Degradation of carbon disulphide (CS₂) in soils and groundwater from a CS_{2 -}contaminated site

This study is the first investigation of biodegradation of carbon disulphide (CS2) in soil that provides estimates of degradation rates and identifies intermediate degradation products and carbon isotope signatures of degradation. Microcosm studies were undertaken under anaerobic conditions using soil and groundwater recovered from CS2-contaminated sites. Proposed degradation mechanisms were validated using equilibrium speciation modelling of concentrations and carbon isotope ratios. A first-order degradation rate constant of 1. 25 × 10-2 h-1 was obtained for biological degradation with soil. Carbonyl sulphide (COS) and hydrogen sulphide (H2S) were found to be intermediates of degradation, but did not accumulate in vials. A 13C/12C enrichment factor of -7. 5 ± 0. 8 ‰ was obtained for degradation within microcosms with both soil and groundwater whereas a 13C/12C enrichment factor of -23. 0 ± 2. 1 ‰ was obtained for degradation with site groundwater alone. It can be concluded that biological degradation of both CS2-contaminated soil and groundwater is likely to occur in the field suggesting that natural attenuation may be an appropriate remedial tool at some sites. The presence of biodegradation by-products including COS and H2S indicates that biodegradation of CS2 is occurring and stable carbon isotopes are a promising tool to quantify CS2 degradation

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The effect of formoterol over 24h in patients with asthma: the role of enantiomers

The single-dose effect of formoterol racemate and enantiomers on bronchodilatation up to 24h was determined. Forty-six reversible asthmatic patients were randomised to this double blind, crossover study. Formoterol was inhaled by nebulizer (HaloLite((R))); 4.5 and 36mug of the racemate (rac-formoterol), 2.25 and 18mug of (R;R)-formoterol, 18mug of (S;S)-formoterol, or placebo. Airway and systemic effects were assessed by serial measurements of forced expiratory volume during the first second, FEV(1) (24h), and heart rate (4h). Rac- and (R;R)-formoterol significantly and dose-dependently increased FEV(1) with similar mean maximal effect. (S;S)-formoterol was without significant effects on FEV(1) and heart rate. (R;R)- and rac-formoterol were still effective 22-24h after single high doses, but this was associated with some systemic side effect (increased heart rate) initially. Average 22-24h FEV(1) was 8% (rac-formoterol 36mug) and 11% ((R;R)-formoterol 18mug) over placebo, respectively. No significant differences in effects were observed between rac- and (R;R)-formoterol. Thus, the single dose bronchodilatating effect of formoterol resides in (R;R)-formoterol. This study does not indicate a clinically important advantage of (R;R)-formoterol as acute bronchodilator compared to the racemate

The effect of formoterol over 24 h in patients with asthma: the role of enantiomers

The single-dose effect of formoterol racemate and enantiomers on bronchodilatation up to 24 h was determined. Forty-six reversible asthmatic patients were randomised to this double blind, crossover study. Formoterol was inhaled by nebulizer (HaloLite(R)); 4.5 and 36 mug of the racemate (rac-formoterol), 2.25 and 18 mug of (R;R)-formoterol, 18 mug of (S;S)-formoterol, or placebo. Airway and systemic effects were assessed by serial measurements of forced expiratory volume during the first second, FEV1 (24 h), and heart rate (4 h). Rac- and (R;R)formoterol significantly and dose-dependently increased FEV1, with similar mean maximal effect. (S;S)-formoterol was without significant effects on FEV1 and heart rate. (R;R)- and rac-formoterol were still effective 22-24 h after single high doses, but this was associated with some systemic side effect (increased heart rate) initially. Average 22-24 h FEV1 was 8% (rac-formoterol 36 mug) and 11% ((R-R)-formoterol 18 mug) over placebo, respectively. No significant differences in effects were observed between rac- and (R;R)-formoterol. Thus, the single dose bronchodilatating effect of formoterol resides in (R;R)-formoterol. This study does not indicate a clinically important advantage of (R;R)-formoterol as acute bronchodilator compared to the racemate