In 1981, in Spain, the ingestion of an oil fraudulently sold as olive oil caused an outbreak of a previously unrecorded condition, later known as toxic oil syndrome (TOS), clinically characterized by intense incapacitating myalgias, marked peripheral eosinophilia, and pulmonary infiltrates. Of the 20,000 persons affected, approximately 300 died shortly after the onset of the disease and a larger number developed chronic disease. For more than 15 years, a scientific committee supported by the World Health Organization's Regional Office for Europe and by the Institute of Health Carlos III in Madrid has guided investigation intended to identify the causal agent(s), to assess toxicity and mode of action, to establish the pathogenesis of the disease, and to detect late consequences. This report summarizes advances in research on this front. No late mortality excess has been detected. Among survivors, the prevalence of some chronic conditions (e.g., sclerodermia, neurologic changes) is high. Attempts to reproduce the condition in laboratory animals have been unsuccessful, and no condition similar to TOS has been reported in the scientific literature. Laboratory findings suggest an autoimmune mechanism for TOS, such as high levels of seric soluble interleukin-2 receptor. Epidemiologic studies integrated with chemical analyses of case-related oils have shown that the disease is strongly associated with the consumption of oils containing fatty acid esters of 3-(N-phenylamino)-1,2-propanediol (PAP). These chemicals have also been found in oils synthesized under conditions simulating those hypothesized to have occurred when the toxic oil was produced in 1981. Whether PAP esters are simply markers of toxicity of oils or have the capability to induce the disease remains to be elucidated.

Major advances have been made during recent years in the understanding of associations between health and environment, and of biological, environmental and social mechanisms involved in this association. More emphasis should be placed on investigations of complex environmental health problems such as complex exposures to different pollutants at different levels and their combined health impact in different populations.

No abstract

No abstract

No abstract

No abstract

Abstract— The effect of 15 h continuous exposure to CS2 on the metaboliam of glucose and free amino acids in the brain of rats was studied. CS2 caused a moderate hypoglycaemia. There were also changes in the amounts of some amino acids in the brain. Glutamate and γ‐aminobutyrate were lower whereas glutamine was markedly increased. Comparative studies in vivo of the metabolism of [2‐14C]glucose and [1‐14C]butyrate indicated that CS2 did not affect glycolysis or the incorporation of 14C from glucose into amino acids except into γ‐aminobutyrate which was reduced. Contrary to the findings with [14C]glucose, CS2 provoked distinct changes in the labelling of amino acids when [14C]butyrate was the precursor. The most notable change was a markedly increased incorporation of 14C into glutamine. Based on the two‐compartment model of brain glutamate the experimental findings indicated that CS2 affected metabolism associated with the ‘small’ pool of glutamate but had a minimal effect on metabolism associated with the ‘large’ glutamate pool. The possibility is suggested that the changes observed involved an increased rate of ammonia removal. The low incorporation of 14C into γ‐aminobutyrate from either precursor is consistent with other evidence showing that CS2 interferes with pyridoxal phosphate‐dependent enzymes.

No abstract