Valve disease associated with ergot alkaloid use: echocardiographic and pathologic correlations.
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Biomedical subjects
Publications and source records attributed to W J Nicholson.
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Using a double polymerase chain reaction a method was devised for detecting and subtyping hepatitis B virus DNA in serum samples. Primers from the S-gene were selected from the sequence analyses of five HBV HBsAg subtypes, to amplify HBV DNA and subtype for y specific DNA. Thirty-eight samples were subtyped for d and y determinants by radioimmunoprecipitation assay (RIPA) and the polymerase chain reaction (PCR). Subtyping by PCR and RIPA was in agreement in 100% of subtype y samples and 83.3% of subtype d, giving an overall correlation of 92.1%. As a third comparison, 12 amplified samples were digested by the restriction enzyme Sau 3A, which differentiates between subtypes y and d. The digest results agreed with PCR in 83.3% of the samples. In addition, we compared our standard phenol/chloroform extraction against a rapid one step method. The phenol/chloroform stage was found to be essential for the removal of nucleases and polymerase inhibitors present in sera.
Chest radiographs were read from a sub-cohort of 386 factory workers with short term exposure to amosite asbestos (median exposure six months) and long follow up (median 25 years). Prevalence of abnormality was determined independently by two readers from the first film available after 20 years from first employment. Serial films were obtainable for 238 men (median interval from first to last film: nine years). Progression was classified with a direct progression scoring scale. Individual dust exposure estimates were derived from dust counts from two similar plants. With as little as one month or less of employment, about 20% of the films showed parenchymal abnormality and about a third showed pleural abnormality. Those in the lowest cumulative exposure stratum (less than 5 fibre-years/ml) were similarly found to have high rates of abnormality. Dose-response relations were present in the data of both readers. Smokers had higher rates of parenchymal abnormality. On multivariate analysis, cumulative exposure was the exposure variable most closely related to parenchymal abnormality, and time from first employment was the variable most closely related to pleural abnormality. Progression (including first attacks) 20 or more years after ceasing employment occurred and was more common for pleural than for parenchymal abnormality. It is concluded that with exposure to high concentrations to amosite such as existed in this factory and with follow up for at least 20 years, (1) exposure for as little as a month was sufficient to produce radiological signs of parenchymal and pleural fibrosis, (2) no cumulative exposure threshold for parenchymal and pleural fibrosis was detectable, and (3) parenchymal and pleural progression were still detectable >/= 20 years after the end of exposure.
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Site-specific cancer trends are particularly useful indicators to identify cancers that should be subject to further case-control research to identify causes of the rate changes. One of the most sensitive of trends is that of the ratio of male-to-female rates, especially by age groups. This ratio is likely to eliminate rate changes due to better diagnosis, treatment, and cancer ascertainment. Also some lifestyle changes may be eliminated by considering the male-female ratio as they equally affect both genders. On the other hand, some may produce substantial effects. The finding of large increases in male-female cancer mortality ratios at specific sites in the United States and in all cancers, except lung, in several countries suggests that case-control studies of some sites are worthy of consideration to identify the gender-related differences. Because most male rates are increasing relative to females, any case-control study should certainly include occupational factors among those investigated.
Two patients with a remote history of pathologically documented giant cell arteritis developed severe regurgitation. The first patient developed severe aortic regurgitation five years after the pathologic documentation of giant cell arteritis of the temporal arteries. Giant cell arteritis involvement of the aortic root was confirmed. The second patient developed aortic regurgitation seven years after pathologic documentation of giant cell arteries of the temporal arteries. Although pathologic confirmation of the aortic root process was not obtained, this case strengthens the clinical association between giant cell arteritis of the temporal arteries and subsequent aortic root dilatation and severe aortic regurgitation. Observation for signs of de novo severe aortic regurgitation is indicated in follow-up of patients with temporal arteritis.
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Benzene exposure can cause leukemia, aplastic anemia, and possibly lymphoma. In 1978, on the basis of strong but incomplete data then available on the risk of benzene-induced leukemia, the U.S. Occupational Safety and Health Administration (OSHA) reduced the permissible occupational exposure standard for benzene from 10 ppm to 1 ppm. Shortly thereafter, the Fifth Circuit Court of Appeals stayed this ruling, and in 1980, the Supreme Court overturned the regulation, citing insufficient evidence of benefit. Thus, from 1978 until the standard was again lowered to 1 ppm in 1987, American workers were exposed to benzene at levels in excess of 1 ppm. An estimated 9600 were exposed to levels between 1 and 10 ppm, and an additional 370 were exposed at levels above 10 ppm. To assess the risk resulting from this delay in regulation, we have conducted an epidemiologic risk analysis. We merged data on numbers of persons (238,000) exposed to benzene in seven occupational categories with dose-response data from three epidemiologic studies. The range of risk in these studies indicates that 44 to 152 excess leukemia deaths will ultimately result from exposure to benzene at 10 ppm over a working lifetime (45 years) and that lower or briefer exposures will result in proportionately fewer deaths. On this basis, we calculated that between 30 and 490 excess leukemia deaths will ultimately result from occupational exposures to benzene greater than 1 ppm that occurred between 1978 and 1987. Deaths from aplastic anemia and lymphoma will likely add to this toll. These data confirm the risk of regulatory delay. They suggest that the courts, in reviewing public health regulations, must beware of facile cost-benefit arguments and be willing to accept strong evidence of health risk even when such evidence is incomplete.
