Novel treatment of dihydrogen sulfide inhalation using hyperbaric oxygen during mass casualty.

Hydrogen sulfide (H2S) is a toxic gas produced via breakdown of organic matter. Hydrogen sulfide exposure can cause symptoms ranging in severity from mild effects (dizziness, headache, nausea) to severe lactic acidosis, respiratory failure, pulmonary edema, cardiac arrhythmias and death. Treatment modalities include oral countermeasures and 100% FiO2 with supportive therapy. However, case studies utilizing hyperbaric oxygen (HBO2) therapy have been reported with general benefit seen in severe cases of toxicity. In this report, cases of mild to moderate H2S toxicity occurred aboard a U.S. Navy ship, resulting in a mass casualty incident of more than 30 patients. Patient symptoms included dizziness, headaches, nausea, vomiting, and one patient with altered mental status. Most patients' symptoms resolved after several hours of supportive therapy, but six patients had symptoms refractory to 100% FiO2 at 1 atm. These six patients received HBO2 therapy with a USN Treatment Table 9 after consultation with the local emergency room and hyperbaric assets. Four separate chambers were utilized, including two chambers onboard USN ships and the local explosive ordnance disposal (EOD) chamber. Complete resolution of symptoms in all six patients was achieved within the first breathing period. Patients were monitored after treatment aboard the USN ship medical department. No patients required emergency department care. These cases demonstrate an expanded use of HBO2 to include moderate cases of H2S toxicity refractory to first-line therapy.

Thalamic GABA levels and occupational manganese neurotoxicity: Association with exposure levels and brain MRI.

Excessive occupational exposure to Manganese (Mn) has been associated with clinical symptoms resembling idiopathic Parkinson's disease (IPD), impairing cognitive and motor functions. Several studies point towards an involvement of the brain neurotransmitter system in Mn intoxication, which is hypothesized to be disturbed prior to onset of symptoms. Edited Magnetic Resonance Spectroscopy (MRS) offers the unique possibility to measure γ-amminobutyric acid (GABA) and other neurometabolites in vivo non-invasively in workers exposed to Mn. In addition, the property of Mn as Magnetic Resonance Imaging (MRI) contrast agent may be used to study Mn deposition in the human brain. In this study, using MRI, MRS, personal air sampling at the working place, work history questionnaires, and neurological assessment (UPDRS-III), the effects of chronic Mn exposure on the thalamic GABAergic system was studied in a group of welders (N=39) with exposure to Mn fumes in a typical occupational setting. Two subgroups of welders with different exposure levels (Low: N=26; mean air Mn=0.13±0.1mg/m3; High: N=13; mean air Mn=0.23±0.18mg/m3), as well as unexposed control workers (N=22, mean air Mn=0.002±0.001mg/m3) were recruited. The group of welders with higher exposure showed a significant increase of thalamic GABA levels by 45% (p<0.01, F(1,33)=9.55), as well as significantly worse performance in general motor function (p<0.01, F(1,33)=11.35). However, welders with lower exposure did not differ from the controls in GABA levels or motor performance. Further, in welders the thalamic GABA levels were best predicted by past-12-months exposure levels and were influenced by the Mn deposition in the substantia nigra and globus pallidus. Importantly, both thalamic GABA levels and motor function displayed a non-linear pattern of response to Mn exposure, suggesting a threshold effect.

Outbreak of Mysterious Illness Among Hospital Staff: Poisoning or Iatrogenic Reinforced Mass Psychogenic Illness?

BACKGROUND: Hospitals are rarely reported as settings for mass psychogenic illness (MPI). The present report scrutinizes an outbreak of probable MPI among hospital staff, with medical intervention reinforcing the course of the illness. CASE REPORT: Four of seven staff members in an emergency department became acutely ill with nonspecific symptoms. After uneventful observation they were discharged, but symptoms worsened at reassembly for debriefing. Poisoning with hydrogen sulfide was suspected, and the victims were transferred by helicopter for hyperbaric oxygen (HBO) treatment. During the following 9 days, 14 possible poisoning victims were identified, 6 of whom were transferred for HBO. After hospital stays with repeated HBO treatment and examinations without identification of significant physical disease, the majority of the 10 HBO-treated victims remained symptomatic, some on prolonged sick leave. The ward was closed for several weeks during comprehensive but negative investigations for toxic chemicals. Clinical data and lack of indication of chemical exposure, together with an attack pattern with only some individuals becoming ill in a shared environment, suggest MPI. Iatrogenic influence from dramatic intervention was probably a strong driving force in the outbreak. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Awareness of MPI may prevent unnecessary and potentially harmful treatment as well as improve health care resilience, particularly with respect to preparedness. Outbreaks of illness in a group of symptomatic victims without indication of significant physical disease should be managed by observation and limited intervention.

