[A case of acute inhalation dinitrogen tetroxide poisoning].

Dinitrogen tetroxide is often used as an oxidant in rocket propellant and has strong irritant and corrosive properties. This paper analyzes the clinical data of a patient with dinitrogen tetroxide poisoning admitted in the 63710 Army Hospital of Chinese People's Liberation Army, so as to further explore the poisoning mechanism, clinical characteristics and key points of acute inhaled dinitrogen tetroxide poisoning.

Acute lung injury following refrigeration coil deicing.

We report a case of a worker who developed ALI requiring mechanical ventilatory support after attempting to melt ice condensate by applying the flame of an oxy-acetylene torch to refrigeration coils charged with a halocarbon refrigerant in a closed environment. A discussion of possible etiologies are discussed, including phosgene, carbonyl fluoride, and nitrogen oxides. Primary prevention with adequate respiratory protection is recommended whenever deicing is performed in a closed space environment.

Dose-response relationships between occupational exposure to potash, diesel exhaust and nitrogen oxides and lung function: cross-sectional and longitudinal study in two salt mines.

OBJECTIVE: Several studies have shown that underground salt miners may have an increased incidence of chest symptoms and sometimes decreased lung function. Miners of two salt mines were investigated to evaluate relationships between the lung function and the workplace exposure. The effect of nitrogen monoxide (NO) and nitrogen dioxide (NO(2)) was investigated in view of the recent debate on European occupational exposure limits. METHODS: A total of 410/463 miners (mine A/mine B) were examined cross-sectional and 75/64% of the first cohort were examined after a 5-year period. Exposure was measured by personal sampling. Personal lifetime exposure doses of salt dust, diesel exhaust, NO(2) and NO were calculated for all miners. Dose-response relationships were calculated by multiple regression analysis. Each exposure component acted as an indicator for the complex exposure. RESULTS: Exposure response relationships were shown in the cross-sectional and longitudinal investigations in both mines. In the 5-year period, the adjusted (age, smoking, etc.) effect of the exposure indicators resulted in a mean decrease of FEV(1) between -18 ml/year (mine A) and -10 ml/year (mine B). The personal concentrations related to this effect were 12.6/7.1 mg/m(3) inhalable dust, 2.4/0.8 mg/m(3) respirable dust, 0.09/0.09 mg/m(3) diesel exhaust, 0.4/0.5 ppm NO(2) and 1.7/1.4 ppm NO (mine A/B). Exposure was related to symptoms of chronic bronchitis only in mine B. CONCLUSION: The effects found in both mines indicate that the mixed exposure can cause lung function disorders in salt miners exposed over a long time. Because of the high correlation of the concentrations it was not possible to determine the effects of a single exposure component separately or to recommend a specific occupational exposure limit. However, possible maximum effects associated with the mixed exposure can be evaluated in the ranges of concentrations of the individual substances in the mines.

Serum clara-cell protein and beta2-microglobulin as early markers of occupational exposure to nitric oxides.

Biochemical effects of NOx on 60 workers (both genders) of nitric acid production were studied. The control group consisted of 61 nonexposed people employed elsewhere in the plant. Although the actual threshold limit valuetime weighted averages (TLV-TWA) were not exceeded in the specific conditions of our study, the subjects were exposed to NO2 and NO during several exposure episodes with peak maximal concentrations of 140 ppm and 515 ppm, respectively. Additional cross-week evaluation of several biochemical biomarkers in 15 NOx-exposed workers from one shift was performed. The objective of the study was to evaluate the value of serum Clara-cell protein (CC16) as a marker of bronchoalveolar epithelium activity. Antioxidant status was assessed by measuring activity of enzymes: glutathione peroxidase (GSH-Px), ceruloplasmin (Cp) in plasma, or superoxide dismutase (SOD), gluthatione S-transferase (GST), and nonenzymatic alpha-tocopherol in erythrocytes and thiobarbituric acid-reactive substances (TBARS) in plasma. Serum hyaluronic acid (HA) determining the connective tissue matrix status of airways, and beta2-microglobulin in serum (beta2M-S) and urine (beta2M-U) as a marker of renal function in occupational exposure to NOx were also employed. Exposure to NOx initiates peroxidative chain depleting of lipoprotein pool (alpha-tocopherol) in blood. Serum CC16 levels in NOx-exposed workers were found to be closely connected with alpha-tocopherol content. In NOx-exposed workers, the beta2M-S level was significantly higher than in the nonexposed ones, with the exception of smokers. Results of the cross-week study confirm cumulative systemic effects of NOx on several examined biomarkers. SOD and GST were found to be depleted. A transient higher level of HA after a 5-d shift significantly inversely correlated with CC16 level. The data imply that NOx-depleted levels of CC16 are detectable already after an 8-h shift. Our results demonstrate that even low NOx human exposure can cause characteristic changes in bronchiolar epithelium cells and renal effects. Serum CC16 level, although a nonspecific marker, was lowest in NOx-exposed subjects. The most sensitive parameters in exposed workers were beta2M-S and a-tocopherol. Spirometric assessment was not useful to describe low occupational exposure to NOx. In studying the effects of NOx on biomarkers, it is essential to carefully select suitable time of sampling. Screening of CC16, beta2M-S, and a-tocopherol can be successfully employed for biological monitoring of exposure to NOx.

