Pollutant source or sink? Adsorption and mobilization of PFOS and PFOA from sediments in a large shallow lake with extended reed belt.

In this study, we i) assessed the occurrence of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in sediments, pore water, and bulk water from three different areas in Lake Neusiedl, Austria, and ii) investigated mechanisms regulating adsorption and remobilization of these substances under different conditions via multiple lab-scale experiments. The adsorption capacity was mainly influenced by sediments' organic matter content, oxide composition, and pre-loading. Results suggest that a further increase of PFAS-concentrations in the open lake can be partly buffered by sediment transport to the littoral zone and adsorption to sediments in the extended reed belt. But, under current conditions, the conducted experiments revealed a real risk for mobilization of PFOS and PFOA from reed belt sediments that may lead to their transport back into the lake. The amount of desorbed PFAS is primarily dependent on water/sediment- or pore water/water-ratios and the concentration gradient. In contrast, water matrix characteristics and oxygen levels played a minor role in partitioning. The highest risk for remobilizing PFOS and PFOA was observed in experiments with sediments taken near the only major tributary to the lake (river Wulka), which had the highest pre-loading. The following management advice for water transport between high and low polluted areas can be derived based on the results. First, to reduce emissions into Lake waters from polluted tributaries like the Wulka river, we recommend diffuse pathways through the reed belt in the lake's littoral to reduce pollutant transport into the Lake and avoid high local sediment loadings. Second, water exchange with dried-up areas with probable higher loadings should be carefully handled and monitored to avoid critical back transport in the open lake. And third, general work in the reed belt or generally in the reed should be accompanied by monitoring to prevent uncontrolled remobilization in the future.

[Diphtheria antitoxin level 2 years after booster vaccination]. / Diphtherie-Antitoxin-Spiegel zwei Jahre nach Auffrischimpfung.

In a prospective, controlled, randomized, multicenter study the immunogenicity of a single (day 0) and two (day 0, 28) booster vaccination against diphtheria were compared in subjects who had received their last diphtheria vaccination more than 10 years ago. Both short-term and long-term immunogenicity was assessed by determining diphtheria antitoxin levels four weeks after vaccination and after one and two years. 102 subjects received the first booster vaccination, and 83 were vaccinated twice. Prior to the first vaccination 27% of the subjects had a diphtheria antitoxin level below 0.01 I.U./ml; after the first booster only 5% were unprotected. The second booster did not show a significant effect, however, in 1 of the 5 subjects who were still unprotected after the first booster the second elicited an antitoxin level of more than 0.01 I.U./ml. After one and two years 7% and 8% of the subjects had diphtheria antitoxin level below 0.01 I.U./ml. A serological effect of a second booster vaccination four weeks after the first one could not be demonstrated neither after one nor after two years.

Severe pulmonary hypertension reversed by antibiotics in a patient with Whipple's disease.

The case is described of a 58 year old man with systemic Whipple's disease with pericardial and pleural effusions and severe pulmonary hypertension. After three months of antibiotic treatment there was a complete resolution, not only of the symptoms known to be associated with Whipple's disease (diarrhoea, arthralgia, pericardial and pleural effusions), but also of pulmonary hypertension.

[Dangerous intoxication from extreme serum concentrations of methaqualone metabolites. Detection and quantification of biosynthesis with gas chromatography-mass spectrometry]. / Lebensbedrohliche Intoxikation durch extreme Serum-konzentration eines Methaqualonmetaboliten. Nachweis und Quantifizierung mittels Biosynthese und Gaschromatographie-Massenspektrometrie.

CLINICAL COURSE: We present a potentially fatal case of acute methaqualone (M) poisoning with very low serum concentrations of M but extremely high levels of its metabolite, 2-methyl-3-(2-hydroxymethyl-phenyl)-4 (3H)-chinazoline (Met-1). A 23-year-old man was admitted to the intensive care unit 2 days after ingestion of 4-5 g M in an suicidal attempt. On admission he was somnolent and poorly responsive to painful stimuli. Physical examination revealed a heart rate of 95 bpm, a blood pressure of 125/65 mmHg, and a normal body temperature. His chest was clear to auscultation, respirations were shallow, and the skin was cyanotic. The electrocardiogram was unremarkable. The chest radiograph showed a normal heart size without pulmonary infiltrates or venous congestion. The pupils were dilated but reactive to light. The neurologic examination was further remarkable for increased limb reflexes, myoclonia, and positive pyramidal signs. During the next 2 days the patient became comatose and developed respiratory insufficiency due to non-cardiogenic pulmonary oedema, which was confirmed by chest radiograph and haemodynamic investigations by means of right heart catheterisation. He required mechanical ventilation for 6 days. Finally, he recovered completely and was discharged in good condition. DIAGNOSTICS: A lumbar puncture revealed neither blood nor pleocytosis in the cerebrospinal fluid. Cranial computed tomography was carried out on an emergency basis, but no abnormality was disclosed. An electroencephalogram did not exhibit any significant pathological findings. Testing for infectious diseases or porphyria gave negative results. Toxicological screening based on enzyme immunoassays (ELISA) was negative for alcohol, tricyclic antidepressants, benzodiazepines, barbiturates, and morphine, but gave a positive result for M. From the moment of admission daily blood samples were taken and analysed by combined gas chromatography and mass spectrometry. These showed very low levels of M but extremely high levels of Met-1. THERAPY: After gastric lavage, continuous enteric lavage with activated charcoal and mannitol was initiated to minimise intestinal absorption. Since M was hardly detectable in the serum, haemoperfusion was not regarded as indicated for drug elimination and treatment was restricted to general supportive measures. To rule out a central anticholinergic syndrome, an anticholinesterase drug (physostigmine) was administered but remained without therapeutic effect. CONCLUSIONS: The presented case is the first report of a life-threatening intoxication after M ingestion primarily caused by Met-1. It supports the significance of this metabolite for the toxic effects of the drug. A toxicological screening test based on ELISA proved helpful due to its cross-reactivity with metabolites. In cases similar to ours, resin haemoperfusion may be indicated to remove the metabolites despite low detectable concentrations of the parent substance in the serum.

Treatment of drug-induced agranulocytosis with recombinant granulocyte colony-stimulating factor (rh G-CSF).

Five patients with drug-induced agranulocytosis received 300 micrograms recombinant human granulocyte colony-stimulating factor (rh G-CSF) subcutaneously twice daily for 2-5 days. G-CSF therapy resulted in a steep increase of the neutrophil count, which was faster than that in patients with spontaneous recovery reported in the literature. In all four patients with infectious complications fever rapidly declined with the increase of granulocytes. G-CSF may be useful in the management of drug-induced agranulocytosis.