A recent interpretation of the pathogenetic role of asbestos fiber size in the development of mesothelioma and in the possibility of mesothelioma prevention needs clarification. This point of view is based on a biased interpretation of the literature. Epidemiologic, experimental, and molecular evidence suggests that the arguments for the role of fiber size relative to dose, dose-response effect, and genetic susceptibility are scientifically unsound. Their proponent also states that means available in the past for the implementation of dust-control measures and/or personal protective equipment would not have contributed to reducing the frequency of mesothelioma among exposed subjects, an argument again based on invalid assumptions.
Discovered in the early 1800s, the use of cadmium and various cadmium salts started to become industrially important near the close of the 19th century, rapidly thereafter began to flourish, yet has diminished more recently. Most cadmium used in the United States is a byproduct from the smelting of zinc, lead, or copper ores, and is used to manufacture batteries. Carcinogenic activity of cadmium was discovered first in animals and only subsequently in humans. Cadmium and cadmium compounds have been classified as known human carcinogens by the International Agency for Research on Cancer and the National Toxicology Program based on epidemiologic studies showing a causal association with lung cancer, and possibly prostate cancer, and studies in experimental animals, demonstrating that cadmium causes tumors at multiple tissue sites, by various routes of exposure, and in several species and strains. Epidemiologic studies published since these evaluations suggest that cadmium is also associated with cancers of the breast, kidney, pancreas, and urinary bladder. The basic metal cationic portion of cadmium is responsible for both toxic and carcinogenic activity, and the mechanism of carcinogenicity appears to be multifactorial. Available information about the carcinogenicity of cadmium and cadmium compounds is reviewed, evaluated, and discussed.
Experimental chemical carcinogenesis, which included long-term tests in experimental animals,had a dominating role in cancer research between the 1920s and the late 1960s. Two events marked a certain decline of confidence in the ability of experimental results to predict human risks: the incapacity of developing methods to identify agents acting on the different steps of the carcinogenesis process, and the incapacity to reproduce experimentally the strong evidence of carcinogenicity of tobacco smoke provided by epidemiological studies. It was at that time that epidemiologists and biostatisticians developed criteria for assessing the causation of chronic-degenerative diseases relying primarily on epidemiological evidence. In 1969 the International Agency for Research on Cancer (IARC) did initiate a programme for identifying the cause of cancer with the aim of promoting the primary prevention of cancer. The programme is focused on the evaluation of the carcinogenicity of environmental agents on the basis of both the experimental and epidemiological evidence and, since the 1990s, a balanced use of the new tools provided by advances in toxicology, molecular biology and genetics. A strong point of the IARC programme is that in the absence of adequate human data it is reasonable and prudent to regard agents for which there is sufficient experimental evidence of carcinogenicity as if they were carcinogenic to humans.
The particular point of view, recently published by Gerolamo Chiappino, on the pathogenetic role of asbestos fibres size in the origin of mesothelioma and on the possibility of mesothelioma prevention until the middle of the '80s needs to be critically clarified. The suggestion of an exclusive role of ultrashort and ultrathin fibres in the origin of mesothelioma is based on a biased interpretation of the literature. A review of the epidemiological, experimental, and molecular literature suggests that Chiappino's statements on the role of dose, dose-response effect, and genetic susceptibility are scientifically unsound Chiappino states that, in the past, in the workplaces where use and exposure to asbestos were not stopped, any reduction in the intensity of exposure by means of dust control measures or personal protective equipment would not have contributed to reduce the frequency of mesothelioma. In the authors' opinion the underlying assumptions are invalid.
During the annual Ramazzini Days, the Mayor of Carpi confers the Ramazzini Award on scientists deemed by the Collegium Ramazzini to have made outstanding contributions to furthering the aims of Bernardino Ramazzini in safeguarding public health. Dr. Lorenzo Tomatis was the Ramazzini Award recipient in 2005, and the presentation of the award was a highlight of the Symposium. The Ramazzini Lecture given by Dr. Tomatis follows.
Key terms cancer; discussion paper; economic pressure; economics; primary prevention; science; sociocultural trend
In spite of claiming primary prevention as their aim, studies of potential occupational and environmental health hazards that are funded either directly or indirectly by industry are likely to have negative results. The authors present three common scenarios in which faulty design of epidemiologic studies skews results, and list 15 study design flaws that lead to results that are dangerously misleading with regard to both the evaluation and the improvement of public health.
