Health effects of static magnetic fields--a review of the epidemiological evidence

Potential health effects of static magnetic fields have received far less attention than, for example, power frequency or radiofrequency fields. Static fields are found in certain occupational settings, e.g. in the aluminium and chloralkali industries, in arc-welding processes, and certain railways systems. Magnetic resonance imaging (MRI) for medical diagnosis is another source. This paper summarizes the epidemiological evidence of static magnetic field exposure and long-term health effects. There are only a few epidemiological studies available, and the majority of these have focused on cancer risks. There are some reports on reproductive outcomes, and sporadic studies of other outcomes. Overall, few occupational studies have focused specifically on effects of static magnetic field exposure, and exposure assessment have consequently been poor or non-existent. Results from studies that have estimated static magnetic field exposure have not indicated any increased cancer risks, but they are generally based on small numbers of cases and crude exposure assessment. Control of confounding has been limited, and it is likely that the “healthy worker” effect have influenced the results. A few studies have reported results on reproductive outcomes among aluminium workers and MRI operators, but limitations in study designs prevent conclusions. A problem in epidemiological studies of static magnetic fields is that workers in exposed occupations are also exposed to a wide variety of other potentially harmful agents, including some known carcinogens. In conclusion, the available evidence from epidemiological studies is not sufficient to draw any conclusions about potential health effects of static magnetic field exposure.     

A Review of the Epidemiology of Trichloroethylene and Kidney Cancer

The occupational epidemiological studies of trichloroethylene (TCE) exposure and kidney cancer are reviewed. Seven occupational cohort studies, conducted in the U.S., Finland, and Sweden involving over 130,000 workers, do not report statistically increased risks of kidney cancer among TCE-exposed workers. These studies were based on well-defined cohorts and exposure assessments involving urine biomonitoring or some type of job exposure matrix. In contrast, two German studies reported eight- to eleven-fold increased risks for renal cancer among TCE-exposed workers. However, numerous methodological and analytical shortcomings severely limit any interpretation of the German studies. We conclude that the more reliable epidemiologic data do not support a causal relationship between kidney cancer and TCE exposure.     

Industrial epidemiology.

Industrial epidemiology is a specialized discipline concerned with the study of disease occurrence in specific subgroups of the general population, i.e., of relatively healthy members of the work force for whom adequate records are available. Although the ultimate purpose of industrial epidemiology--the prevention of disease--is a logical extension of programs of industrial medicine and occupational and community health, epidemiologic methods must draw on interdisciplinary skills. The existence of centralized records kept in the course of business may make it easier to collect information about industrial populations than to gather data relative to other population subgroups. Many deficiencies in epidemiologic studies of worker groups, however, can be related to poor methods of data-gathering, inadequate record keeping, and an incomplete data base. Sources of information for epidemiologic studies of worker groups may include personnel and medical records, government reports, insurance files, production records, industrial hygiene measurements, surveys and questionnaires, and an organized follow-up program. In some cases, the ready availability of multiple sources of information may lead to differential information bias, and this should be avoided.     

Accuracy of industry and occupation on death certificates of electric utility workers: implications for epidemiologic studies of magnetic fields and cancer

A substantial epidemiologic literature has relied on occupation and industry information from death certificates to make inferences about the association of electric and magnetic field exposure with cancer, but the validity of the occupational data on death certificates is questionable. We compared occupation and industry information from death certificates to company work histories for 793 electric utility workers who died from brain cancer (n=143), leukemia (n=156), lung cancer (n=246, randomly sampled), and non-cancer causes (n=248, randomly sampled). Nearly 75% of death certificates correctly indicated utility industry employment and of those, 48% matched the longest held occupation derived from company work histories. Hence, only 36% matched on both industry and occupation. We computed odds ratios relating occupations involving magnetic field exposure to brain cancer and leukemia both for the occupation listed on the death certificate and for the longest-held occupation based on company records in order to examine the impact of exposure misclassification based on reliance on the death certificate information. For brain cancer, the odds ratio was 1.2 based on death certificates and 1.7 based on company work history, suggesting some attenuation due to misclassification. For leukemia, death certificate information yielded an odds ratio of 0.9, whereas company work histories yielded an odds ratio of 1.3. Although work histories are limited to the period of employment in a specific company, these data suggest that there is substantial misclassification in use of death certificate information on industry and occupation of utility workers, as found in other industries. The limited quality of occupation and industry information on death certificates argues against relying on such information to evaluate modest associations with mortality.     

