatography–electrospray tandem mass spectrometry (LC–MS/MS). An aliquot of each diluted urinary sample was directly injected into an autosampler through a trap column to reduce contamination, and then the retained target compounds were eluted by back-flush mode into an analytical column for separation. Negative electrospray ionization tandem mass spectrometry was utilized for quantification. The coefficients of correlation (r2) for the calibration curves were greater than 0.995. Reproducibility was assessed by the precision and accuracy of intra-day and inter-day precision, which showed results for coefficient of variation (CV) that were low 0.9 to 6.6% and 3.7 to 8.5%, respectively, and results for recovery that ranged from 90.8 to 108.9% and 92.1 to 107.7%, respectively. The limits of detection (LOD) and limits of quantification (LOQ) were determined to within 0.010 to 0.769ngmL−1 and 0.033 to 2.564ngmL−1 in this study. A stability study test included 3 freeze/thaw cycles during short-term storage at room temperature for 36h and long-term storage at −20°C for 1 month, and the CV (coefficient of variation) showed less than 8.4, 7.4 and 9.7%, respectively. To the best of our knowledge, this is the first study to provide simple, small injection volumes (40µL) and a rapid LC–MS/MS method combined with an on-line SPE step for the simultaneous detection, identification, and quantification of seven metabolites derived from five VOCs in human urine for evaluation of the future risk of human exposure to volatile organic compounds.

Influence of usage time on exposure of snus users to nicotine, NNN and NNK from snus pouches

Poster POS1-23 presented at 2012 SRNT 18th Annual Meeting, March 13-16, Houston, Texas, USA. This study was entirely funded by British American Tobacco INTRODUCTION Measuring the amount of constituents extracted by snus consumers during use is a valuable step in estimating exposure to tobacco constituents. A factor potentially influencing the extent of exposure is the length of time that individual consumers keep snus pouches in their mouths during use. A 2007/2008 survey of snus use in Sweden established that, on average, use of pouched snus extends from approximately 30 minutes to just less than 120 minutes1. The objective of this study therefore was to quantify the importance of use duration on constituent transfer from pouched snus to the consumer over this timescale. The constituents selected for evaluation were nicotine and the two tobacco-specific nitrosamines (TSNAs) classified by IARC as Group 1 (sufficient evidence of carcinogenicity in humans)2, 4-(N-Methylnitrosamino)-1-(3-pyridinyl)-1-butanone (NNK) and N-Nitrosonornicotine (NNN).

The International Agency for Research on Cancer (IARC) evaluation of the carcinogenicity of outdoor air pollution: focus on China.

The International Agency for Research on Cancer (IARC) has classified outdoor air pollution and the particulate matter (PM) in outdoor air pollution as carcinogenic to humans, as based on sufficient evidence of carcinogenicity in humans and experimental animals and strong support by mechanistic studies. The data with important contributions to the evaluation are reviewed, highlighting the data with particular relevance to China, and implications of the evaluation with respect to China are discussed. The air pollution levels in Chinese cities are among the highest observed in the world today and frequently exceed health-based national and international guidelines. Data from high-quality epidemiologic studies in Asia, Europe, and North America consistently show positive associations between lung cancer and PM exposure and other indicators of air pollution, which persist after adjustment for important lung cancer risk factors, such as tobacco smoking. Epidemiologic data from China are limited but nevertheless indicate an increased risk of lung cancer associated with several air pollutants. Excess cancer risk is also observed in experimental animals exposed to polluted outdoor air or extracted PM. The exposure of several species to outdoor air pollution is associated with markers of genetic damage that have been linked to increased cancer risk in humans. Numerous studies from China, especially genetic biomarker studies in exposed populations, support that the polluted air in China is genotoxic and carcinogenic to humans. The evaluation by IARC indicates both the need for further research into the cancer risks associated with exposure to air pollution in China and the urgent need to act to reduce exposure to the population.

