Exposure to glycols and their renal effects in motor servicing workers

Ten car mechanics frequently exposed to glycol-based cooling liquids were followed during a workshift. Airborne ethylene and propylene glycol concentrations in the car mechanics' environment were measured. The car mechanics gave urine samples after the workshift and their excretion of ethylene glycol, propylene glycol, oxalic acid, calcium and ammonia was analysed and compared to that of unexposed office workers. Urinary succinate dehydrogenase activity and glycosaminoglycans were also measured in both groups. Airborne ethylene and propylene glycol concentrations in the car mechanics' environment were negligible. Urinary ethylene glycol excretion in exposed workers was significantly higher than that in unexposed workers, but propylene glycol excretion was at the same level as in controls. In the exposed group, the excretion of the end metabolite of ethylene glycol, oxalic acid (47 ± 11 mmol/mol creatinine, mean ± SD, n= 10) differed slightly from that of controls (36 ± 14 mmol/mol creatinine, mean ± SD, n= 10). Urinary excretion of ammonia was higher among exposed workers than office workers. The excretion of calcium did not differ from that of controls. A marginally decreased urinary succinate dehydrogenase activity was found in the exposed men. The excretion of glycosaminoglycans was significantly lower in exposed workers. Therefore, it seems that ethylene glycol is absorbed by skin contact. The internal body burden is associated with oxaluria and increased ammoniagenesis typical of chronic acidosi

Kriisit hallintaan työpaikoilla

Vaasan yliopiston koordinoimassa Fokus työhyvinvoinnin johtamiseen! -hankkeessa on tuotettu kaikkien toimialojen työpaikkojen käyttöön Fokus kriisien hallintaan -ohje sekä KriisiApuri-sovellus. Netistä ladattavien ohjeiden tai sovelluksen avulla ja tarvittaessa työterveyshuollon tuella yritykset voivat laatia eri kriiseihin tarkoitetut varautumissuunnitelmat ja harjoitella niiden toimivuutta.©2021 Suomen Työterveyslääkäriyhdistys ryfi=vertaisarvioimaton|en=nonPeerReviewed

A Case of Optic Nerve Atrophy with Severe Disc Cupping after Methanol Poisoning

We report a rare case of optic nerve atrophy with severe disc cupping resulting from methanol poisoning. A 30-year-old man presented to the hospital complaining of decreased visual acuity in both eyes a day after drinking alcohol containing methanol. His initial visual acuity allowed for only visualizing hand motion and not corrected in either eye. Initial intraocular pressure was within normal limits in both eyes. Initial fundus examination showed optic disc swelling in both eyes. Four years later, he visited our hospital for an eye evaluation. Visual acuity in both eyes still only allowed for visualizing hand motion. No nystagmus was observed in either eye during the optokinetic nystagmus test, and no waves were found in a visual evoked potential test. No specific change was noted on brain magnetic resonance imaging. On fundus examination, there was disc pallor in both eyes and disc cupping with a high cup/disc (C/D) ratio above 0.9 in the left eye. C/D ratio of the right eye was 0.5. Methanol poisoning may induce glaucomatous disc cupping in the late stage as well as optic atrophy. One possible mechanism of disc cupping is ganglion cell loss due to acute demyelination of the retrobulbar optic nerve. This report is the first photographic evidence of methanol induced optic disc cupping in Korea

The European Registered Toxicologist (ERT) : Current status and prospects for advancement

Acknowledgements We would like to thank the participants of the five workshops in which the issues presented in this paper were discussed and the revised guidelines prepared, as well as the EUROTOX Executive Committee and the societies of toxicology of Sweden, the Netherlands, Switzerland, Austria and France for their support which allowed the workshops to take place.Peer reviewedPostprin

The dose response principle from philosophy to modern toxicology: The impact of ancient philosophy and medicine in modern toxicology science

Since ancient times the concept of dose response, from a toxicological perspective, has been a matter of concern. Already by the 8th century BC and over the years, many enlightened people have attempted to interpret this phenomenon, observing and coming across its results and practical implementation through exposure to chemical substances, either from natural or synthetic sources. Nowadays, the environmental exposure of human populations to chemicals in terms of quantity and quality might differ. Nevertheless, dose response still remains an issue joining hands with scientific and technological progress. The aim of the present review is not only to briefly recount the history of the dose response concept, from ancient time theories to novel approaches, but also to draw the outline of challenges and requirements toxicology science needs to fulfill

Olive oil with high polyphenolic content induces both beneficial and harmful alterations on rat redox status depending on the tissue