Numerous sources of asbestos exist that may contribute to non-occupational exposures, among the important ones being building surfacing materials that have been damaged or allowed to deteriorate. Even more important is the potential exposure from improperly controlled maintenance activities in buildings. Evidence exists suggesting that vehicle braking makes a significant contribution to ambient asbestos levels, but more data are required to establish its extent. Many asbestos materials are present in homes, and fibres may be released during home renovations or repairs. Little information exists on the levels of other mineral fibres in the non-occupational environment or on the relative contributions from potential sources.
Three cases are described with documented ventricular fibrillation shortly after the patients received disopyramide in moderate dosage. Electrocardiograms showed markedly prolonged Q-T intervals in two patients and a prominent U wave with a prolonged Q-U interval in one patient, but no change in QRS width. Disopyramide-induced ventricular fibrillation appears to be similar to that caused by quinidine and is an indication to discontinue the drug.
Among a cohort of 544 men with at least 20 years of employment in chrysotile mining and milling at Thetford Mines, Canada, 16% of the deaths were from lung cancer and 15% from asbestosis. The excess over expected deaths from these causes account for 43 of 178 deaths in the group. The risk of death of asbestosis, at equal times fron onset of exposure, is very similar in miners and millers, factory workmen and insulators. The ratio of observed to expected deaths from lung cancer is similar in the miners and millers and factory workers, but higher in insulators. The risk of death of mesothelioma in miners and millers is decidedly less than the other two groups. The exact causes of the reduced risk in this category are not yet completely clarified.
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Iron ore called taconite is mined in the Biwabik Iron Formation in the Eastern Mesabi region of the Mesabi Range, in eastern Minnesota. After mining, ore is shipped to Silver Bay, Minnnesota for processing and wet magnetic extraction. Tailings from the process are dumped, as a slurry, into a man-made containment delta constructed in Lake Superior. Submicroscopic amphibole fibers and/or cleavage fragments, a component of the gangue, apparently escape from the delta at Silver Bay, and enter Lake Superior. These particles contaiminate the potable water supplies of municipalities drawing directly from the lake. One of the gangue minerals is the amphibole grunerite, whose asbestiform variety is called amosite. Major emphasis of this study was directed at identification of submicroscopic particle pollutants, based on morphology, structure and chemical composition. Quantitative determination of fibrous amphibole phases, present in a range of water samples, was undertaken. Transmission electron microscopy, selected area electron diffraction, and an electron microprobe technique was used for identification and enumeration and this information was compared with data sets determined from standards. Grunerite fiber and/or acicular cleavage fragments, in some instances indistinguishable from asbestiform grunerite, are present in the tailings, lake water and drinking water of a number of municipalities, a result of contamination of the lake at the Silver Bay milling operation. This amphibole is found in drinking water in concentrations which range from 0.6 to 2.8 X 10(6) fiber/liter. The risk to health, associated with direct ingestion of grunerite fiber is unknown and is extrapolated from the asbestiform grunerite (amosite) data base. The biological activity of other fibrous amphiboles observed, unrelated to any asbestiform silicate variety, is presently unknown and warrants investigation.
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Four cases are presented of aortic root dissection after aortocoronary bypass surgery in which the origin of the intimal tear was at or very near the aortic site of saphenous vein anastomosis. Two cases were documented at autopsy. In one of two cases diagnosed with aortography, the patient underwent surgical correction and survived. All patients had long-standing severe hypertensive cardiovascular disease or severe generalized atherosclerotic disease, or both. Clinical awareness of aortic dissection after coronary bypass surgery in this group of patients should make early diagnosis with successful surgical correction feasible.
A group of 560 individuals has been identified as employed on 1 May 1960 with at least five years seniority in a plant manufacturing styrene and polystyrene. In this plant workplace exposures included styrene, benzene and ethylbenzene, among other materials. All of the 560 individuals have been traced through 1975 and their vital status determined. Expected and observed deaths, by cause, were determined from 1 May 1960 or the tenth anniversary of employment in the plant through 31 December 1975. Over this relatively short period of time a deficit of deaths compared to that of the general population was observed (106.41 expected versus 83 observed). Among the 83 deaths, one was of leukemia, one of lymphoma and an additional death was accompanied by leukemia. A review of 361 additional death certificates revealed five additional cases of leukemia and four of lymphoma. The available information from the limited follow-up in time of the time of the cohort and from the randomly collected death certificates, while suggestive of a possible risk, is not definitive.
A review is presented of the various factors important in the identification of carcinogenic disease from occupational and environmental exposure to asbestos and vinyl chloride. The long lapsed period, usually of 20 or more years from first exposure to these materials, is discussed, as well as the requirement for sufficiently long observation periods in prospective epidemiological studies. The multiple-factor etiology of lung cancer involving cigarette smoking and asbestos exposure is illustrated. The risks of asbestos-related cancers to other than those directly working with the material are discussed in a variety of circumstances, and finally the effectiveness of control procedures for vinyl chloride and asbestos are compared.