Carcinogenicity of implanted synthetic grafts and devices

Cancer in women is a common cause of morbidity and death,and the aetiology is frequently unknown. Potential carcino-genic agents are all around us: in the air we breathe, the foodand fluids we digest, and in the background radiation thatsurroundsus.Also,diagnosticandtherapeuticagentshavethepotential to induce cancer in some patients under some cir-cumstances: X-ray investigations, radiation treatment, drugsand hormones with oestrogen are well-known examples. Toprove these associations and calculate risk is always a longand arduous scientific process, but what can be even moredifficultistoprovethatthereisnoriskorassociationbetweenvarious environmental factors or medical treatments and can-cer. There will always be an inherent risk of cancer occurringin any individual, but is this increased, and if so by howmuch? A recent example is the reported association betweenmobilephoneuse,low-level exposuretoradiofrequencyelec-tromagnetic fields and brain tumours. The evidence to datefrom multiple studies is that there is no increased risk ofacoustic neuroma [1] or brain tumours [2], but larger andlonger-term studies are needed.Implantable devices and grafts also have the potential toinduce cancer; thus, it is an important matter that is discussedby Ostergard and Azadi [3] in this issue of our journal. Theauthorsraisetheissueofthecarcinogenicityofpolypropylene(PPL) in animals and humans. Despite extensively searchingthe literature on PPL they found little evidence of carcinoge-nicity in humans, with only two cases in patients with poly-ester mesh grafts who had chronic infection and developed asquamous cell carcinoma 6 and 24 years following insertion[4]. As stated by Ostergard and Azadi [3], chronic inflamma-tionoflongdurationisaknowncauseofcancer.Themeshdidcontribute to the infection and inflammation, but is it in itselfcarcinogenic?By 3 months after implantation, PPL mesh is surroundedbymature connectivetissueand only rarely becomes infectedunless inappropriately situated, for instance, protruding intothe bowel, bladder or vagina. Synthetic mesh, including PPL,has been used in urogynaecological surgery since the 1960s[5, 6], and even more widely in other forms of reconstructivesurgery, such as hernia repair. Despite the millions of patientsworldwide who have had PPL implanted, the authors couldfind no evidence of an association with cancer, or any casereports.Thisshouldgiveourpatientsconsiderableconfidencethat their PPL implants will not cause cancer. However, thereare risks associated with graft and mesh usage; these do needto be carefully weighed against the potential benefits whenused in reconstructive surgery.WehavebalancedtheOstergardandAzadiarticlewithtwoother contributions written by experts in urogynaecology andPPL mesh and biomaterials [7, 8]. We hope that open discus-sionleads to a better understanding of thissensitive issue,notonlybyclinicians,butalso,justasimportantly,bythebroadercommunity, who can be reassured that even the most difficultissues will be scientifically assessed and discussed.References

The Weight of Evidence Does Not Support the Listing of Styrene as “Reasonably Anticipated to be a Human Carcinogen” in NTP's Twelfth Report on Carcinogens

ABSTRACT Styrene was listed as “reasonably anticipated to be a human carcinogen” in the twelfth edition of the National Toxicology Program's Report on Carcinogens based on what we contend are erroneous findings of limited evidence of carcinogenicity in humans, sufficient evidence of carcinogenicity in experimental animals, and supporting mechanistic data. The epidemiology studies show no consistent increased incidence of, or mortality from, any type of cancer. In animal studies, increased incidence rates of mostly benign tumors have been observed only in certain strains of one species (mice) and at one tissue site (lung). The lack of concordance of tumor incidence and tumor type among animals (even within the same species) and humans indicates that there has been no particular cancer consistently observed among all available studies. The only plausible mechanism for styrene-induced carcinogenesis—a non-genotoxic mode of action that is specific to the mouse lung—is not relevant to humans. As a whole, the evidence does not support the characterization of styrene as “reasonably anticipated to be a human carcinogen,” and styrene should not be listed in the Report on Carcinogens.

Use of Meta-analyses by IARC Working Groups

Use of Meta-analyses by IARC Working Groups

Hepatocellular adenoma associated with long-term exposure to phenobarbital: a paediatric case report