Facteurs de risques environnementaux et/ou professionnels du cancer du testicule

Despite a low overall incidence (1% of all malignant neoplasms), testicular cancer is the most common malignancy among young men. Over the last 40 years, this incidence rate has substantially risen in most industrialised countries. However, the aetiology of testicular cancer remains largely unknown. Only cryptorchidism, and to a lesser extent a family history of testicular cancer, may be considered to be well established risk factors. Numerous attempts have been made to assess the potential role of occupational exposures in adult life as a risk factor for TC, but no clear hypotheses have yet emerged from previous studies in this field. A major limitation of all occupational studies is that no single toxic substance has been clearly identified, and consequently the significant association observed between some job titles and risk of testicular cancer must be interpreted very carefully. In this respect, comparative occupational studies of exposed and non-exposed workers including rigorous and valid job-matrix exposure assessment are needed to study potential relationships between certain occupational exposures and testicular cancer.     

The use of common genetic polymorphisms to enhance the epidemiologic study of environmental carcinogens

Overwhelming evidence indicates that environmental exposures, broadly defined, are responsible for most cancer. There is reason to believe, however, that relatively common polymorphisms in a wide spectrum of genes may modify the effect of these exposures. We discuss the rationale for using common polymorphisms to enhance our understanding of how environmental exposures cause cancer and comment on epidemiologic strategies to assess these effects, including study design, genetic and statistical analysis, and sample size requirements. Special attention is given to sources of potential bias in population studies of gene--environment interactions, including exposure and genotype misclassification and population stratification (i.e., confounding by ethnicity). Nevertheless, by merging epidemiologic and molecular approaches in the twenty-first century, there will be enormous opportunities for unraveling the environmental determinants of cancer. In particular, studies of genetically susceptible subgroups may enable the detection of low levels of risk due to certain common exposures that have eluded traditional epidemiologic methods. Further, by identifying susceptibility genes and their pathways of action, it may be possible to identify previously unsuspected carcinogens. Finally, by gaining a more comprehensive understanding of environmental and genetic risk factors, there should emerge new clinical and public health strategies aimed at preventing and controlling cancer.     

Extremely low frequency electric fields and cancer: Assessing the evidence

Much of the research and reviews on extremely low frequency (ELF) electric and magnetic fields (EMFs) have focused on magnetic rather than electric fields. Some have considered such focus to be inappropriate and have argued that electric fields should be part of both epidemiologic and laboratory work. This paper fills the gap by systematically and critically reviewing electric‐fields literature and by comparing overall strength of evidence for electric versus magnetic fields. The review of possible mechanisms does not provide any specific basis for focusing on electric fields. While laboratory studies of electric fields are few, they do not indicate that electric fields should be the exposure of interest. The existing epidemiology on residential electric‐field exposures and appliance use does not support the conclusion of adverse health effects from electric‐field exposure. Workers in close proximity to high‐voltage transmission lines or substation equipment can be exposed to high electric fields. While there are sporadic reports of increase in cancer in some occupational studies, these are inconsistent and fraught with methodologic problems. Overall, there seems little basis to suppose there might be a risk for electric fields, and, in contrast to magnetic fields, and with a possible exception of occupational epidemiology, there seems little basis for continued research into electric fields. Bioelectromagnetics 31:89–101, 2010. © 2009 Wiley‐Liss, Inc.     

