Urinary excretion of n-hexane metabolites. A comparative study in rat, rabbit and monkey

Exposure to n-hexane, a component of many industrial solvent mixtures, is known to cause polyneuropathy in man. The concentration of metabolites in urine following exposure may be useful in biological monitoring. In a comparative study experimental animals (rat, rabbit and monkey) were subjected to single inhalatory treatments of 6, 12 and 24 h with 5,000 ppm of pure n-hexane. At the end of the treatments and at intervals thereafter, urine, and in rats also blood, were collected and analyzed for n-hexane and its metabolites. While the urine of rats contained 2-hexanol, 3-hexanol, methyl n-butyl ketone, 2,5-dimethylfuran, y-valerolactone and 2,5-hexanedione, rabbit and monkey urine were found to contain only 2-hexanedione, rabbit and monkey urine were to contain only 2-hexanol, 3-hexanol, methyl n-butyl ketone and 2,5-hexanedione. Within 72 h of the end of exposure, the principal metabolite was 2,5-dimethylfuran in rats and 2-hexanol in rabbits and monkeys. In all three species the excretion rates of methyl n-butyl ketone, 3-hexanol and 2-hexanol peaked several hours earlier than 2,5-hexanedione (and gamma-valerolactone and 2,5-dimethylfuran in rats). In all species 2,5-hexanedione was still detectable in urine 60 h following exposure. n-Hexane metabolites in rat blood were 2-hexanol, methyl-n-butyl ketone, 2,5-dimethylfuran and 2,4-hexanedione. The first two, as well as n-hexane itself, were found in maximum concentration immediately after termination of exposure, while 2,5-dimethylfuran and 2,5-hexanedione, with the longer exposure times, peaked some hours later. The data from urine collected at the end of exposure were compared with those obtained in a parallel study in humans occupationally exposed to a mixture of hexane isomers. Humans chronically exposed to 10-140 ppm n-hexane had 2,5-hexanedione concentrations in urine ranging from 0.4 to 21.7 mg/l, i.e., in the same proportion as rats exposed once for 6 or 12 h to 5,000 ppm

Modeling interventions to reduce deforestation in Zambia

CONTEXT Agriculture faces tremendous pressure to supply both growing and wealthier populations with more food, fiber, and fuel, while recognizing the limits of agricultural ecosystems. But it remains unclear whether it is possible to increase agricultural and food production without increasing deforestation and associated greenhouse gas emissions. OBJECTIVE The objective of this study was to advance the understanding of landscape-level implications of sustainable intensification of agriculture on forest conservation in Zambia. Sustainable intensification aims to increase agricultural yields and reduce deforestation. Miombo woodlands, a dry forest ecosystem common throughout the region, are the dominant biome in much of Zambia, and they are suitable for the production of charcoal, a commonly used cooking fuel among urban households. METHODS We used participatory system dynamics modeling to examine the drivers of deforestation in two provinces in Zambia. We modeled four scenarios to examine their effects on reducing deforestation over a 50-year simulation period: (i) an increase in maize yield from adoption of SI practices, and (ii) occasional moderate and severe drought events, (iii) adoption of efficient charcoal cookstoves, and (iv) full electrification. RESULTS AND CONCLUSIONS We found no effects of adoption of sustainable intensification practices on agricultural encroachment into forested ecosystems. The clearing of forested land for agriculture was found to be largely driven by the rising demand for wood fuels for cooking and heating, particularly charcoal in urban areas. Charcoal was increasingly dominant as a driver of deforestation in both provinces such that changes in land practices and economic returns to farmers are unlikely to reveal measurable changes in land use. SIGNIFICANCE The findings have implications for the development of integrated approaches to address the challenges of food and energy insecurity, as well as for national-level policies aimed at climate change mitigation and reducing greenhouse gas emissions. This study provides a unique and innovative approach to integrating social and biophysical/ecological data through the application of system dynamics modeling. Furthermore, the study contributes to the literature on the environmental implications of agricultural land use and the drivers of deforestation

Complete genome sequences of two <em>Rhodococcus</em> spp. strains with large and linear chromosomes, isolated from apple rhizosphere.

Members of the genus Rhodococcus are usually able to catalyze a number of processes, which are of great interest for ecosystem performance as well as biotechnology. Here, we report the complete genome sequences of two Rhodococcus strains that were isolated from rhizosphere soil from an apple orchard in northern Germany

Experimental neurotoxicity and urinary metabolites of the C5-C7 aliphatic hydrocarbons used as glue solvents in shoe manufacture

Rats were intermittently exposed (9 to 10 h/d, 5 to 6 d/week) to controlled concentrations of single analytical grad solvents in ambient air. After periods ranging from 7 to 30 weeks the animals were perfused with glutaraldehyde and samples of nerves were processed for light microscopy of sections and of teased fibers. Animals treated with n-hexane at 5000 ppm (14 weeks) or 2500 ppm (30 weeks) developed the typical giant axonal degeneration already described in rats treated continuously with 400 to 600 ppm of the same solvent for 7 weeks or more. No such alterations were found in rats subjected to the following intermittent respiratory treatments: n-hexane 500 ppm (30 weeks) or 1500 ppm (14 weeks), cyclohexane 1500 or 2500 (30 weeks), n-pentane 3000 ppm (30 weeks), n-heptane 1500 ppm (30 weeks), 2-methylpentane 1500 ppm (14 weeks), and 3-methylpentane 1500 ppm (14 weeks). The following metabolites were found in the urine of rats according to treatment (in parenthesis): 2-methyl-2-pentanol (2-methylpentane); 3-methyl-2-pentanol and 3-methyl-3-pentanol (3-methylpentane), 2-hexanol, 3-hexanol, gamma-valerolactone, 2,5-dimethylfuran, and 2,5-hexanedione (n-hexane). 2-Hexanol was found to be the main urinary metabolite of n-hexane, while 2,5-hexanedione was present only in a lesser proportion. This feature of rat metabolism suggests that in this species 2,5-hexanedione reaches an effective level at its site of action during intermittent respiratory treatment with n-hexane with difficulty and explains the high concentrations necessary to cause polyneuropathy in rats subjected to this treatment