Hepatocellular adenoma is a rare, benign liver tumour diagnosed predominantly in women on oral contraceptive therapy [1, 2]. Hepatocellular adenoma has also been described in patients taking anabolic androgenic steroids [3] and in those with some inherited metabolic disorders, as type 1 glycogen storage disease [4, 5]. Hepatocellular adenoma is a benign proliferation of hepatocytes in an otherwise normal liver and it constitutes 0.6% of all liver tumours [1–3]. Phenobarbital is the most widely used antiepileptic drug in the developing world and in many industrialised countries. It has many advantages, including affordable cost, broad spectrum of action and ease of use. Phenobarbital demonstrates overall tolerability similar to that of other established antiepileptic drugs, and serious systemic side effects are uncommon. Hepatotoxicity and teratogenicity are rare potential side effects of phenobarbital [6]. Early studies and epidemiological latest reports found an association between phenobarbital and hepatocellular tumour [7–12]. Phenobarbital was one of the first drugs for which carcinogenicity was demonstrated in several animal experiments [13– 15]. However, despite several long-term pharmacoepidemiological data being available for phenobarbital, evidence for human carcinogenicity is not consistent and phenobarbital is considered only possibly carcinogenic to humans [16]. A liver tumour-promoting action of some antiepileptic drugs, as oxcarbazepine, sodium valproate and carbamazepine, has known, also in young patients [17–19]. To date, there are no reports in the paediatric population of hepatocellular adenoma associated with phenobarbital therapy. Herein, we describe one case concerning a 13-year-old girl with hepatocellular adenoma associated with long-term use of phenobarbital.

Update of carcinogenicity studies in animals and humans of 535 marketed pharmaceuticals

This survey is a compendium of information retrieved on carcinogenicity in animals and humans of 535 marketed pharmaceuticals whose expected clinical use is continuous for at least 6 months or intermittent over an extended period of time. Of the 535 drugs, 530 have the result of at least one carcinogenicity assay in animals, and 279 (52.1%) of them gave a positive response in at least one assay. Only 186 drugs (34.8%) have retrievable information on carcinogenicity in humans, and 104 of them gave to a variable extent evidence of a potential carcinogenic activity. Concerning the correlation between results obtained in animals and epidemiological findings, 58 drugs gave at least one positive result in carcinogenicity assays performed in animals and to a variable extent displayed evidence of carcinogenicity in humans, but 97 drugs tested positive in animals and were noncarcinogenic in humans or vice versa. Our findings, which are in agreement with previous studies, indicate that the evaluation of the benefit/carcinogenic risk ratio should be always made in prescribing a drug.

Formaldehyde and cancer risk – an updated quantitative review of cohort studies

ObjectivesIn 2006, IARC concluded that the evidence for carcinogenicity in humans was adequate for nasopharyngeal cancer. In the most recent meta-, a non-significantly raised relative risk was determined for nasopharyngeal...

A Compendium of Challenges: Assessing the State of the Science on Occupational Carcinogens

Uncertainties abound about the adverse health effects of exposure to carcinogens found in today’s workplaces. Even with substantial toxicologic evidence of carcinogenicity, cancer risks for humans often remain inconclusive, thus delaying regulatory action and the search for safer alternatives. A new systematic review by the International Agency for Research on Cancer (IARC) identifies research gaps and needs for 20 agents prioritized for review on the basis of evidence of widespread human exposures and potential carcinogenicity in animals or humans [EHP 118(10):1355–1362; Ward et al.]. Drawing from an international collaboration by 25 health and research agencies and institutions, the report summarizes recommendations and broaches key topics pertaining to several chemicals, metals, dusts, and physical agents for which there is widespread human exposure, predominantly in occupational settings. The authors emphasize that carcinogenic agents can act through multiple pathways and mechanisms, including oxidative stress, epigenetic mechanisms, and immuno- and hormonal modulation. They then discuss overarching issues pertinent to the study of these mechanisms. For example, regarding the validation of oxidative stress biomarker assays, they write, “Research is needed to examine the relationship between exposure to toxic agents and oxidative stress biomarkers, and between these biomarkers and risk of cancer, while controlling for the many individual factors that contribute to oxidative stress.” Concerning genetic susceptibility to carcinogenic exposures, the authors caution that stable and reproducible associations are few. Examining genetic polymorphisms related to carcinogen metabolism and/or DNA repair may aid the identification of higher cancer risks in susceptible subgroups and clarify the role of specific agents in mixed exposures. Nonetheless, the magnitude of such associations may be modest and could entail multiple genes or metabolic pathways—thus making them hard to detect. The report deals with only a fraction of the potentially carcinogenic agents found in today’s workplaces, most of which have sufficient evidence of carcinogenicity in animals but limited evidence for carcinogenicity in humans. Because of a paucity of well-designed animal bioassays and human studies, insufficient evidence exists to evaluate animal or human carcinogenicity for most other agents. The report ends on a somber note, noting that substantial challenges for the study of environmental carcinogens remain, including a recent decline in funding for occupational cancer research, and that fewer scientists are entering the fields of epidemiology, toxicology, and exposure assessment.

