Metabolism of methanol, methyl ethers, esters and amides give rise to formic acid. This acid is an inhibitor of the mitochondrial cytochrome oxidase causing histotoxic hypoxia. Formic acid is a weaker inhibitor than cyanide and hydrosulphide anions. The body burden of formate in methanol poisoning is high enough to cause acidosis, and other clinical symptoms. Part of the protons can be attributed to formic acid whereas the most significant acid load results from the hypoxic metabolism. The acidosis causes e.g. dilatation of cerebral vessels, facilitation of the entry of calcium ions into cells, loss of lysosomal latency and deranged production of ATP. The latter effect seems to impede parathormone-dependent calcium reabsorption in the kidney tubules. Besides, urinary acidification is affected by formic acid. Its excretion causes continuous recycling of the acid by the tubular cell Cl-/formate exchanger. This sequence of events may partially explain an accumulation of formate in urine. Occupational exposure to vapours of methanol and formic acid can be quantitatively monitored by urinary formic acid determinations. Formic acid toxicity may prove a suitable model for agents causing histotoxic hypoxia.

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Epidemiological evidence from Western countries indicates that the prevalence of diseases associated with alterations in the immune response, such as asthma, certain autoimmune diseases and cancer, are increasing to such an extent that it cannot be attributed to improved diagnostics alone. There is some concern that this trend could be, at least, partially attributable to new or modified patterns of exposures to chemicals, including pesticides. The purpose of this article is to review the evidence on pesticide immunotoxicity in humans. Overall, the available data are inadequate to draw firm conclusions on the immunotoxic risk associated with pesticide exposure. The available studies on the effects of pesticides on the human immune system have several limitations, including limited data on exposure levels, heterogeneity of the applied methods, and difficulties in assessing the prognostic significance of observed slight changes and in the interpretation of the reported findings. Further studies are needed and preferably as prospective studies, comparing pre- and post-exposure data in the same group of subjects and including an appropriate non-exposed control group. More knowledge is required regarding the prognostic significance of the small changes observed.

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