We find by examination that the acid used contained no appreciable amount of nitrous acid and was of about 38 per cent. About ten gallons of it escaped. Coronavirus Resource Center. Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy Continue.
Twitter Facebook. This Issue. August 5, HALL, M. Workers may be harmed from exposure to nitric acid. The level of exposure depends upon the dose, duration, and work being done. Nitric acid is used in many industries.
Nitric acid is also used in the polymer industry. Some examples of workers at risk of being exposed to nitric acid include the following:. If you work in an industry that uses nitric acid, please read chemical labels and the accompanying Safety Data Sheets for hazard information. The following resources provide information about occupational exposure to nitric acid.
Search the HHE database for more information on chemical topics. Skip directly to site content Skip directly to page options Skip directly to A-Z link. A latent period has then been described which will last anywhere from hours ending with the development of symptoms of pulmonary edema and can develop into respiratory failure [ 1 — 3 ].
Here, we report the case of a year-old male working with nitric acid that developed pulmonary edema 12 hours after being exposed. A year-old male nonsmoker, with no past medical history, was working with nitric acid in an enclosed area.
Upon noticing a reddish-brown sweet smelling gas emanating from the bottom of a gallon drum, he turned on exhaust fans but continued to work. He did not put on any kind of protective mask or respirator on. He felt the sensation of eye and throat irritation and shortness of breath.
During the course of the six-hour exposure, he, on multiple occasions, retreated to the outside area and felt an amelioration of symptoms. Approximately 12 hours later he experienced paroxysms of cough and shortness of breath and was driven to the emergency department by his wife. He presented to the emergency department in moderate to severe respiratory distress. There were no murmurs rubs or gallops. Diminished breath sounds were appreciated on lung examination. There were frequent paroxysms of cough which were exacerbated by deep inhalation; there was no use of extra inspiratory muscles and no cyanosis appreciated.
The remainder of the exam was normal. He was placed on supplemental oxygen at 2 liters per minute with an increase in his oxygen saturation to 85 percent. The supplemental oxygen was increased to 4 liters per minute with an increase in his oxygen saturation to 92 percent and he was given bronchodilator treatments.
On 2 liters of supplemental oxygen by nasal cannula, his arterial blood gas showed a pH of 7. Carboxyhemoglobin and methemoglobin levels were unappreciable.
Normal blood gas values are pH of 7. All other laboratory values were within normal limits with the exception of a white blood cell count of Chest radiography showed bilateral pulmonary infiltrates and pulmonary edema Figure 1. Electrocardiogram showed normal sinus rhythm with a ventricular rate of 87 beats per minute with a normal axis and normal intervals. He was admitted to the intensive care unit, supplemental oxygen was continued, and bronchodilator treatments using albuterol and ipratropium 2.
Pulmonary care for this patient was at the discretion of the pulmonologist on the case. Over a seven-day hospital course he had progressive improvement in his symptoms and his chest X-ray Figure 2. One month after discharge the patient presented to pulmonary re-evaluation and followup. At the time of outpatient followup the patient denied any complaints at that time. During the visit standard pulmonary function testing was performed which included forced vital capacity, forced expiratory volume in the first second, peak expiratory flow, and maximum mid-expiratory flow.
These pulmonary function tests were found to be within their normal parameters. After this visit, he was lost to follow up. Oxides of nitrogen are emitted from a variety of sources.
Of the nitrogen oxides, nitrogen dioxide is the most important with regard to human exposure. The major contribution of atmospheric nitrogen dioxide is from the combustion of fossil fuels and emissions from motor vehicles [ 4 ]. Indoor exposure of nitrogen dioxide can occur through the use of gas stoves and heaters, including kerosene space heaters. Additionally, cigarette smoke can be a source of nitrogen dioxide.
Potential exposure to nitrogen oxides can occur in various occupational settings. Electroplaters, acetylene welders, nitrocellulose combustion, explosive detonation, and the application of nitric acid are all potential occupational exposure risks. In the agricultural setting the generation of nitrogen dioxide can occur from the decomposition of organic materials corn, grains that are deposited in silos [ 5 ]. Ice skating rink resurfacing machines Zamboni have the potential to generate nitrogen dioxide resulting in lung injury [ 6 , 7 ].
Cold blast furnace syndrome, resulting from exposure to nitrogen oxides, has also been described [ 8 ]. The magnitude of exposure, duration, and comorbidities determine the severity of illness after nitrogen dioxide exposure. These deleterious effects that lead to lung injury affect both type I and type II alveolar cells.
Throughout the literature, symptoms of nitric acid inhalational injury have been generalized into three phases—acute, subacute, and delayed onset. The acute exposure leads to an immediate onset of chest pain, wheezing, shortness of breath, cough or palpitations, nausea and vomiting, and diaphoresis; sudden death secondary to laryngospasm and bronchospasm has been described as well. Patients who present with subacute disease have nonspecific symptoms that can include dyspnea, cough, generalized weakness, and nausea; the symptoms can persist for up to 2 weeks but rarely persist for that length of time.
Those patients, who present with delayed symptoms, as with our patient, typically present with onset of symptoms within 4 to 12 hours after exposure; the delayed symptoms include dyspnea, tachypnea, cyanosis, bronchospasm, hemoptysis, tachycardia, and chest pain. Delayed symptoms are caused secondary to the development of frank pulmonary edema and progression of the patient into acute respiratory distress syndrome ARDS [ 1 ].
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