SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cyclosporine is an important therapeutic agent for transplant recipients and for a growing number of autoimmune diseases. Experimental animal and human data has indicated that cyclosporine is unlikely to be genotoxic. In contrast, azathioprine, an agent often given with cyclosporine, is considered to be genotoxic making the assessment of the independent effects of cyclosporine difficult. Cyclosporine does appear to be related to the development of tumors, primarily lymphomas, in animals and humans, but the basis of its potential carcinogenicity is not completely understood. In terms of reproductive and developmental toxicity, cyclosporine produces some adverse effects in both experimental animals and humans. In animals, the effects are seen at high doses sufficient to cause maternal toxicity. In humans, outcomes such as growth retardation have been noted, but the confounding effects of renal toxicity and resultant pregnancy complications cloud the interpretation. An increase in congenital anomalies and genetic disease have not been found reported in human studies that are limited in sample size. Given that the present data indicate the lack of genotoxicity, a mutation epidemiology study of cyclosporine is not recommended. As indicated above, such a study is probably impractical for many genetic endpoints of interest. However, well-conducted, large multicenter studies of transplant patients and their offspring would allow for routine monitoring of an increased risk for some reproductive and developmental (possibly non-genetic) endpoints that are of public health importance.
The liberation and use of organisms that have been manipulated by genetic engineering must be viewed against the background of criteria related to human toxicology and general and public health as far as the production of foods and foodstuffs is concerned. This interdisciplinary study yielded the result that the examinations performed for the purpose of discovering possible pathogenic effects do not by themselves safeguard human health if they are based on the classical mechanistic model. Rather, the structural changes brought about by genetic engineering result in technicalising living organisms. Concepts such as "health" can no longer be applied to organisms manipulated by genetic engineers. The loss of characteristics typical of life within the horizon of human knowledge is fraught with impeding health risks. From the viewpoint of philosophy, the conceptual areas of causality, time and spontaneity are affected by the manipulations of gene technology. The authors point out that these areas lose their pretechnological meaning subject to changes conditioned by gene technology.
Recently, a working group of six European scientists published a report on exposure to environmental tobacco smoke and the risk of lung cancer. The report concludes that environmental tobacco smoke is not a primary lung carcinogen. Critical evaluation of the report, however, shows that this conclusion is not justified. Results of recent epidemiologic studies support the earlier conclusion of the American Environmental Protection Agency (EPA) that environmental tobacco smoke does cause lung cancer. Furthermore, the working group fails to present compelling evidence that the results of the epidemiological studies in this field can be explained by bias or confounding, or that the association between environmental tobacco smoke and lung cancer is biologically implausible. Therefore, we see no reason to modify the conclusion of the EPA that passive smoking causes lung cancer.
The success of our national environmental policies depends upon the capacity of states to implement them. This article presents the findings of an examination of the state level organization of environmental health and protection services. The goals of the project were to conduct a descriptive analysis of the structure, functions, and funding of state environmental health and protection services, and to examine the impact of the major federal environmental statutes on the organization of the state infrastructure. Future environmental progress will depend upon an improved understanding of the relationship between human health and the environment. This will require a commitment to improving the public health training of environmental professionals, and improved cooperation between health and environmental agencies to assure that they do not lose sight of their fundamental mission--the protection of public health.
The Food Quality Protection Act (FQPA) of 1996 mandates that the U.S. Environmental Protection Agency consider both aggregate and cumulative risks. Aggregate assessments account for multiple sources and routes of exposure for a single chemical. Cumulative assessments combine exposures to two or more chemicals that share a common mechanism of toxicity. Probabilistic risk assessment methods are described for determining a population's distribution of the dose from exposure and the combination of that exposure characterization with appropriate toxicological information to form a risk assessment. An individual's dose from exposure is characterized as a set of chemical- and route-specific dose profiles over time. For each individual and each chemical and route, a margin of exposure (MOE) is calculated by dividing a toxicologically relevant benchmark dose (e.g., an ED(10)) by the individual's dose from exposure. The set of these MOEs for an individual is combined into the individual's Total MOE. The distribution of the Total MOEs in a population is compared to an Acceptable MOE. Advantages of the Total MOE approach over approaches based on reference doses are discussed. Some general comments on risk metrics are made, and some general guidance for cumulative risk assessments is provided.