Journal of environmental pathology and toxicology最新文献

The multiplicity of potential teratogenic mechanisms requires that a practical screening system for developmental hazards simultaneously assess effects on as wide a variety of developmental phenomena as possible. The system also must provide the relevant dose level based on adult toxicity. A fresh water coelenterate fashioned into an artificial "embryo" may provide the former, while exposure of adult polyps may provide the latter. The system appears to separate the two dose levels as adequately as standard laboratory rodents but as significantly lower cost in time and effort.

The zinc/copper hypothesis, which invokes relative or absolute deficiency of copper in the etiology of ischemic heart disease, was described. The belief that calcium (and, perhaps, magnesium) is a substance in hard water which protects against ischemic heart disease by altering copper and zinc metabolism was presented. The amounts of copper and zinc in drinking water usually are too small to produce important increases in the amounts of these elements in diets. Occasionally tap water high in copper may be an important supplement to a diet low in copper.

The toxicity and mutagenicity of N-chloropiperidine (NCP) and piperidine (PD) were tested in C57Bl/J6 mice and in Salmonella tester strains. Toxicity studies, based on single intraperitoneal administration of the test compounds, revealed that while the toxic effect of PD in aqueous solution decreased with time, the toxicity of aqueous solution of NCP increased on standing at room temperature for 24 or more hr. Direct incorporation assay of NCP and PD for mutagenic activity, using Salmonella tester strains as the test system, showed that the number of revertants induced by NCP was about 2.4 fold of that induced by PD. The results further indicated that TA100 and TA1535 were the most sensitive strains. A modified host-mediated assay, involving the analysis of urine, peritoneal fluid and faecal material from control and NCP-treated mice, indicated that peritoneal fluid from treated animals generated more revertants; moderate levels of revertants were produced by faecal material and urinary and urinary preparations produced the least number of revertants.

Responsible evaluation of energy production effects on human health requires prior accounting for the socioeconomic, cultural, and climatic characteristics known to influence mortality rate and cause. Fifteen population characteristics and environmental variables (education, income, occupation, industrial mix, socioeconomic status, housing quality, climate, urban residence, geographic residence, internal migration, cigarette consumption, alcohol consumption, marital status, foreign birth or stock, and religious affiliation) and three age subgroups are discussed. An initial set of eight variables is indicated for mortality rate standardization, based on the reliability of their relationships with mortality. These eight variables are: education, occupation, industrial mix, urban residence, marital status, ethnic mix, and cigarette and alcohol consumption. Education and occupation are negatively related to mortality. Occupational exposure to toxicants (indicated by industrial mix), cigarette consumption, and alcohol consumption have positive linear relationships with various specific causes of mortality. Urban residence, marital status, and ethnicity have non-linear relationships with mortality and show consistent patterns for certain causes of death. In addition to these characteristics three age subgroups ( less than 1 year, 1-14 years, greater than or equal to 65 years) are discussed because of their relatively high or low rates compared to the rest of the population. A brief review of water and air pollution effects on mortality is included for completeness. Unique to this review is the quantitative summary (presented as an appendix) of the variables influencing adult mortality. It is a compilation of numerical relationships, derived either directly or indirectly from the published data, that support the choice of influencing variables.

Because chlorinated surface drinking water supplies have been implicated in an increased risk of cancer, alternative methods of disinfection are being proposed; chlorine dioxide is the most seriously considered. This study reports that chlorine dioxide exposure of two strains of laboratory mice (A/J and C57L/J) to 100 ppm chlorine dioxide in their drinking water for 30 days produced no changes in 11 hematological parameters measured. Chlorite (a product formed from chlorine dioxide disinfection) produced increases in MCV (mean corpuscular volume); osmotic fragility; G6PD (glucose-6-phosphate dehydrogenase) activity; and the number of acanthocytes at exposure to 100 ppm, but not 1.0 or 10.0 ppm. These findings are consistent with membrane damage to the red cell and, in particular, the lipid fraction. Since chlorite is formed at a rate of 50 percent of the chlorine dioxide demand, serious consideration must be given to limiting chlorite formation before chlorine dioxide is adopted as a disinfectant to replace chlorine.

The in vivo effects of patulin on hepatic monooxygenase enzymes in male mice were examined after single and multiple exposures (i.p.) to the mycotoxin. The animals were exposed to a single dose of 1, 3 or 4.5 mg patulin/kg or daily doses of 1.0 mg/kg for 5 or 14 days. After single exposure no significant effect was observed on hexobarbital hydroxylation while aniline hydroxylase increased significantly at 3 mg/kg and at 48 hr. The demethylation of aminopyrine and ethylmorphine increased significantly 48 and 72 hr after 3.0 or 4.5 mg patulin/kg doses. A 12% increase was observed in cytochrome P-450 content 48 hr after exposure to 1 or 3 mg/kg. NADPH-cytochrome C reductase was enhanced significantly at all 3 dose levels at 48 hr. At 24 hr hepatic NADPH-dependent dehydrogenase activity increased 38 and 46% in animals exposed to a single dose of 3 mg patulin/kg, respectively. No effect of patulin was observed on the hepatic drug metabolizing enzymes examined except hexobarbital oxidation in mice exposed to multiple doses of patulin. Patulin at best was a weak inducer of the hepatic mixed function oxidase system.

Asbestos fibers were tested for possible mutagenic activity using the Fluorescent Plus Giemsa (FPG) sister chromatid exchange (SCE) technique. Amosite, crocidolite, and chrysotile fibers were added to cell cultures at final concentrations of 10 and 100 micrograms/ml. Chrysotile completely inhibited cell growth at both concentrations; cells exposed to amosite and crocidolite proliferated but only at the lower concentration. Crocidolite significantly elevated the SCE rate and larger (greater than 5 mu) chromosomes were most sensitive. Amosite appeared to have a lesser effect on SCE frequency. Asbestos fibers are capable of disturbing cellular processes associated with chromosomal stability and effects vary with the asbestos type.