Toxicology and Pharmacokinetics of Halogenated Hydrocarbons

Halogenated hydrocarbons encompass a diverse group of industrial and clinical chemicals, including chlorofluorocarbons, halogenated anaesthetics and industrial solvents. Their lipophilicity facilitates rapid absorption via inhalation, dermal contact or ingestion, followed by widespread distribution to lipid-rich tissues such as liver, brain and adipose compartments. Biotransformation is primarily mediated by cytochrome P450 enzymes in the liver, yielding reactive intermediates—acyl halides, halogenated aldehydes and free radicals—that can bind cellular macromolecules, promote oxidative stress and trigger membrane lipid peroxidation. Elimination pathways include urinary excretion of conjugated metabolites, pulmonary exhalation and, in some cases, enterohepatic recirculation. Pharmacokinetic parameters such as volume of distribution and half-life vary markedly with the degree and pattern of halogenation, influencing both acute and chronic toxic potential. Organ-specific toxicity commonly manifests as hepatotoxicity, nephrotoxicity, cardiotoxicity and neurotoxicity. Persistent halogenated pollutants pose environmental and human health risks, underscoring the need for refined risk assessment, exposure monitoring and the development of safer alternatives with lower bioaccumulative and reactive metabolite profiles. Applications span ozone-depleting substance replacement, occupational safety in manufacturing and clinical use of inhalational anaesthetics.

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Toxicology and Pharmacokinetics of Halogenated Hydrocarbons publication trend

The graph below shows the total number of articles in toxicology and pharmacokinetics of halogenated hydrocarbons across all publications each year (not limited to Nature Index journals).

Technical terms

Biotransformation: Enzymatic conversion of chemicals into more water-soluble metabolites.

Cytochrome P450: A family of hepatic enzymes responsible for oxidation of xenobiotics.

Hepatotoxicity: The capacity of a compound to cause liver injury.

No-observed-adverse-effect level (NOAEL): The highest exposure at which no significant toxic effects are detected.

Approximate lethal dose (ALD): An estimated dose likely to cause fatality in exposed organisms.

References

1. HCFC-123-induced toxic hepatitis and death at a Korean fire extinguisher manufacturing facility: a case series. Annals of Occupational and Environmental Medicine (2018).
2. In Vivo Evaluation of the Oral Toxicity of the Chlorobutanol. Toxics (2022).
3. Chlorinated paraffin metabolism and its importance for understanding CP toxicity. Journal of Environmental Exposure Assessment (2023).