DNA adducts as markers of exposure and risk

Many carcinogens exert their biological effects through the formation of DNA adducts by metabolically activated intermediates. Detecting the presence of DNA adducts in human tissues is, therefore, a tool for molecular epidemiological studies of cancer. A large body of evidence demonstrates that DNA adducts are useful markers of carcinogen exposure, providing an integrated measurement of carcinogen intake, metabolic activation, and delivery to the target macromolecule in target tissues. Monitoring accessible surrogate tissues, such as white blood cells, also provides a means of investigating occupational or environmental exposure in healthy individuals. Such exposure to carcinogens, e.g. to polycyclic aromatic hydrocarbons, has been demonstrated in several industries and in defined populations, respectively, by the detection of higher levels of adducts. Adducts detected in many tissues of smokers are at levels significantly higher than in non-smokers, although the magnitude of the elevation does not predict the magnitude of the risk. While such associations do not demonstrate causality, they do, importantly, lend plausibility to observed associations between smoking and cancer. However, there is still resistance to the notion that such monitoring can inform, rather than merely confirm, epidemiological investigations of cancer causation. Interestingly, smoking was recently causally linked to cervical cancer after years of being considered a confounding factor; yet smoking-related adducts have been known to be present in cervical epithelium for some time. In the few prospective studies thus far, elevated adduct levels have been found in individuals who subsequently developed cancer compared with individuals who did not. The potential for biomarker measurements, such as DNA adducts, to provide answers to the origin of many cases of human cancer for which an environmental cause is suspected, needs to be exploited more fully in future epidemiological studies.     

Assessment of personal protective equipment use and occupational exposures in small industries in Jeddah: Health implications for workers

Small-scale industries account for a large proportion of jobs and play a vital role in most countries’ economic growth and prosperity. Due to the very low use of personal protective equipment (PPEs), employees are exposed to numerous physical, chemical, and accidental hazards in small-scale industries. PPEs are very effective in minimizing occupational injuries, accidents, and other hazards which otherwise result in substantial manpower and financial losses. The study objective was to assess the availability and use of PPEs as well as self-reported occupational exposures among workers in surveyed small industries in Jeddah. The study involved 102 workers from 28 small-scale industries (vehicle repair, welding, and paint). A survey was conducted to gather data of socio-demographic characteristics, self-reported occupational exposures, and frequency of PPEs used by workers. The occupational exposures (never exposed, sometimes exposed and always exposed) were reported in percentages including; noise exposure (19.6, 73.5 and 6.9%); dust/smoke exposure (9.8, 69.6 and 20.6%); vapors/fumes exposure (11.8, 60.8 and 27.5%); and direct sunlight (43.1, 56.9 and 0%), respectively. The reported use of different PPEs in descending order was; knee joints mats (50%), welding shields (50%), safety glasses (33.3%), gloves (27.5%), face masks (26.5%), safety shoes (10.8%) and earplugs/ muffs (8.8%). On the basis of this study findings, hand hygiene and general OSH awareness like interventions can be developed which will help in minimizing workplace exposures among small-scale industry workers.     

Theory and practice of primary cancer prevention

The primary aim of cancer prevention is to stop carcinogens from entering the body. Since the low doses involved in carcinogenesis do not cause true toxicological effects, usual toxicological analytic methods do not allow the detection of the early effects of carcinogens. Exposure to chemical carcinogens causes damage to nuclear chromatin, the most vulnerable part of the cell, by inducing DNA damage, chromosomal abnormalities and mutations, which foreshadow the danger of cancer development. In such cases intervention is possible in two ways. On the one hand, we attempt to remove the causative agent from the environment, while on the other we aid the elimination of somatic mutations. The latter is called active prevention; the introduction of substances into the body that can help the elimination of defective cells (apoptosis induction) or stop processes responsible for elongation errors (i.e. with antioxidants). Concerning our own studies, we present the results of 25 years of research on the genotoxicological characteristics of workers exposed to various chemicals, which show that active prevention can in fact be effective in conjunction with information on specific biomarkers. We present in detail the genotoxic changes found in hospital nurses who routinely administer intravenous cytostatic therapy, and the relationship of these changes to their immunotoxic and clinical laboratory parameters. Genotoxic substances decrease the oxidative burst and natural killer (NK) cell activity, which may explain the immunosuppressive effects of occupational exposures. We also present the detailed results of a follow-up study involving two groups of industrial workers. We monitored the status of workers involved in benzene production for 15 years and of asphalt industry workers for 8 years. In both studies we concluded that genotoxic effects can be decreased by ensuring appropriate working conditions, while a temporary lapse in these conditions or accidental changes lead to increases in genotoxic parameters. Since genotoxic effects develop over an extended period (4-5 months), they are independent of hygienic conditions at any single inspection and, thus, their detection also offers a way to ascertain true exposure levels. Our studies also show a connection between genotoxic effects and immune function, which is adversely affected not only by occupational exposures, but also by medications and smoking. From our results with workers in the oil and asphalt industries, we concluded that the levels of chromosomal aberrations (CAs) and sister chromatid exchange (SCE) increase in proportion to exposure levels and decrease with a certain delay following the attenuation of the exposure. We could not detect an increased frequency of any chronic disease in industrial workers. The increased numbers of iron deficiency anemia and thyroid disease in nurses providing cytostatic therapy was, however, related to their occupational exposure.     

