Journal of environmental pathology and toxicology最新文献

Although humans may accept fairly large amounts of orally ingested copper (0.25 to 1.0 gm) without visible harmful effects, patients with Wilson's disease, and persons with G6PD deficiency may represent persons at unusual risk to hemolytic anemia from ingestion of Cu(II). This study reports that in vitro exposure of G6PD deficient red blood cells to copper produced marked elevations of methemoglobin and decreases in GSH when compared with normal red cells. Chlorite, a by-product of chlorine dioxide disinfection of water, produced decreases in GSH and G6PD activity, while increasing methemoglobin levels markedly over red cells with normal G6PD activity. The combined action of chlorite and copper was additive in producing increased levels of hemoglobin and decreases in levels of GSH and G6PD deficient cells. The combined ingestion of copper and chlorite may represent an increased risk to persons with G6PD deficiency.

Studies of water hardness and cardiovascular disease are briefly reviewed, and the probability that the reported associations are those of cause-and-effect is assessed. While the verdict is "not proven", further studies are desirable because of the potential benefits that might accrue from water treatment. Future studies, however, need to be much more definitive than the ecological investigations of the past. Although such studies have been useful as pilot studies, the effects of a possible water factor cannot be disentangled from the effects of many personal characteristics that also vary with geography.

Technical BHC and the alpha, beta, gamma and delta isomers of BHC are carcinogenic for the liver of mice and rats. Mice given the isomers of BHC developed carcinomas and hyperplastic nodules of the liver as early as 24 weeks. Several strains of mice (dd, ICR-JLC, CL1, DDY, IRC, DBA/Z, C3H/HEN, C57BL/6 were susceptible. Male mice were more susceptible to hepatic carcinogenesis than female mice and they appeared to be more susceptible to alpha-BHC. The incidence of neoplasms of the liver was increased when beta-, gamma-, or delta-BHC were each given together with alpha-BHC. PCB-5 promoted the induction of hepatic neoplasms when administered with beta-BHC. Technical BHC and its isomers are carcinogenic for the liver of male and female Wistar rats. Beta-BHC is carcinogenic for the liver of Osborne-Mendel male rats. Osborne-Mendel rats receiving delta-BHC developed cirrhosis of the liver, portal vein thrombosis, and focal necrosis of the skeletal muscle. Male rats ingesting technical BHC or the beta or delta isomers also had atrophic testes.

Epidemiologic data can be extremely important in arriving at quantitative estimates of human cancer risk, expressed either as (a) attributable risk, or (b) relative risk. While case-control studies have a low cost/benefit ratio, cohort studies are more likely to yield data relating risk to amount of exposure, and to allow precise calculation of risk. However, cohort studies are long, expensive, and difficult to administer. Attrition and resultant unrepresentative composition can be major problems. Cohorts should be followed to extinction to permit accurate calculation of risk, which must take into account prolonged latency periods, competing risks, and the likelihood of increasing risk with time (or age). In view of certain limitations in epidemiologic and virologic methods, critical re-evaluation of the viral and oncogene theories are called for. The use of animal data for assessing human cancer risk requires further investigation of the assumptions and facts supporting two kinds of extrapolation: That from high to low dose carcinogen exposure, and cross-species extrapolation (i.e., from experimental animals to man). Large pieces of these two approaches rest on testable hypotheses which deserve further attention.

Building on prior work on sodium (Na) in drinking water and its effects on blood pressure (BP), two variations of the initial University of Massachusetts studies were carried out in other locations using the same methodology as the original investigations. A Texas/Oklahoma study compared the BP of 7th graders in two economically similar communities whose drinking water Na levels were 25 mg/L and 275 mg/L, a difference 2 1/2 times that in the original University of Massachusetts studies. A second study in Ohio, within only one community, compared the BP's of the 7th graders with a home water softener to their peers drinking the same water unsoftened (400 ppm total hardness). Although both studies have some complicating factors, the preliminary results indicate some effect of elevated Na in drinking water upon blood pressure in normotensive children.

The negative association between water hardness and cardiovascular disease found by several authors in different countries has also been found in the present investigation. All cases of myocardial infarction were registered in a standardized way at 15 WHO Collaborating Centres in Europe; information on the hardness of drinking water used by the population studies was also collected. Higher rates of myocardial infarction were usually found in towns served by softer water.

An epidemiological study amongst hypertensives and normotensives in Renfrew, Scotland, where drinking water hardness is very low (5 p.p.m.) and water-lead levels are commonly high, has shown a significant association between high blood-lead levels and high blood pressure. No association was found with indices of renal function, plasma renin or angiotensin II concentrations or serum uric acid levels. In a parallel study of blood-lead levels in Birmingham, England, where water hardness is low (20 p.p.m.) but water-lead levels are also low, high blood-lead levels were not found, no relationship was found with blood pressure and the prevalence of hypertension was lower than in Renfrew. We conclude that sub-clinic lead exposure from drinking water may be a factor in the development of hypertension. A study of blood-cadmium levels has shown no association between high blood pressure and sub-clinical cadmium exposure, but confirmed a close relation between blood-cadmium and cigarette smoking. We conclude that previous reports of a cadmium-blood pressure link may be confounded by failure to allow for the cigarette smoking habits of the subjects studied.

Epidemiological and clinical studies suggest that the incidence of atherosclerosis is higher in soft-water areas than in hard-water areas. In an attempt to discern the factor(s) in drinking water that may be associated with these observations, the current studies were performed to determine the effects of several elements associated with hard (i.e., calcium and magnesium) or soft (i.e., cadmium and lead) water in the induction and progression of atherosclerosis in the white carneau pigeon. The effect of these elements on lipoprotein metabolism was also assessed because it has been suggested that changes in the metabolism of lipoprotein may play a role in the etiology of atherosclerosis. Results show that the number and size of atherosclerotic plaques in the aorta were increased in pigeons given drinking water containing lead and/or cadmium. The effects of these elements were antagonized by the addition of calcium to drinking water containing lead and/or cadmium. Although lead and cadmium altered the profile of lipoproteins, this change did not appear to be related to an increase in the number and size of atherosclerotic plaques of the aorta. However, in pigeons treated with calcium alone the low-density lipoprotein (LDL) increased fourfold, and arteriosclerosis of the coronary arteries was observed. This result suggests that marked increases in the LDL protein may be related to arteriosclerosis of the coronary arteries. Based on these preliminary results, we suggest that lead, cadmium, and the LDL protein may be important factors in the induction and progression of atherosclerosis and arteriosclerosis in the pigeon.