Occupational Diseases and Toxicology · MU Plovdiv

9. Occupational intoxications with irritant gasses (fluorine, hydrogen fluoride, chlorine, hydrogen chloride or sulfide, ammonia, sulfur dioxide). Etiology, pathogenesis, clinical manifestations, diagnosis, treatment, medical expertise.

Inside: 8 sections · 1 table · 15 flashcards · 7 min

Topic 9 of 60 in the MU Plovdiv syllabus for Occupational Diseases and Toxicology (Medicine, Year 3). The free AceMed note covers it in 8 sections, about 891 words (7 min of reading), with 15 flashcards.

In this note

  1. Introduction
  2. General principles of irritant gas toxicity
  3. Fluorine and hydrogen fluoride
  4. Chlorine and hydrogen chloride
  5. Hydrogen sulfide
  6. Ammonia and sulfur dioxide
  7. Diagnosis and differential diagnosis
  8. Medical expertise

Introduction

This topic covers occupational poisoning by irritant gases: fluorine and hydrogen fluoride, chlorine and hydrogen chloride, hydrogen sulfide, ammonia and sulfur dioxide. For each agent you should be able to give the sources of exposure, the mechanism of toxicity, the acute and chronic clinical picture, the diagnostic approach, the treatment and the principles of medical expertise.

General principles of irritant gas toxicity

Irritant gases damage tissue on contact. The depth of injury depends mainly on their water solubility. Highly soluble gases are absorbed in the upper airways, so they cause nose, throat and larynx injury quickly. Less soluble gases reach the bronchioles and alveoli, where they cause the most dangerous effects: chemical pneumonitis and non-cardiogenic pulmonary oedema. The main pathogenic events are direct epithelial necrosis, loss of surfactant, bronchospasm, increased capillary permeability and, in some patients, sensitisation of the airways.

Fluorine and hydrogen fluoride

Exposure occurs mainly through inhalation of HF vapour or fluoride dust, and through skin contact with HF solutions. Elemental fluorine is extremely reactive and is rarely encountered outside specialised chemical plants. The toxicity of HF is due to the fluoride ion, which binds calcium and magnesium.

  • Acute inhalation: irritation of the airways, cough, dyspnoea and delayed pulmonary oedema.
  • Skin and eye contact: deep tissue necrosis that may be painless at first and appear hours later, because the fluoride penetrates the tissue.
  • Systemic effects after large or dermal exposures: hypocalcaemia, hypomagnesaemia and hyperkalaemia, which may cause arrhythmia and cardiac arrest.
  • Chronic exposure leads to skeletal fluorosis, with increased bone density, periarticular calcification of ligaments, joint stiffness and pain. Staging is based on radiographic bone changes together with clinical findings; early stages are often asymptomatic and found only on X-ray.

Treatment of skin exposure includes copious water irrigation and topical calcium gluconate gel. Severe or deep burns may require subcutaneous or intra-arterial calcium gluconate and ECG monitoring. Serum calcium, magnesium and potassium must be checked and corrected. Fluoride levels in blood or urine are useful for confirming exposure.

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