Occupational cancer: experience in Ontario.

This paper reviews the experience of the Workmen''s Compensation Board of Ontario in identifying cases of cancer that could be attributed to occupational hazards. Worker''s claims for compensation are allowed if there is reasonable medical evidence that their cancer was caused by exposure to risk factors associated with their occupation. Details of the types of cancer associated with specific carcinogens or fields of employment are discussed. About 50% of the cases were related to exposure in particular industrial operations that functioned for relatively brief periods. The number of deaths from cancer identified as being caused by occupational factors is compared with the total for cancer from all causes in Ontario during the period 1971 through 1975. Although all workers eligible for compensation may not have been identified, the data suggest that less than 1% of cancer is presently caused by occupational factors.     

Issues in Exposure and Dose Assessment for Epidemiology and Risk Assessment

Epidemiologic studies have been effective in identifying human environmental and occupational hazards. However, most epidemiologic data has been difficult to use in quantitative risk assessments because of the vague specification of exposure and dose. Toxicologic animal studies have used applied doses (quantities administered, or exposures with fixed duration) and well characterized end points to determine effects. However, direct use of animal data in human risk assessment has been limited by uncertainties in the extrapolation. The applied dose paradigm of toxicology is not suited for cross species extrapolation, nor for use in epidemiology as a dose metric because of the complexity of human exposures. Physiologically based pharmacokinetic (PBPK) modeling can estimate the time course of tissue concentrations in humans, given an exposure-time profile, and it has been used for extrapolating findings from animals to humans. It is proposed that human PBPK modeling can be used in appropriately designed epidemiologic studies to estimate tissue concentrations. Secondly, tissue time courses can be used to form dose metrics based on the type and time course of adverse effects. These dose metrics will strengthen the determination of epidemiologic dose-response relationships by reducing misclassification. Findings from this approach can be readily integrated into quantitative risk assessment.     

Molecular mechanisms in urinary bladder carcinogenesis

Urinary bladder cancer accounts for approximately 5% of all newly diagnosed malignancies in the developed world. Smoking, occupational exposure and dietary factors constitute the most important exogenous risk factors for bladder carcinogenesis. Yet, individuals with seemingly equal exposure to environmental carcinogens develop bladder cancer in an unpredictable manner. This is probably attributed to the fact that DNA repair capacity varies in human populations, pointing the role of genetic susceptibility in human cancer. Numerous studies demonstrated that certain genetic and epigenetic alterations are fairly constant. Loss of heterozygosity (LOH) at chromosome 9 is an aberration found in urothelial cell carcinoma (UCC) of all stages and grades as well as in dysplastic urothelium, possibly representing an early event in urinary bladder carcinogenesis. On the contrary, gains of 3p can only be found in tumors demonstrating highly malignant behavior. Microsatellite instability (MSI) is another frequent finding in urinary bladder cancer. This has led many investigator groups to employ the analysis for MSI for early diagnosis of UCC with promising results. The silencing of certain genes such as p16(INK4A) and DAPK by aberrant methylation of their promoter region also represents an important mechanism in carcinogenesis. Similarly, alterations in certain tumor suppressor genes and proto-oncogenes result in uncontrolled cell proliferation, reduced apoptosis and have been associated with more aggressive UCC phenotypes. Undoubtedly, the application of these observations in clinical practice will make a breakthrough in the management of bladder cancer.     