Electric and magnetic fields at power frequencies

Exposures to electric and magnetic fields are among the most ubiquitous exposures that the Canadian population experiences. Sources of electric and magnetic field exposures may be occupational or residential and include proximity to certain types of electrical equipment, transmission and distribution power lines as well as appliance use. The early studies of children tended toward a consistent association between risks for leukemia and brain cancer and residential proximity to power lines having high wire configuration. More recent studies-and studies which have attempted to improve upon the measurement of exposure by using calculated fields, point-in-time or personal monitoring-have been inconsistent, with some suggesting increased risk and others not. Occupational exposures have suggested an increase in risk for leukemia, and to a lesser extent brain cancer and Non-Hodgkin lymphoma. However, studies of residential exposures and cancer in adults generally have suggested no effect. Laboratory work has been unable to demonstrate a biological mechanism which might explain the epidemiological findings. In spite of extensive efforts over the past 20 years and many expert reviews, it has been difficult to reach consensus regarding the carcinogenic effects of electric and magnetic fields. Exposure assessment has proven to be complex, and agreement on the relevant exposure metric has not yet been obtained. There is justification to question whether point-in-time measures in homes are appropriate indices of the relevant etiological exposure, as they fail to account for changes over time, peak exposures or time-varying fields. Nevertheless, it is probably desirable to err on the side of caution in not placing too much weight on the inconsistencies. The IARC has classified EMF as a "possible carcinogen" which refers to the circumstances where there is limited evidence of carcinogenicity in humans and inadequate evidence in experimental animals. The IARC review indicated limited evidence for the carcinogenicity of extremely low-frequency magnetic fields in relation to childhood leukemia at high level exposure in the residential environment (average residential magnetic field strength >0.4 μT). Even higher levels of exposure in the occupational environment may increase the risk of leukemia in adults.

Cancer and the environment: Ten topics in environmental cancer epidemiology in Canada

This Chronic Diseases in Canada supplement is a compilation of literature reviews by scientific experts. It was initiated as follow-up to the Green Plan, the federal government's environmental agenda in the 1990s. In recognizing that Canadians are concerned about the environment and its relationship to their health, this document attempts to address some of these concerns in relation to cancer by reviewing and summarizing the epidemiological literature for ten environmental exposures, and highlighting future research needs. The topics include three types of radiation exposure (ultraviolet, radon and electromagnetic (powerfrequency electromagnetic fields)), three classes of chemical exposure (organochlorines, disinfection by-products, and pesticides), two types of air pollution (environmental tobacco smoke and outdoor air pollution), and two industrial sources (pulp and paper milling, and metal mining and processing). This publication is intended to provide a base of information for researchers interested in environmental cancer epidemiology and to assist with the formulation of research priorities. The ten topics reviewed here were selected because concern about them has been expressed or because they involve known animal carcinogens. Complete elimination of exposures to carcinogens in the environment, synthetic or natural, is not technically feasible if cancer can potentially occur at any level of exposure (i.e., the linear non-threshold theory). Consequently, it is important to have an operational concept of safety which is more practical than that of zero risk. Such an approach uses the concept of acceptable or essentially negligible risk to determine the exposure levels at which carcinogens are regulated. Acceptable risk has been defined as one that is "so small, whose consequences are so slight, or whose associated benefits (perceived or real) are so great that persons or groups in society are willing to take or be subjected to that risk". The level of risk where remedial action is recommended will vary according to the "agent or process being regulated, the economic and social costs and benefits and technology factors". In accordance with the system used by the International Agency for Research on Cancer (IARC) to assess the strength of the evidence for human carcinogenicity, the ten exposures reviewed here can be grouped into three broad categories, with some exposures occupying more than one and the first category-human carcinogens-should be subdivided. Tables 1-4 refer to these categories. For many of the exposures discussed here, ongoing etiological research awaits methods development, particularly in exposure assessment.