Low air levels of benzene: correlation between biomarkers of exposure and genotoxic effects.

This study was aimed to identify useful biomarkers of exposure and effect in workers exposed to low levels of benzene, and to evaluate any correlations existing between these parameters. Benzene exposure was measured in 33 petrochemical industry operators (PIO), 28 service station attendants (SSA), 21 gasoline pump maintenance workers (GPMW) and 51 non-exposed controls by GC-FID analysis. Samples were collected with personal passive samplers (Radiello). End-shift urine samples were collected for t,t-muconic acid (t,t-MA) determination by HPLC and for S-phenylmercapturic acid (S-PMA) measurement by HPLC-MS/MS. The alkaline version of the comet assay and, in a subgroup of 19 SSA and 16 control subjects, chromosomal aberrations (CA) and glutathione (GSH) levels were measured in peripheral blood lymphocytes. Personal benzene exposure was significantly higher in PIO, SSA and GPMW as compared to controls. The urinary excretion of the two metabolites showed a significant increase in SSA (p=0.0258 and p=0.0001, for t,t-MA and S-PMA, respectively) and in PIO (p=0.0013 and p=0.0001, for t,t-MA and S-PMA, respectively) as compared with the control group, while no such increase was observed for GPMW, for whom occupational exposure was not continuous and occurred on specific working days only. Significant increases of DNA damage were found by the comet assay for tail moment (TM) and tail length (TL) in SSA (p<0.0001 and p=0.008, for TM and TL, respectively) and PIO (p<0.0001 and p<0.0001, for TM and TL, respectively) when compared with controls. The PIO group also displayed a significant increase in the number of cells with comet (p<0.0001). Smoking habits did not appear to interfere with these results in any of the groups. No difference was found in percentage of CA between exposed workers and controls. Significant correlations were found, in all groups, between benzene exposure and the more representative comet parameter TM (r=0.509, p=0.007; r=0.525, p=0.017 and r=0.420, p=0.046 in SSA, GPMW, and PIO, respectively). A trend of negative correlation was observed between DNA damage and either GSH or urine S-PMA for exposed workers. In summary, in present study urinary S-PMA and DNA damage by the comet assay were both sensitive to exposure to low levels of benzene, and GSH seems to play an important defence role against benzene-dependent DNA damage.

[Acute respiratory distress syndrome induced by hydrogen fluoride gas inhalation].

A 21-year old man was referred to our hospital with severe respiratory distress and diffuse infiltrative shadows on chest radiograph. He had been exposed to irritant gas when polishing the inside of a stainless tank using a chemical cleaner containing hydrofluoric acid and nitric acid. He felt sick immediately after exposure and experienced respiratory distress within a few hours. He was successfully treated with intensive care including mechanical ventilation and administration of high dose methylprednisolone. Later, his illness was diagnosed as acute lung damage induced by hydrogen fluoride gas inhalation based on the findings of increased fluoride concentration in serum and urine specimen, and decreased serum calcium level.

Inhalational nickel carbonyl poisoning in waste processing workers.

BACKGROUND: Nickel carbonyl is formed when carbon monoxide comes into contact with active nickel. The inhaled nickel carbonyl is rapidly absorbed and distributed mainly to the lungs, brain, adrenal glands, and kidneys. In severe cases, acute nickel carbonyl exposure has been reported to cause death. DESIGN: Descriptive study. PATIENTS: Seven young men presented with fever, chills, substernal pleuritic chest pain, and exertional dyspnea. Extensive microbiological and toxicological investigations (including blood, urine, and bronchial specimens) for known pathogens and occupational toxins were performed. The clinical course and radiologic findings of each patient, including autopsy findings of three patients who died, were described. RESULTS: Four patients received treatment in the ICU. Elevated urinary nickel concentration was detected in all patients. Results of extensive microbiological investigations were unremarkable. No patients received chelating agents. Pulmonary consolidation, edema, hemorrhage, and fibrosis were observed at autopsy in patients who died. An out-of-date chemical used during neutralization of nickel waste was implicated as the source of nickel carbonyl poisoning. CONCLUSIONS: High mortality was reported in patients who presented subacutely following nickel carbonyl exposure. Further studies should be performed to clarify the role of chelation therapy in the subacute phases following nickel carbonyl exposure.

Clinical analysis of 43 cases of chronic benzene poisoning.

