A continuous-culture device was used to select and enrich for microorganisms, from sewage and agricultural runoff, that were capable of using the organophosphorus insecticide parathion as a sole growth substrate. Parathion was dissimilated by the highly acclimated symbiotic activities of Pseudomonas stutzeri, which non-oxidatively and cometabolically hydrolyzed the parathion to ionic diethyl thiophosphate and p-nitrophenol, and P. aeruginosa, which utilized the p-nitrophenol as a sole carbon and energy source. Ionic diethyl thiophosphate was found to be inert to any transformations. Methyl parathion was dissimilated in an analogous way. The device functioned as a chemostat with parathion as the growth-limiting nutrient, and extraordinarily high dissimilation rates were attained for parathion (8 g/liter per day) and for p-nitrophenol (7 g/liter per day). This is the first report of parathion utilization by a defined microbial culture and by symbiotic microbial attack and of dissimilation of an organophosphorus pesticide in a chemostat.
A first toxicity identification evaluation (TIE) was conducted in three phases using the Microtox test to identify the major toxicant(s) in effluent discharged from a dyeing plant in Hong Kong. In Phase I toxicity characterization indicated that anions were likely to be the major toxicants for the entire effluent. In Phase II concentrations of sulfite and other anions in the original and the anion exchange resin-treated effluent samples were determined by ion chromatography. Anions, which were found in the effluent at comparatively high concentrations and were suspected of being responsible for the toxicity to luminescent bacteria, were selected for further study in Phase III. Investigation in Phase III using the spiking and mass balance approaches confirmed that the sulfite ion was the major toxicant in the effluent.
ISEE-922 Objective: Previous studies showed that arsenic was associated with increased prevalence of metabolic syndrome (MS) which has been demonstrated as a strong predictor for type 2 diabetes incidence in middle-aged people. The objective is to evaluate MS prevalence 2 decades (1970–1990) after high arsenic exposure in 1920–1970, and to assess the importance of arsenic relative to conventional risk factors for MS occurrence in a perspective cohort from the arseniasis endemic area of southwestern Taiwan. Material and Methods: Subjects were based on the cohort recruited in 1990 (Chen et al, 1996 Hypertension) consisted of 1297 men and women over 40 years from Putai village. We followed the subjects during 1993, 1996, and 2002 for MS-related disease profiles. In 2002, 700 subjects were successfully followed for. Adult Treatment Panel III (2001) criteria were adopted according to reviews and comparisons. Five risk factors (fasting glucose, triglycerides, high density lipoprotein, systolic or diastolic blood pressure, and waistline) were used to define MS which was defined as the presence of 3 or more of the risk factors mentioned above. Conclusions: Two hundred fifty-nine subjects developed MS among 700 subjects in 1993. The incidence was 31.2 (95% CI: 21.8–40.6), 42.1 (33.4–50.9), and 45.8 (36.4–55.2) per 1000 person-years for DMA/MMA ratio tertiles of <5.50, 5.50–12.0, and >12.0, respectively. The odds ratio was significantly higher in middle (2.62, 95% CI: 1.27–5.51) and higher tertiles (2.61, 95% CI: 1.24–5.50) compared with lower tertile after adjustment for age and gender. We found that arsenic exposure was related to increased MS incidence even after 20 years of tap water use. This experience suggests that diabetes mellitus risk would need to be monitored even after the cessation of arsenic exposure from drinking water.
The suspect milk-borne carcinogen, aflatoxin M1 (AFM), was produced and isolated from the rice culture of the fungus Aspergillus flavus NRRL3251 for confirmation and determination of the potency of its carcinogenicity in the male adult Fischer rat. The carcinogen was mixed into an agar-based, semisynthetic diet at 0, 0.5, 5, and 50 ppb (microgram/kg) and was fed to groups of animals continuously for 19-21 months. Aflatoxin B1 (AFB), of which AFM is a metabolite, at 50 ppb was used as a positive control. Hepatocarcinogenicity of AFM was detected at 50 ppb, but not at 5 or 0.5 ppb, with a potency of 2-10% that of AFB. A low incidence of intestinal adenocarcinomas was found in the AFM 50 ppb group, but not in any other groups. At 0.5 ppb, the action level enforced by the U.S.A. Food and Drug Administration, AFM induced no liver lesions in the rats but stimulated the animals' growth. On the average, the rats in the 0.5 ppb group weighed 11% (p less than 0.001) more than those in the control group. This increased growth was associated with increased feed intake. Based on the biological activity of AFM at the relevant low doses and the estimated level of human exposure to AFM through consumption of milk, the cancer risk posed by this contaminant for human adults is assessed to be very low. For infants, further studies are warranted because milk constitutes the major ingredient of the infant diet and because infant animals have been shown to be more sensitive to the carcinogenicity of AFB than adult animals.
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