A.. n issue relevant to scientifit integrity has arisen in ·connection with a court case in the Amazon, wherein the Amazonian people are seeking redress for environmental damage and deleterious health effects related to the operations of Texaco in the Amazon region of Ecuador. It has been estimated that in its more than 20 years of oil exploitation·· in Ecuador (1971-1992), Texaco discharged into the environment 16.8 million gallons of' crude oil and· 20 billion gallons of toxic wastes.1 The. environmental damage caused by Texaco can be compared to 10.8 million gallons of crude oil spilled in Alaska in the Exxon. Valdez tanker disaster in 1989. Mor~over, six hundred open pits filled with toxic waste were apparently left in the surrounding' communities in . Ecuador.2,3 In 1995, the company signed' an agreement with Ecuador's government to undertake clean up activities in return for releasing the company from future responsibility related' to its former oil operations.4 On February 10, 2005, during the ongoing court proceedings, major newspapers in Ecuador ran a full-page (presumably paid) advertisement citing reports by scientists 'retained by Texaco who critiqued studies published in prestigious peer-reviewed journals that suggest links between adverse health effects and oil development in the Amazon.5-1oTexaco's consultant scientists, Kenneth Rothman, Felix Arellano, Alvaro Felipe Davalos Perez, Lowell Sever, DavidJ. Hewitt, and Laura Green, pointed to alleged weaknesses in the ..published studies. The ad was, to us, a blatant effort by the company to sway. public opinion as the legal case was being heard. The Web site is available at: . Epidemiologic studies, however meticulously conducted, may have inherent limitations, as allepidemiologists are aware. Epidemiology is not laboratory science but a study of the' real world, and thus always subjectto challenge in its ability to control for. all potential· effects. Especially, in .vulnerable study .populations, exact· details of the· populations.at risk, as well as the extents, natures, and durations of exposures, are difficult· to document, and ascertainment of 'outcomes is limited by the quality of health services available. However, epidemiologic findings' can confidently detect trends, and it is the body of evidence that should influence policy.' The scien.tificprocessof peer. review ascertains .whether the potential weaknesses of any' study raise doubts sufficient. to preclude publication of its .findings and' conclusions. Texaco's consultants went to great pains to find flaws.in the studies. Some of the so-:-calledweaknesses they point out are not even themselves of particular concern, e.g., while "memory bias of respondents" may be .a confounder in some circumstances, it· is hardly a factor in the case of remembering < pregnancy and spontaneous abortion ..·Self-reported health effectsof which they also seem to question the validity-is a widely used· and accepted practice. The onus cannot be put on sci.;. entists to ensure that data are available· 'to evaluate adverse health impacts. It is far more logical to require' a company extracting minerals· or biological raw materials to accept responsibility, as good corporate citizens, for determining what protective measures it would be prudent to impose, and to monitor its success in controlling poten>tial adverse human health and environmental effects. If this did not occur, should we not be asking "why not"? In 'many" jurisdictions,environmental health, impact assessments are now ,required-:7"putting the onus where it belongs: on those who, are responsible for the poten':' tial health impacts. In fact, environmental health impact assessments are 'increasingly addressing. not only direct (toxicologic),. but also indirect ,impacts, of development· projects (health effects mediated by changes in ecologic and social systems).1l,12Texaco's Web site maintains that the primary causes of disease in the region are poverty, poor sanitation, naturally occurringbacteria and. parasites, a lack ·of access to clean water, and insufficient infrastructure, adding that, "it is both irresponsible and inaccurate for the plaintiffs to ignore. these well-documented conditions." Yet nowhere does Texaco mention how oil development has conceivably:' altered these conditions, nor does it state that such conditions' increase vulnerability to the environmental exposures of concern. Responsible environmen tal health scientists, cognizant of the need to.assess indirect as well as direct health effects of operations such as these, would have raised these issues \n an open and comprehensive discussion. Texaco's protagonists, whether or not, they agree, about the adverse health impacts of the social and ecologic disruptions related to the oil company's operations, can hardly believe· that the agents involved in drilling, and in the extracted oil, are innocuous. The hired experts.never referred to industrial and environmental exposure records, so presumably either the company failed to collect and maintain these data or the containment of the toxic agents was ineffective, and therefore not mentioned: The consultants commissioned by Texaco might have reasonably been expected to note that in the light of the monitoring, control, and mitigating measures provided to· them by the company
To investigate in an animal model whether preconceptual X-ray exposure leads to an altered tumor rate and spectrum in the offspring, a transgeneration carcinogenesis study was carried out. Female mice received X-ray irradiation (2×2 Gray) 2 weeks prior to mating with untreated males. After weaning, half of the descendants were exposed for 6 months to the immunomodulating and tumor-promoting compound cyclosporine A (CsA) by diet, the others remained untreated. The animals were maintained for their entire lifespan, terminal sacrifices were carried out after 28 months. Complete autopsy was performed, and three protocol organs (lung, liver and spleen) were examined histologically, together with any suspicious lesions in other organs. Fertility and the lifetime of the maternal mice were reduced by the X-ray irradiation, and their incidence of lung and liver tumors was increased as compared to non-irradiated mice. The descendants of all groups revealed comparable body weights and mortality rates. The incidence of hematopoietic/lymphoreticular tissue tumors increased in the female hybrids by 6 months of CsA-treatment. A higher incidence of lung and liver tumors in the sham-treated male progeny of irradiated mothers was detected, pointing to a possible germ cell-transmitted alteration initiated by the preconceptual maternal X-ray exposure.
LetterOpen AccessAsbestos and international organizations. Lorenzo Tomatis Lorenzo Tomatis Search for more papers by this author Published:1 May 2004https://doi.org/10.1289/ehp.112-a336bAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit FiguresReferencesRelatedDetails Vol. 112, No. 6 May 2004Metrics About Article Metrics Publication History Originally published1 May 2004Published in print1 May 2004 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.
The Republic of Korea (hereafter referred to as Korea) is located in Northeast Asia, on the southern half of the Korean Peninsula, jutting out from the far east of the Asian landmass. Seoul, the capital city of Korea, is located at 37°25′–37°41′N and 126o45′–127o 11′E in the midwest of the Korean Peninsula, covering a total area of 605.5 km2. The Han River flows through the city from east to west, dividing it into north and south. The city consists of 25 districts. The population of the city has grown rapidly since the Korean War to about 10 million – representing around 20% of the total population of Korea. Seoul is well known for its high population density and its metropolitan area is one of the most densely populated cities in Asia. Economic growth and industrialization have stimulated population growth in Seoul, and this growth has been profitable to the city as it has become a center of governance, education, culture, commerce, and production.