Olive oil (OO) possesses a predominant role in the diet of Mediterranean countries. According to a health claim approved by the European Food Safety Authority, OO protects against oxidative stress‑induced lipid peroxidation in human blood, when it contains at least 5 mg of hydroxytyrosol and its derivatives per 20 g. However, studies regarding the effects of a total OO biophenols on redox status in vivo are scarce and either observational and do not provide a holistic picture of their action in tissues. Following a series of in vitro screening tests an OO containing biophenols at 800 mg/kg of OO was administered for 14 days to male Wistar rats at a dose corresponding to 20 g OO/per day to humans. Our results showed that OO reinforced the antioxidant profile of blood, brain, muscle and small intestine, it induced oxidative stress in spleen, pancreas, liver and heart, whereas no distinct effects were observed in lung, colon and kidney. The seemingly negative effects of OO follow the recently formulated idea in toxicology, namely the real life exposure scenario. This study reports that OO, although considered a nutritional source rich in antioxidants, it exerts a tissues specific action when administered in vivo

The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals : 137. Ammonia

Ammonia (NH3) is a colourless gas with a distinctly pungent odour at normal atmospheric temperatures and pressures. The odour threshold is approximately 5 ppm. Ammonia can be liquefied under pressure. In aqueous solution, NH3 acts as a base yielding ammonium (NH4+) and hydroxide (OH-) ions. Because of the high water solubility ammonia dissolves in moisture on the mucous membranes, eyes and skin, forming ammonium hydroxide, which may cause alkali burns and liquefaction necrosis of the tissues. Ammonia occurs naturally in the environment and is endogenously produced in humans and other mammalians. It is also man-made in vast quantities. Occupational exposures may occur in ammonia plants, fertiliser manufacturing, and animal production. The primary route of occupational exposure to ammonia is inhalation, although dermal exposure may also occur during handling of liquid ammonia or aqueous ammonia solutions. The critical effect of exposure to ammonia is irritation. In controlled human exposure studies (3-4 hours) clear signs of mild respiratory and eye irritation appear somewhere between 25 and 50 ppm. In one of these studies very slight irritation was seen at 5 ppm. NEG considers 5 ppm as a pragmatic NOAEL and 25 ppm as a LOAEL for irritation. Chronic exposure to average ammonia levels above 25 ppm has been associated with an increase in respiratory symptoms (cough, wheezing, phlegm, and dyspnoea) and bronchial asthma. High acute exposure levels may result in reactive airways dysfunction syndrome (RADS), an asthma-like syndrome with persistent bronchial hyperreactivity but no sensitisation. Massive exposure to ammonia can cause eye damage, skin burns, severe inflammation of the respiratory tract (laryngitis, tracheobronchitis, and pulmonary oedema), and death. With very limited data available, there is no evidence that ammonia possesses genotoxic, carcinogenic or reprotoxic potential.Ammoniak (NH3) är en färglös gas med en påtagligt stickande lukt vid normal temperatur och tryck. Lukttröskeln har angivits till ungefär 5 ppm. Ammoniak kondenserar till vätska vid högt tryck. Ammoniak är en svag bas som i vatten bildar ammonium- (NH4+) och hydroxidjoner (OH-). Den höga vattenlösligheten gör att ammoniak löser sig i slemhinnor, ögon och hud och bildar ammoniumhydroxid som i sin tur kan orsaka frätskador och nekros. Ammoniak förekommer naturligt i vår omgivning och bildas endogent hos människor och andra däggdjur. Ammoniak framställs också industriellt i stora kvantiteter. Förutom vid råvaru- och handelsgödselproduktion förekommer ammoniakexponering framförallt inom jordbruket i samband med djurhållning. Yrkesmässig exponering för ammoniak sker främst genom inhalation. Hudupptag kan ske vid hantering av flytande ammoniak eller vattenlösningar av ammoniak. Den kritiska effekten vid exponering för ammoniak är irritation. I kontrollerade exponeringsstudier på människa (3-4 timmar) uppträder tydliga tecken på mild irritation i övre luftvägar och i ögon någonstans mellan 25 och 50 ppm. I en av dessa studier noterades en mycket svag irritation vid 5 ppm. NEG bedömer 5 ppm som en pragmatisk icke-effektnivå (NOAEL) och 25 ppm som lägsta observerade effektnivån (LOAEL) för irritation. Kronisk exponering för en genomsnittlig ammoniaknivå över 25 ppm har rapporterats vara förenat med en ökning av luftvägssymptom (hosta, pipande andning, slem och andnöd) och bronkiell astma. Akut exponering för höga halter ammoniak kan ge upphov till ett astmaliknande sjukdomstillstånd, s k RADS (reactive airways dysfunction syndrome) som kännetecknas av kvarstående bronkiell hyperreaktivitet men ingen sensibilisering. Massiv exponering för ammoniak kan orsaka frätskador på hud och ögon, allvarlig inflammation i luftvägarna (laryngit, trakeobronkit och lungödem) och leda till döden. Det går inte att bedöma om ammoniak har genotoxisk, carcinogen eller reproduktiontoxisk potential med tillgängliga data. Nyckelord: ammoniak, astma, frätskador, irritation, hygieniskt gränsvärde, RADS, toxicitet, översik