Occupational health problems among migrant and seasonal farm workers.

Migrant and seasonal farm workers are one of the most underserved and understudied populations in the United States. The total US population of such farm workers has been estimated at 5 million, of whom about 20% live or work in California. Farm workers perform strenuous tasks and are exposed to a wide variety of occupational risks and hazards. Low socioeconomic status and poor access to health care also contribute to existing health problems in this population. Potential farm work-related health problems include accidents, pesticide-related illnesses, musculoskeletal and soft-tissue disorders, dermatitis, noninfectious respiratory conditions, reproductive health problems, health problems of children of farm workers, climate-caused illnesses, communicable diseases, bladder and kidney disorders, and eye and ear problems. Few epidemiologic studies exist of these occupational health problems. No comprehensive epidemiologic studies have assessed the magnitude of occupational health problems among migrant and seasonal farm workers and their dependents. Although the migratory nature of this population makes long-term studies difficult, the development of standardized data collection instruments for health consequences and scientific assessment of farm work exposures and working conditions are vital to characterize and reduce the occupational health risks in farm workers.     

Papillomviren und Krebs. Wie aus einem Anfangsverdacht ein Impfstoff wurde

Since a long time epidemiologic studies suggested a sexually transmitted infectious agent as cause of cervical cancer. Human papillomaviruses (HPV) were considered as causative agents since members of the papillomavirus family can induce tumors in animals, and genital infections with papillomaviruses in man are common. Several discoveries ranging from the identification of the plurality of HPVs, the regular finding of genomes of certain, so called high‐risk HPV types within tumor biopsies, insights into the transforming mechanism and informative epidemiological surveys finally led to the conclusion within the scientific community of a causative link between these viruses and cervical cancer as well as other human malignancies. This awareness triggered the development of HPV‐specific vaccines as means of cancer prevention.     

Tea drinking and cancer risk: epidemiologic evidence

Tea and tea compounds have been shown to inhibit carcinogenic processes in experimental animals, raising the possibility that tea drinking may lower cancer risk in humans. However, epidemiologic studies have produced inconsistent evidence on the relation between tea drinking and cancer risk. Ecological data show considerable international variation in tea consumption but relatively small differences in cancer rates. Results from case-control and cohort studies also are inconclusive. Nevertheless, high consumption of tea has been linked to a reduced risk of digestive tract cancers in a number of epidemiologic studies. A lack of detailed information on duration and amount of tea drinking, a narrow range of tea intake in some study populations, inadequate control for confounding, and potential biases in recall and reporting of tea drinking patterns in case-control studies may have contributed to the diverse findings. Further research is needed before definitive conclusions on tea's impact upon cancer risk in humans can be reached.     

Years of Potential Life Lost Due to Occupational Fatal Injury in the United States

Fatal injury surveillance data coupled with life expectancy data may be used to assess the impact of occupational fatal injuries on years of potential life lost (YPLL). We compare three definitions of YPLL and trends over time in YPLL. Two definitions determine YPLL as expected life lost to fixed life expectancies of 65 or 85 years. The third definition uses actuarial adjustments of life expectancy given survival to a given age stratified by gender and race. Fatalities from the National Traumatic Occupational Fatality (NTOF) database are used to illustrate the three definitions of YPLL. The three YPLL measures were similar in magnitude and direction of the trend in YPLL over 1980-1992. Proper interpretation of these trends can only be made in conjunction with other measures (e.g., rates). Almost all YPLL trends are declining, implying that over time fatal injuries are shifting to older workers. The exception is the increasing trend in YPLL for the retail trade industry, injury rates have also been increasing over time for this industry. Mining and construction have the highest YPLL among all industries. This analysis suggests efforts to prevent the occupational fatalities of younger workers should focus on the retail trade, mining, and construction industries.     

