Volatilisation of crop protection chemicals from crop and soil surfaces under controlled conditions--prediction of volatile losses from physico-chemical properties.

Volatilisation of crop protection chemicals from soil and crop surfaces is one of a number of processes that may contribute to their dissipation in the environment. Therefore, information on the potential of a chemical to volatilise from these surfaces is required by international and national registration authorities. This paper reports the results of more than 190 experiments, which were carried out with 80 different crop protection chemicals under controlled conditions (laboratory and/or greenhouse) according to the BBA guideline. Percent loss values observed during 24 h after application are reported for 123 soil and 71 crop volatility studies. Generally, volatile losses from crop surfaces were found to be greater than from soil surfaces under comparable experimental conditions. It has been previously proposed that volatile losses from soil surfaces, from crops, and from aqueous systems can be estimated from physico-chemical parameters. The data are therefore analysed to determine whether a correlation exists between volatilisation and physico-chemical parameters, such as vapour pressure, Henry's law constant, water/air and soil/air distribution coefficients. It was found that these parameters can be used to make reasonable predictions of volatile losses from crop and soil surfaces, which can be expected for crop protection chemicals under controlled conditions. Vapour pressure was the best predictor of losses from soil and crops. The use of the soil/air distribution coefficient is an alternative for predicting/estimating the volatility potential of a chemical from soil. Based on direct measurements, no noticeable volatility can be expected from compounds with a vapour pressure below 10(-3) Pa from soil and 10(-4) Pa from crops, this is fully confirmed by indirect measurements. A tiered volatility testing scheme including appropriate trigger values is proposed.

Dietary copper supplementation reduces atherosclerosis in the cholesterol-fed rabbit.

There has been considerable debate about how copper status may affect the biochemical and cellular processes associated with atherogenesis. In the present study we have attempted to address this issue directly by investigating the effects of dietary copper supplementation on processes likely to contribute to atherogenesis, using the cholesterol-fed New Zealand White rabbit model. Age matched rabbits (n = 16) were fed a 0.25-1% cholesterol diet to maintain plasma cholesterol concentrations at approximately 30 mmol/l. Eight of these animals also received 0.2% copper acetate. Control animals (n = 8) received rabbit chow without supplements. After 13 weeks on the experimental diets the animals were killed. Integrated cholesterol levels were similar for the cholesterol-fed animals (31.1+/-2.5 vs. 29.9+/-1.9 mmol/l weeks; P>0.05). Although integrated plasma copper levels were higher in the animals receiving the copper supplements, these did not differ significantly (19.0+/-4.8 vs. 15.1+/-2.9 micromol/l weeks; P>0.05). Tissue concentrations of copper were higher in the copper fed animals compared to those on cholesterol alone in aortic 14.0+/-0.75 vs. 1.8+/-0.2 microg/g wet tissue; P<0.05), carotid artery (11.4+/-3.5 vs. 4.9+/-0.9 microg/g wet tissue; P<0.05), and hepatic (332.5+/-28.6 vs. 3.3+/-1.1 microg/g wet tissue; P<0.0001) samples. The concentration of copper within the carotid artery was also significantly higher than that within the aorta (7.5+/-1.8 vs. 2.4+/-0.4 microg/g wet tissue; P<0.05). In animals fed a normal rabbit chow aortic, carotid and hepatic copper concentrations were 3.7+/-0.8, 9.4+/-3.4, and 5.0+/-1.6 microg/g, respectively. These values did not differ significantly from the cholesterol-fed animals (P>0.05). Plasma concentrations of caeruloplasmin, the major copper carrying protein, were estimated as plasma ferroxidase activity and were similar for the groups (P>0.05), as were aortic superoxide dismutase activity levels (P>0.05). Copper supplementation was associated with increased mononuclear cell adhesion to the endothelium of the carotid endothelium, with 2.6+/-0.3 adherent monocytes/1000 endothelial cells in the cholesterol plus copper-fed animals compared to 1.3+/-0.3 in the cholesterol-fed group (P = 0.0006), and 0.1+/-0.1 in the control animals (P<0.002). This may reflect the higher concentrations of copper found within the carotid artery. Histology of the thoracic aorta at the level of the third and sixth intercostal arteries, showed that copper supplementation was associated with significantly smaller intimal lesions (P<0.05 and P<0.01, respectively). These data suggest that copper supplements possibly inhibit the progression of atherogenesis.