Neurotoxic Effects of Ozone-Depleting Solvents
Summary
Ozone-depleting solvents, notably halogenated hydrocarbons such as 1-bromopropane and methyl bromide, have been widely employed in industrial cleaning, fumigation and degreasing. Increasing evidence indicates that chronic or high-level exposure to these compounds can impair both central and peripheral nervous systems. Clinical observations in occupational settings reveal sensory disturbances, slowed nerve conduction and cognitive deficits, while laboratory studies report neuronal apoptosis, oxidative imbalance and alterations in neurotransmitter systems. The neurotoxic profile of these solvents arises from their lipophilicity, facilitating penetration of the blood–brain barrier and accumulation in neural membranes, where they induce lipid peroxidation and mitochondrial dysfunction. Human case series and rodent models converge on consistent findings: peripheral neuropathy characterised by diminished vibration sense, slowed sensory nerve conduction velocity, and central effects including memory impairment and mood alterations. Given ongoing use in certain regions and potential for environmental release, a comprehensive understanding of mechanisms, exposure thresholds and mitigation strategies is essential. This overview synthesises the current state of research, highlights global health implications and underscores the need for preventive measures in occupational and regulatory contexts.
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Neurotoxic Effects of Ozone-Depleting Solvents publication trend
The graph below shows the total number of articles in neurotoxic effects of ozone-depleting solvents across all publications each year (not limited to Nature Index journals).
Technical terms
Ozone-depleting solvent: A halogenated organic compound that accelerates stratospheric ozone destruction and can pose toxicological risks.
Peripheral neuropathy: Dysfunction of peripheral nerves leading to sensory loss, motor weakness or paresthesia.
Oxidative stress: An imbalance between reactive oxygen species production and antioxidant defence mechanisms, resulting in cellular damage.
Electroencephalogram (EEG): A non-invasive recording of electrical activity in the brain used to detect functional alterations.
Apoptosis: Programmed cell death involving caspase activation, leading to controlled neuronal loss in neurotoxic conditions.
References
- Neurologic Abnormalities in Workers of a 1-Bromopropane Factory. Environmental Health Perspectives (2004).
- Identify Melatonin as a Novel Therapeutic Reagent in the Treatment of 1-Bromopropane(1-BP) Intoxication. Medicine (2016).
- Negative effect of methyl bromide fumigation work on the central nervous system. PLOS ONE (2020).
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