[Progress in the protective medicine against [correction of aganist] rocket propellents].

To review the progress in the major assignment, the organization and implementation of protection against liquid rocket propellent. The safety detection methods of the rocket [correction of rocked] propellent in the launching field were also discussed. Three steps of the sanitation and protection of the liquid propellent, the toxicity and the toxicology of hydrazine on central nervous system, blood circulatory system, assimilation system, respiratory system, immune system, liver, kidney, eye, skin and its hereditary toxicology were described. In addition, the clinical types of poisoning, the current principle and the common ways of the prevention and treatment of hydrazine and nitrogen oxides poisoning were summarized.

Reactive airways dysfunction syndrome after exposure to dinitrogen tetroxide.

BACKGROUND: Reactive airways dysfunction syndrome (RADS) is characterized by persistent bronchial hyperreactivity and asthmatic symptoms in a previously healthy individual after a single intense exposure to an irritant fume, vapor, or gas. On October 23, 1995, a cloud of dinitrogen tetroxide (N2O4) escaped from a railroad tanker car in Bogalusa, Louisiana, exposing an estimated 4,000 citizens to the gas. METHODS: A sample of 234 patients with respiratory complaints after the spill received a complete history and physical examination, a symptom questionnaire, and pulmonary function tests. Patients whose previously undocumented asthma-like symptoms persisted for 3 months after exposure to N2O4 had methacholine challenge testing. RESULTS: Of the 234 patients evaluated, six met the criteria for a diagnosis of RADS. The distance of these six patients from the source of the leak, their durations of exposure, and initial symptoms were not different from those of the sample patients who did not have RADS. CONCLUSIONS: After evaluation of 234 symptomatic patients who were exposed to N2O4, we diagnosed six cases of RADS. There were no demographic characteristics or initial symptoms that identified patients who were at risk of having this syndrome. We believe we are the first to report cases of RADS due to N2O4 exposure.

[Accidental poisoning with silo gas]. / Przypadkowe zatrucie gazem silosowym.

Eight cases of poisoning in workers cleaning silo are presented. Silo gas, produced during fermentation of vegetable material, contains very toxic nitrogen oxides. In this group three workers died within silo, four patients were hospitalized (one of them with acute toxic pulmonary oedema, two with sings of pneumonia, one had only transient decrease of consciousness) and recovered without detectable sequelae. One patient, in general good condition, refused hospitalization and recovered.

[Changes in the lipid spectrum of the lungs in poisoning by nitrogen oxides or adrenaline]. / Izmeneniia v lipidnom spektre legkikh pri intoksikatsii oksidami azota ili adrenalinom.

The content of lipids and fatty acids was measured in lung tissue of intact rats and animals with lung edema caused by nitrogen oxide or adrenaline. Lung edema was found to involve disagreement between the phospholipid and fatty acid spectra and to increase the permeability of membranes. The toxic and adrenaline-induced edemas were found identical as regards the type of changes in the ratio of fractions of neutral lipids, phospholipids, and fatty acid spectrum, that is, these shifts represent a nonspecific reaction of lung tissue to aggression.

[Collective acute poisoning by nitrous gases]. / Intoxication aiguë collective par les vapeurs nitreuses.

A collective nitrous fumes poisoning (five cases) is reported. Two patients (case 3 and case 4) were comatose, in severe respiratory distress. Shock and slate blue cyanosis were noted. Physical examination and chest X ray revealed acute pulmonary edema-Methemoglobin levels were 71,3% (case 3) and 58% (case 4). Despite treatment both of them died from severe hypoxia resulting in cardiorespiratory arrest. Post-mortem examination was performed upon these four men. On admission the last one (case 5) was conscious, and in good hemodynamic condition. Acute pulmonary edema and cyanosis were present. Methemoglobin level was 37,3%. This patient recovered appropriate therapy. For case 1 and 2 acute anoxia due to methemoglobinemia seems to be cause of death. For cases 3 and 4 death is due to hypoxemia associated with pulmonary edema.

Determination of nitrate content in whey and milk powders at a dairy after an occupational accident with nitric acid.

A case of accidental occupational intoxication by fumes of nitrogen oxides and the application of an indirect method for the analysis of nitrate, nitrite, and nitro groups to establish the origin of the intoxication are presented. The method is based on the formation of a copper neocuproine complex, and extraction of the complex with methyl isobutyl ketone. The amount of copper in the organic phase is directly proportional to the nitrate content. This copper complex is determined by atomic absorption spectrophotometry. The results, which showed that samples from the contaminated workroom contained 0.1-0.2% nitrate, while blanks contained less than 0.02%, strongly support the hypothesis proposed for the course of the accident.