Biological monitoring to assess dermal exposure to ethylene oxide vapours during an incidental release.

During a short incident in an ethylene oxide (EO) producing plant, EO vapour was released under high pressure. Operators wore full respiratory protection during repairs to fix the leak. To check the adequacy of the applied personal protective equipment and to address concerns about potential dermal exposure and subsequent uptake of EO, biological monitoring was applied by determination of the haemoglobin adducts of EO in blood. Based on the results of the biomonitoring, a risk assessment of dermal exposure to EO vapour was made. Calculations to estimate dermal exposure, based on two recently published models and using the relevant physical-chemical properties of EO, indicate that the dermal contribution to total exposure is expected to be negligible under normal operating circumstances. However, the models indicate that under accidental circumstances of product spillage, when high air concentrations can build up quickly and where incident response is conducted under respiratory protection with independently supplied air, the systemic exposure resulting from dermal absorption may reach levels of concern. The model estimates were compared to the actual biomonitoring data in the operators involved in the accidental release of EO vapour. The results suggest that when incidental exposures to high EO vapour concentrations (several thousand ppm) occur during periods in excess of 20-30 min, additional risk management measures, such as wearing chemical impervious suits, should be considered to control dermal uptake of EO.

Mortality study update of ethylene oxide workers in chemical manufacturing: a 15 year update.

OBJECTIVE: To investigate the long-term mortality patterns of workers with past exposure to ethylene oxide (EO). METHODS: We redefined and updated a cohort of male workers employed in industrial facilities where EO was produced or used. All 2063 men were employed between 1940 and the end of 1988 and were observed for mortality through 2003. Cause specific Standardized Mortality Ratios were calculated. Internal analyses were made by applying Cox proportional hazards models to the data. RESULTS: No indications were found for excess cancer risks from EO exposures, including the lymphohematopoietic malignancies. There were 11 leukemia deaths and 11.8 expected and 12 non-Hodgkin lymphoma deaths and 11.5 expected. Proportional hazards modeling for all cause, leukemia and lymphoid malignancies mortality revealed no trends or associations with cumulative exposure. CONCLUSION: Despite the relatively high EO exposures in the past and extensive mortality follow-up, the cause specific mortality rates are comparable with those of the general US population. The Standardized Mortality Ratio analyses and the proportional hazards modeling for all cause mortality, leukemia and lymphoid malignancies mortality do not indicate exposure related effects in this cohort.

Toxicology primer: understanding workplace hazards and protecting worker health.

Hazardous substances are ubiquitous in the environment and common in industrialized societies. Serious harm can occur with sufficient exposures under certain conditions. However, much harm can be avoided if hazardous substances are handled with respect and appreciation for their use and potential. Occupational health nurses must be aware of potential hazards to employees in the work environment and apply scientific principles to their practice of promoting worker safety and health.

[Ototoxic study spiral ganglion neurons in the pig guinea with ethylene oxide remained in absorbable gelatin sponge].

OBJECTIVE: To measure ethylene oxide remained in absorbable gelatin sponge, and to observe change of ultrastructure in spiral ganglion neurons after deposited in otic vesicle of pig guinea with ethylene oxide sterilized absorbable gelatin sponge. METHOD: To use comparative colour technique measuring ethylene oxide remained in absorbable gelatin sponge, by means of transmission electron microscope to observe change of ultrastructure in spiral ganglion neurons after 3 months deposited in otic vesicle of pig guinea with ethylene oxide sterilized absorbable gelatin sponge. RESULT: The mean value of ethylene oxide remained in absorbable gelatin sponge were 438.32 mg, while nation standard are less 10 mg, FDA standard(1978) less 25 mg. ultrastructural appearance showed condensed matric electron dense of spiral ganglion mitochondria and dark crista of mitochondria, vacuolated cytoplasm. Ultrastructural observation also demonstrated dissolution or necrosis of ganglion cells, satellite cells, and vacuolated myelin. These changes were near Donson reported(1997) intracochlear perfusion with aminoglycosides. CONCLUSION: The mean value of ethylene oxide remained in absorbable gelatin sponge were 40 times nation standard. Toxic changes of ethylene oxide remained in absorbable gelatin sponge in spiral ganglion neurons were similar to intracochlear perfusion with aminoglycosides.