Benzene can result in bone marrow suppression. Chronic benzene poisoning (CBP) can be found among workers with excessive benzene exposure. CBP could give the appearance of different types of disorders such as leukopenia, agranulocytosis, anemia, pancytopenia, aplastic anemia (AA), myelodysplastic syndrome (MDS), and leukemia. This paper describes 43 CBP cases with the patients' ages ranging from 18 to 36 years (average: 23 years). Among them, 13 (30%) were male and 30 (70%) were female. Their job titles were furniture maker, shoemaker, industrial painter and metal shop worker. Their work durations ranged from 1.5 to 72 months (average: 14 months). Benzene levels in these workplaces exceeded 30 mg/m3. Ten of the 43 cases (23%) were diagnosed as mild cases of CBP, another 10 (23%) were moderate, and 23 (53%) were severe. Treatment for CBP included the following: cessation of benzene exposure, general supportive therapy, antibiotics, vitamins, corticosteroids, androgens, colony-stimulating factors (G-CSF, GM-CSF), blood component therapy, and traditional Chinese medicine. Thirty-three (77%) of the cases recovered completely, nine (21%) cases improved, and one (2%) died. In general, prognosis of CBP cases is optimistic when appropriate treatment is given. However, a few of the benzene-induced AA cases showed no response to treatment, which raises questions about the traditional view of the pathogenesis of the illness. Furthermore, only a part of the population with the same level of benzene exposure would suffer from the disease. Still, CBP cases with the same benzene exposure level exhibited different extents of severity of the illness. This evidence suggests strongly the existence of individual susceptibility. Detection of the biological markers regarding the individual susceptibility would be valuable for screening workers who are not suitable to be exposed to benzene.

Health effects of tank cleaners.

A total of 29 tank cleaners and 31 referent controls participated in the study. In most cases, the tank cleaners were employed in small companies, usually specialized subcontractors such as firms only working in refineries cleaning oil tanks and handling oil spills. The air concentrations of hydrocarbons (HCs) in tanks containing residuals from heavy fuel oil were generally low, unless the oil was still warm. Addition of light fuel oil to facilitate the cleaning of tanks containing viscous, heavy fuel oils resulted in total airborne HC levels of 1000-1500 mg/m3. High levels of HC were measured in tanks with low-boiling petroleum fractions (naphtha and light fuel oils) of 1000-2600 mg/m3 (maximum). Today, most cleaners use air-supplied respirators or air-purifying respirator cartridges inside tanks with petroleum products or other chemicals. The exception is small firms handling fuel oils for heating purposes where only 50% of the workers use protective equipment regularly; the other workers only occasionally use protective equipment even if the air concentrations of HC are high. Protective equipment is rarely used in small, domestic tanks. Measurements of heart rate showed that tank cleaning is, at times, a highly strenuous job. No differences between tank cleaners and controls were found with respect to spirometry, liver enzymes, or frequency of micronuclei. Acute intoxications were not frequently reported in this group. However, this investigation may underestimate the true risk, as it is a cross-sectional study that found that exposures were highly variable, both quantitatively and qualitatively. In many cases, the tank cleaners knew very little about the potential hazards or the proper use of protective equipment.(ABSTRACT TRUNCATED AT 250 WORDS)

Mineral profile of serum in experimental copper intoxication of sheep from industrial emissions.

We studied the dynamics of Cu, Fe, Zn, Mo, As, Cd, Pb and Se in the serum of sheep during experimental copper (Cu) intoxication from emissions from a Cu factory. From the food and the dosed emission, the daily intake was 466.8 mg Cu, 1253.93 mg Fe, 11.67 mg Zn, 0.74 mg Mo, 34.75 mg As, 0.091 mg Cd, 2.13 mg Pb, and 2.57 mg Se/experimental ewe. After the onset of Cu intoxication the first ewe died on the 65th d and the last one on the 84th d of the experiment. Hypercupremia was observed from the 50th d after the beginning of emission administration. Significant changes were observed in serum Cu on the 50th, 70th and 77th d (P less than 0.01). Changes in the dynamics of the other elements were recorded at the end of the cumulative phase and during the hemolytic crisis by also determining Fe, Zn, Mo, As, Cd, Pb and Se in serum of the Cu-poisoned sheep.

Interactions between copper and selenium in sheep in the course of experimentally-produced copper intoxication.