Historical review of occupational exposures and cancer risks in medical radiation workers

Epidemiological studies of medical radiation workers have found excess risks of leukemia, skin and female breast cancer in those employed before 1950 but little consistent evidence of cancer risk increases subsequently. Occupational radiation-related dose-response data and recent and lifetime cancer risk data are limited for radiologists and radiologic technologists and lacking for physicians and technologists performing fluoroscopically guided procedures. Survey data demonstrate that occupational doses to radiologists and radiologic technologists have declined over time. Eighty mostly small studies of cardiologists and fewer studies of other physicians reveal that effective doses to physicians per interventional procedure vary by more than an order of magnitude. For medical radiation workers, there is an urgent need to expand the limited information on average annual, time-trend and organ doses from occupational radiation exposures and to assess lifetime cancer risks of these workers. For physicians and technologists performing interventional procedures, more information about occupational doses should be collected and long-term follow-up studies of cancer and other serious disease risks should be initiated. Such studies will help optimize standardized protocols for radiologic procedures, determine whether current radiation protection measures for medical radiation workers are adequate, provide guidance on cancer screening needs, and yield valuable insights on cancer risks associated with chronic radiation exposure.     

Prostate cancer association studies: pitfalls and solutions to cancer misclassification in the PSA era

Widespread screening of American men for elevated PSA has changed the characteristics of prostate cancer cases in the U.S. The influence of the changed nature of prostate cancer cases in the PSA era and the need for careful consideration of who is a "case" and who is a "control" on the ability to detect associations of risk factors with prostate cancer in etiologic epidemiologic studies merits discussion. Issue 1: prostate cancer cases diagnosed in the PSA era are enriched with a pool of early lesions, which may differ in etiology, and are deficient in advanced lesions, which are the most likely to be the product of promotion and progression events. By admixing the two types of cases (i.e., imperfect specificity), the associations previously detected using epidemiologic designs when the majority of cases were clinically detected may no longer be apparent in the PSA era when the majority of cases are now detected in the pre-clinical phase. Researchers must now tailor hypotheses such that they are testable using early stage cases or specifically augment the number of advanced cases when testing hypotheses related to extraprostatic growth and progression. Issue 2: even when controls are screened for elevated PSA to rule out the presence of prostate cancer, some proportion of those controls currently will have one or more foci of prostate cancer. The imperfect sensitivity of the PSA test coupled with diagnostic work-up may in part result from (a) lack of PSA elevation in some men with prostate cancer or (b) failure of biopsy to sample the tumor focus in men with elevated PSA. Misclassification of men with undetected prostate cancer as controls usually produces a bias that tends to deflate associations. Given this type of disease misclassification, whether an association still can be statistically detected depends on the extent of misclassification, the magnitude of the true association, the prevalence of the exposure in the true controls, and the sample size, although in general moderate nondifferential misclassification does not lead to profound attenuation. However, under the same scenario attenuation does not occur in cohort or case-cohort studies in which the rate or risk ratio (RR) is calculated. That prostate cancer cases diagnosed in the PSA era are enriched with early stage, minimally invasive disease in our opinion is likely to pose a far more serious obstacle to epidemiologic research on the etiology of clinically important prostate cancer than the issue of inclusion as controls some men who have undiagnosed prostate cancer because of imperfect sensitivity of PSA screening and biopsy sampling error.     

Occupational lung cancer and smoking: a review in the light of current theories of carcinogenesis.

This paper considers modern theories of carcinogenesis as they apply to the induction of lung cancer by tobacco smoking and occupational exposure to carcinogens. Some of the known and postulated factors affecting carcinogenesis are discussed, with particular reference to syncarcinogenesis and thresholds. Factors affecting the intensity of smoking exposure are reviewed, and the generally accepted occupational lung carcinogens are listed. Relative risks for the various carcinogens according to smoking status (where known) are presented. The carcinogens are considered individually, and known or postulated interactions with smoking are discussed. It is concluded that the effects of lung carcinogens can be explained on the basis of current theories that support a rational definition of priorities for the prevention of occupational lung cancer.