Two episodes of ethylene oxide poisoning--a case report.

Ethylene oxide is used as a sterilizer, a solvent, a plasticizer and in the manufacture of special solvents, antifreeze, polyester resins and non-ionic surfactants. Its toxicity is caused by an alkylating reaction with most organic substances in the body. Four workers, without any protection, managed the leakage of ethylene oxide from the collecting tank improperly on July 29, 2000. In the same factory, the overflow of ethylene oxide in process resulted in leakage of ethylene oxide again on Aug. 7, 2000. Two workers were poisoned despite wearing full-face respirators with ethylene oxide approved canisters. In these two events, the workers all smelled an ether-like odor. Six workers experienced nausea, vomiting, chest tightness, shortness of breath, dizziness, cough and ocular irritation. One worker had transient loss of consciousness. Oxygen therapy and supportive care were used. Patients were discharged in stable condition. The permissible exposure limit of ethylene oxide in air is 1 ppm as an eight hour TWA. Above 50 ppm, the odor threshold, a positive-pressure supplied air respirator is needed to protect the worker. Full-face respirators with ethylene oxide approved canisters could not protect our cases who smelled the odor and were exposed to an unknown concentration. It is important to wear positive-pressure self-contained breathing apparatuses equipped with full facepieces to clean up the contamination area and rescue the patients.

Intoxicación por contacto con óxido de etileno / Intoxication by contac with ethylene oxide

Una lactante eutrófica, durante una cirugía ortopédica tuvo contacto en su muslo derecho con una venda hemostática de látex contaminada con óxido de etileno (OE). Desarrolló una quemadura química intensa en el área expuesta y una intoxicación de efectos generalizados. Se discute el peligro al manipular objetos estrilizados con este método. Además se recomiendan pautas para evitar futuros accidentes (AU)

Intoxicación por contacto con óxido de etileno / Intoxication by contac with ethylene oxide

Una lactante eutrófica, durante una cirugía ortopédica tuvo contacto en su muslo derecho con una venda hemostática de látex contaminada con óxido de etileno (OE). Desarrolló una quemadura química intensa en el área expuesta y una intoxicación de efectos generalizados. Se discute el peligro al manipular objetos estrilizados con este método. Además se recomiendan pautas para evitar futuros accidentes

Ethylene oxide neurotoxicity: a cluster of 12 nurses with peripheral and central nervous system toxicity.

Ethylene oxide (EO) is commonly used to sterilize heat-sensitive products used by hospital patients and personnel. Ethylene chlorohydrin (EC), a by-product, is considered highly toxic. We report a cluster of 12 operating-room nurses and technicians who developed symptoms after a 5-month exposure to high levels of EO and EC in disposable surgical gowns. All patients reported a rash on the wrist where contact was made with the gowns, headaches, and hand numbness with weakness. Ten of 12 patients complained of memory loss. Neurologic evaluation revealed neuropathy on examination in nine of the 12 patients, elevated vibration threshold in four of nine, abnormal pressure threshold in 10 of 11, atrophy on head MRI in three of 10, and neuropathy on conduction studies in four of 10. Neuropsychological testing demonstrated mild cognitive impairment in four of six patients. Sural nerve biopsy in the most severely affected patient showed findings of axonal injury. Several patients in this group display signs of peripheral and CNS dysfunction following exposure to EO. Possible mechanisms of neurotoxicity include direct exposure of peripheral nerves through cutaneous absorption and central involvement through inhalation and vascular dissemination. The frequency of central and peripheral nervous system symptoms, supported by objective testing in these EO-exposed patients, suggests other healthcare personnel may be at similar risk.

Polyneuropathy due to ethylene oxide, propylene oxide, and butylene oxide.