This work evaluated the effect of interactions between copper (Cu) and selenium (Se) in the course of experimentally-produced Cu intoxication with industrial emissions on the animals' life spans and the Cu and Se concentrations in serum, liver and kidneys. We selected 15 Valaska ewes 1.5 y old. After the morning feeding all the animals were given emissions from a nearby Cu plant that contained 16.5% Cu and 0.0093% Se. Seven of the animals (group B) were given 5 ml SELEVIT injectable (Biotika, Slovenska Lupca)/head before starting the experiment and again on days 30 and 60. In the animals without Se supplementation (group A) the daily Cu and Se intakes from the emission and food were 466.0 mg and 2.56 mg, respectively. The average life span of the sheep in group A was 77 d and in group B it was 79.83 d. The first death due to intoxication occurred on the day 65 in group A and on day 69 in group B. During the emission feeding period no statistically significant differences were observed in cupraemia between the ewes with Se supplementation and those without it. Hypercupraemia was found in both groups from day 50 till death. Only at the end of the experiment was the serum Cu of group A statistically lower than that in group B. Cu concentrations in the liver and kidneys (dry matter) of the sheep that died with Cu intoxication in group A was 2138 +/- 1090.96 mg/kg and 272.94 +/- 197.16 mg/kg, and in group B they were 2603 +/- 1332.9 mg/kg and 341.65 +/- 307.45 mg/kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of hyperbaric oxygenation on the status of the oxidation- reduction system and bioenergetics in phosphorus-processing industry workers]. / Vliianie giperbaricheskoi oksigenatsii na sostoianie okislitel'no- vosstanovitel'noi sistemy i bioénergetiki u rabotaiushchikh v fosfornoi promyshlennosti.

Prolonged contacts with the hazardous substances in phosphorus processing caused noticeable changes in the oxidation-restoration system and bioenergetics. Therapeutic and preventive hyperbaric oxidation procedures improved the processes of bioenergetic supply in the body, which was caused by more active oxidation processes and decreased tissue hypoxia.

Recent advances in occupational cancer.

The contribution of occupational and environmental exposures to the etiology of cancer is a topic of considerable scientific and public interest. If an occupational environmental exposure is associated with cancer in man, then both the exposure and the disease are preventable by appropriate protection. In order to enhance the awareness and timeliness of new information concerning occupational cancer, the University of California, San Francisco, School of Medicine in conjunction with the Northern California Occupational Health Center and the National Institutes of Occupational Safety and Health, the American Cancer Society sponsored a two day meeting in San Francisco at the end of 1983. Five of the presentations are highlighted in this review. In addition, twenty special questions of clinical relevance concerning occupational and environmental cancers are reviewed with the consensus answers given.

[Industrial hygiene studies in the production of various fibers and plastics]. / Trudovokhigienni izsledvaniia v proizvodstvoto na niakoi vlakna i plastmasi.

The results from the labour-hygienic and clinical laboratory studies on working environment and workers engaged in production of polyamide (PAS) and polyacrylnitrile fibres (PAN) are summed up as well as in the production and processing of polyvinylchloride resin, polyurethan, polysterene and glass fibre laminates. The main deleterious factors in those productions are the chemical ones: caprolactam, acrylonitrile,tolyl diisocyanate, vinylchloride, styrene, etc. Noise and microclimate are the other unfavourable on-the-job factors. The concentrations of the toxic substances in the air of the working environment are pointed to be far over MAC, in spite of the new plants. Experiments are reported aiming at the determination of the real exposure of the workers - via individual sample collecting and elaboration of BMAC. The measures for the improvement of the conditions of the working environment in the production of synthetic fibres and plastics are summed up as well as the reduction of occupation risk of the workers.

Cancer among workers exposed to arsenic and other substances in a copper smelter.

A study of the mortality experience of 2802 men who worked one year or more during the period 1940-4964 at a copper smelter in Tacoma, Washington, where arsenic exposure occurred showed a twofold excess in respiratory cancer deaths. Using a time-weighted measure of exposure, a life table method for accumulating dose, and a 10-year lag period, the excess ranged from 1.5 in the lowest exposure category to 2.5 in the highest exposure category. Neither duration of exposure nor time since first exposure contributed strongly to the respiratory cancer excess. The twofold excess in respiratory cancer deaths held for workers with relatively short exposures (less than 10 years) and with a relatively short latency period (less than 20 years) as well as for those with longer exposure and latent periods. This appeared to be because the respiratory cancer excess tended to disappear with time for workers who terminated employment alive, and because workers in high-exposure jobs tended to terminate more quickly than workers in low-exposure jobs. A somewhat unorthodox analytic method showed a weak relationship between the respiratory cancer excess and exposure duration when exposure intensity was held constant. Here, arsenic exposure intensity made an independent contribution to the respiratory cancer excess.