Guy Patin and his martyrology of those dead because of antimony.

Antimony was a chemical drug, similar to arsenic and lead, which was used in medicine since the 16th century. It brought intense controversy: for his supporters, it possessed exceptional properties, with three simultaneous effects, summarized by Libavius formula : vomere, cacare, sudare ... appreciable qualities at a time when Humorous theory was anchored in the minds. The detractors of antimony, among whom Guy Patin (1602-1671), pointed out that many patients treated with this remedy died... Patin's reflexions against the use of antimony in medicine are found in his letters, with a cumulative list of accidents that Patin liked to call his "martyrology of antimony", an expression he used, for example, in a letter to Andri Falconet on March 20, 1654. Our aim is to place Guy Patin's writings in the medical and social debate of his time, when several writers such as Benserade, Molire and Boileau also participated.

Pseudo-outbreak of antimony toxicity in firefighters - Florida, 2009.

Antimony oxides, in combination with halogens, have been used as flame retardants in textiles since the 1960s. Uniforms made from fabric containing antimony are common among the estimated 1.1 million firefighters in the United States. In October 2008, CDC received a report from the fire chief of a fire department in Florida (fire department A) regarding an outbreak of antimony toxicity among 30 firefighters who had elevated antimony levels detected in hair samples. This report summarizes the ensuing health hazard evaluation conducted by CDC to determine the source of antimony exposure. In February 2009, CDC administered questionnaires to and collected urine samples from two groups of firefighters: 20 firefighters from fire department A who did not wear pants made from antimony-containing fabric, and 42 firefighters from fire department B (also located in Florida) who did. All 20 firefighters from fire department A and 41 (98%) from fire department B had urine antimony concentrations below or within the laboratory reference range. CDC concluded that wearing pants made from antimony-containing fabric was not associated with elevated levels of urinary antimony. Only validated methods (e.g., urine testing) should be used for the determination of antimony toxicity. Accurate and timely risk communication during suspected workplace exposures should underscore the importance of using validated tests, thereby refuting an unproven hypothesis, allaying unsubstantiated concerns, and enhancing public trust.

Antimony in lung, liver and kidney tissue from deceased smelter workers.

Tissue concentrations of antimony in lung, liver, and kidney tissue from a group of deceased smelter workers from northern Sweden have been compared with those of a group of persons without occupational exposure from a nearby area. Neutron activation analysis was used to determine the antimony concentration of lung tissue from exposed workers; these concentrations were 12-fold higher than those of referents (p less than 0.001). For lung tissue there was no tendency towards decreased antimony concentrations with time (up to 20 a) after the cessation of exposure, and this result indicates a long biological half-time. The highest values were found for workers who had worked for many years at the roasters and in the arsenic and selenium departments. There was no significant difference between the antimony concentration of the lung tissue from workers who had died of lung cancer and those of persons who died of other malignancies, cardiovascular disease, or other causes. This finding does not however rule out the possibility of a role for antimony in the etiology of lung cancer among smelter workers since multiple factors may have been operating. The antimony concentration of the liver tissue and the kidney cortex did not differ from the corresponding values of the reference group; this finding indicates either a short biological half-time or insignificance for the systemic distribution of antimony.

Cardiovascular disease and work place exposures.

The typical occupational cohort study includes all causes of mortality. However, emphasis is usually placed on the presence or absence of excess cancer mortality. A systematic review of completed occupational cohort studies to assess the findings and patterns of cardiovascular mortality would be useful. Although many of these studies will illustrate the "healthy worker effect" with deficits in mortality, particularly from cardiovascular causes, a thorough review should indicate certain exposures needing further research. A recently published study of heart disease mortality in the rubber industry illustrates the potential use of such a literature review with subsequent follow up. Production workers in the rubber industry have shown small excesses in CAHD mortality. A follow-up study at one plant confirmed the known association between carbon disulfide and atherosclerosis, as well as suggested two new causal associations between CAHD and the use of phenol and ethanol as solvents. What additional techniques can be used to generate hypotheses on heart disease and occupation? Some possibilities include: A recent article describes the use of the results of occupational disease surveillance systems for occupational cancer research. A review of such systems for heart disease would be equally useful. It would be useful to review the quality and quantity of occupational data that has been collected in prospective cohort studies, such as those in Framingham and Evans County. The importance of examining the association between occupational exposures and heart disease include: Assessing whether adequate protection is afforded by current limits on exposure to substances known to cause heart disease (carbon disulfide, nitrates, and carbon monoxide).(ABSTRACT TRUNCATED AT 250 WORDS)

[Mechanism of the cardiotoxic effect of various industrial poisons (metals)]. / Mekhanizm kardiotoksicheskogo deistviia nekotorykh promyshlennykh iadov (metallov).

The effect of acute and repeated action of cobalt, lead, antimony on the metabolism of the heart muscle is shown. High doses of the metals of approximately 1/5 LD50 were studied in the acute experiment and doses one fifth these in the repeated experiment. The data obtained indicated that due to the effect of all the poisons studied changes developed early in catecholamine metabolism - the myocardial noradrenaline content decreased and the blood and urine monamine levels rose. Increase in the content of pyruvic acid, intensification of glycogenolysis processes (increase in phosphorylase a activity and decrease in the glycogen level), and diminished activity of lactate dehydrogenase in the myocardium attested to changes in its metabolism. High doses of the metals caused an increase in the free activity of the lysosome enzymes, cathepsins and of acid phosphatase, which indicated that the permeability of the membranes of these organelles was disturbed. The mechanism of the cardiotoxic effect of the metals is discussed.

Poisoning by antimony: a case report (Oliver Goldsmith).

Poisoning by antimony led to the death of a great individual in English literature. This case report gives as much of the history of the illness as can be found and tells a little about the individual.

Continuous pH monitoring with monocrystalline antimony electrodes: toxicity considerations from studies on heparinized human plasma.

Monocrystalline antimony electrodes can be used as pH sensors for continuous monitoring in vivo. The electric potential of the electrodes stems from a corrosion reaction in which antimony metal dissolution constitutes the anodic reaction. In this study the amount of antimony which leaves a monocrystalline antimony sensor, when monitoring pH in thermostatically controlled sterile human heparinized plasma, was determined by neutron activation analyses. From these results the toxicity hazard of using such electrodes in vivo is assessed. It is concluded that the amount of antimony released from a monocrystalline pH sensor, when used in a biological medium, is small compared with the amount of antimony accepted for administration as a medical therapeutic. Thus it should be safe from the toxicological point of view to use monocrystalline antimony electrodes for in vivo pH monitoring.

Arsine (arsenic hydride) poisoning in the workplace.

The National Institute for Occupational Safety and Health (NIOSH) recommends that appropriate workpractices be implemented to reduce the risk of worker exposure to arsine (AsH3) gas. There is a high potential for the generation of arsine gas when inorganic arsenic is exposed to nascent (freshly formed) hydrogen. This recommendation is based on several reports of worker exposure to arsine resulting in severe toxic effects or death. Most of the reported cases occurred when arsine was accidently generated during an industrial process. NIOSH would like to inform the occupational health community of some of the circumstances in which workers have been poisoned by arsine, with particular emphasis on the underlying mechanisms of generating the gas. We request that producers and distributors of arsenic and materials containing arsenic transmit information to their customers and employees, and that professional associations and unions inform their members. Stibine (SbH3), another toxic gas, if formed when antimony is exposed to nascent hydrogen. In most situations where arsine can be formed if antimony is present. Therefore, similar work practices should be implemented to reduce the risk of worker exposure to stibine.