Axonal neuropathy occurs due to occupational ethylene oxide (EtO) exposure. The experimental model of human EtO neuropathy was established. In addition, the neurotoxic effects of propylene oxide (PpO) and butylene oxide (BtO) were demonstrated in rats. Although no human neuropathy due to PpO or BtO is reported, both chemicals must be considered to be neurotoxic, based on this study.

[Parkinsonism secondary to ethylene oxide exposure: case report]. / Parkinsonismo secundário a exposição a óxido de etileno. Registro de caso.

Ethylene oxide is a gas widely used in the production of industrial chemicals. It is also used to sterilize heat-sensitive medical supplies. Previous reports of acute and chronic exposure have described neurotoxic effects like peripheral neuropathy and cognitive impairment. We describe a pure parkinsonian syndrome following acute ethylene oxide intoxication. A 39-years-old male was referred to our Movement Disorders Clinic for evaluation of a parkinsonian syndrome. He was acutely exposed to ethylene oxide four years before and remained comatose for three days, and gradually regained consciousness. At that time he showed a global parkinsonian syndrome including bradykinesia, rigidity and rest tremor, with a severe motor disability; no other neurological disorders were found. The symptomatology was partially controlled with biperidene and levodopa plus carbidopa. Two years later he developed L-dopa induced dyskinesias. Four years after the intoxication he was evaluated at our clinic. General examination showed no abnormalities. Neurologic examination revealed a normal mental status. Motor evaluation disclosed moderate bradykinesia, rigidity and rest tremor, shuffling gait, poor facial mimic, stooped posture, and his speech was low and monotonous; deep tendon reflexes were brisk. The Hoehn-Yahr disability score was degree IV. Routine laboratory and radiological exams showed results within normal limits. The CSF examination was normal. Brain computed tomography and magnetic ressonance were normal. A trial with bromocriptine and levodopa plus carbidopa did not improve dyskinesia, and he was put on a schedule including amantadine and biperidene with improvement to grade III in Hoehn-Yahr scale. In the present case there was a clear relation between the acute exogenous intoxication and irreversible parkinsonism.(ABSTRACT TRUNCATED AT 250 WORDS)

Parkinsonismo secundário a exposiçäo a óxido de etileno: registro de caso / Parkinsonism secondary to ethylene oxide exposure: case report

Parkinsonismo consequente a intoxicaçöes exógenas tem sido relatado desde o início do século. Os agentes mais comumente implicados säo o manganês, o monóxido de carbono e o sulfureto de carbono. No presente relato descreve-se síndrome parkinsoniana consequente a exposiçäo aguda ao óxido de etileno. Manifestaçöes neurológicas como neuropatia periférica e distúrbios cognitivos relacionados à exposiçäo a este gás foram previamente descritas, porém näo foi encontrada na literatura registro de parkinsonismo consequente a esse tipo de intoxicaçäo exógena

Cytogenetic changes in ethylene oxide-exposed workers: a challenge to occupational medicine.

Ethylene oxide is a colorless gas that can cause neoplastic disease (leukemia, stomach cancer) in animals and humans. Its mutagenic potential is expressed by chromosome aberrations and sister chromatid exchange, as has been shown in numerous studies of groups exposed to ethylene oxide. The results of our pilot study on the effects of exposure to high levels of ethylene oxide show chromosome breakage in exposed individuals at twice the frequency of the normal population. Although these are preliminary findings, they justify urgent, specific protection from further exposure.

[A survey of ethylene oxide sterilization in a hospital].

The health and environmental problems of ethylene oxide gas sterilization in a hospital are reported. Eight nurses who had been engaged in the gas sterilization, sometimes operated the auto-sterilizer in an inadequate manner; they exposed more than several hundred ppm of ethylene oxide once or twice a week. The main acute effects on these nurses after massive exposure were headaches, general fatigue and irritation of the eyes and throat. But no signs of polyneuropathy were seen. This survey suggests that there is a great risk of ethylene oxide poisoning while sterilizing instruments in a hospital.