Epidemiological data base for a health effects study at a coal gasification plant.
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Biomedical subjects
Publications and source records attributed to S C Morris.
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This article quantifies potential public health risks from tumor-producing pollutants emitted from two synthetic-fuel plants (direct liquefaction--Exxon Donor Solvent: and indirect liquefaction--Lurgi Fischer-Tropsch) located at a representative site in the eastern United States. In these analyses gaseous and aqueous waste streams were characterized; exposures via inhalation, terrestrial and aquatic food chains, and drinking water supplies were modeled. Analysis suggested that emissions of "polycyclic aromatic hydrocarbons," "aromatic amines," "neutral N, O, S heterocyclics," "nitriles," and "other trace elements" pose the largest quantifiable risks to public health. Data and analysis for these pollutant categories should be refined to more accurately match compound-specific estimated exposure levels with tumorigenic potency estimates. Before these results are used for regulatory purposes, more detailed analysis for selected pollutant classes are needed, and more sophisticated aquatic exposure models must be developed. Also, differences in geographic scales among the environmental transport models used need to be rectified.
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Important clinical, chemical, and immunological advances in coelenterate venom research have been made in recent years. Perhaps the most dramatic advance has been in the communication of research data and clinical cases between investigators in this field. Results have been processed by the International Consortium for Jellyfish Stings through their newsletter and the forthcoming publication of the Marine Stinger Book by the University of New South Wales Press.
Mortality experience was determined over a 13-year period (1960-72) for sample populations in two small Pennsylvania communities with widely different air pollution levels. The sample populations had been the subject of a Public Health Service study at the beginning of the period and air quality measurements were made at that time. The influence of smoking on mortality was clearly evident. A relationship was suggested between mortality rate and length of residence in the polluted community (age-adjusted), but not in the control community. The hypothesis is suggested that immigrants to a polluted area are a self-selected, unusually healthy group. While the small population size precluded definitive conclusions on the influence of air pollution on mortality, it appears that those with over 20 years exposure to air pollution in the polluted community (151 mug/m3 suspended particulate, 3.7 mg/100 cm2/day sulfation rate) have about one-tenth the excess mortality of those smoking one pack of cigarettes a day in the control community (109 mug/m3, 0.6 mg/100 cm2/day). The data are consistent with the hypothesis that the effects of smoking and air pollution are additive.
We have investigated the influence of background genes in the MRL strain, as compared to C57BL/6, on the induction of autoimmunity in homozygous lpr/lpr mice. We have concentrated on two autoantibodies, anti-Sm and anti-chromatin. The propensity to make anti-Sm is controlled by dominant genes from the MRL background. However, the prevalence of this response is under the control of additional recessive genes. The anti-chromatin response is found in both MRL/Mp-lpr/lpr and in C57BL/6-lpr/lpr mice, but it appears earlier and in higher titers in the former strain. This high responder effect is controlled by dominant genes. In F1 mice between these two strains, both anti-Sm and anti-chromatin antibodies preferentially use the b Igh allotype from the low responder B6/lpr parent. In addition, in the progeny of backcross of the F1 to the MRL/lpr strain, the production of both anti-Sm and anti-chromatin is linked to the b allotype. These results demonstrate the contribution of dominant genes from the MRL background on the induction of severe autoimmunity. They also suggest that the B6 background expresses an Igh allotype particularly amenable to autoantibody production, in spite of the relatively mild SLE-like syndrome in this strain.