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Chronic solvent-induced encephalopathy


Chronic solvent-induced encephalopathy

Chronic solvent induced encephalopathy (CSE) is a condition induced by long-term exposure to organic solvents, typically in the workplace, that lead to a wide variety of persisting sensorimotor [1][2][3][4][5] The multiple names of solvent induced syndromes combined with inconsistency in research methods makes referencing this disease difficult and its catalog of symptoms vague.[1][3][6]


  • Classification 1
  • Causes 2
  • Symptoms 3
    • Neurological 3.1
    • Pathophysiological 3.2
    • Psychological 3.3
  • Diagnosis 4
  • Treatment 5
  • History 6
  • References 7


Introduced by a working group from the Raleigh-Durham, NC (United States) released a second diagnostic criterion which recognizes four stages as symptoms only (type 1), sustained personality or mood swings (type 2A), impairment of intellectual function (type 2B), and dementia (type 3). Though not identical, the WHO and Raleigh criteria are relatively comparable. WHO type I and Raleigh types 1 and 2A are believed to encompass the same stages of CSE, and WHO type II and Raleigh type 2B both involve deficiencies in memory and attention. No other international classifications for CSE have been proposed, and neither the WHO nor Raleigh criteria have been uniformly accepted for epidemiological studies.[1][2][7]


Organic solvents that cause CSE are characterized as volatile, blood soluble, lipophilic compounds that are typically liquids at normal temperature.[2][7] These can be compounds or mixtures used to extract, dissolve, or suspend non-water-soluble materials such as fats, oils, lipids, cellulose derivatives, waxes, plastics, and polymers. These solvents are often used industrially in the production of paints, glues, coatings, degreasing agents, dyes, polymers, pharmaceuticals, and printing inks.

Exposure to solvents can occur by inhalation, ingestion, or direct absorption through the skin. Of the three, inhalation is the most common form of exposure, with the solvent able to rapidly pass through lung membranes and then into fatty tissue or cell membranes. Once in the bloodstream, organic solvents, due to their lipophilic properties, easily cross the hydrogen sulfide, formaldehyde, acetates, and alcohols.


Two characteristic symptoms of CSE are deterioration of memory (particularly short-term memory), and attention impairments. There are, however, numerous other symptoms that accompany to varying degrees. Variability in the research methods studying CSE makes characterizing these symptoms difficult, and some may be questionable regarding whether they are actual symptoms of solvent-induced syndromes, simply due to how infrequently they appear. Characterizing of CSE symptoms is more difficult because CSE is currently poorly defined, and the mechanism behind it is not understood yet.


Reported neurological symptoms include

  1. ^ a b c d e f g h i j van der Laan, Gert; Markku Sainio (2012). "Chronic Solvent induced Encephalopathy: A step Forward". NeuroToxicology. 
  2. ^ a b c d e f Bast-Pettersen, Rita (April 19, 2009). "The neuropsychological diagnosis of chronic solvent induced encephalopathy (CSE)--A reanalysis of neuropsychological test results in a group of CSE patients diagnosed 20 years ago, based on comparisons with matched controls". NeuroToxicology: 1195–1201. 
  3. ^ a b c d e Baker, Edward L; Richard E Letz; Ellen A Eisen; Lucille J Pothier; Dianne L Plantamura; Marilyn Larson; Rodney Wolford (February 1988). "Neurobehavioral Effects of Solvents in Construction Painters". Journal of Occupational Medicine 30: 116–123. 
  4. ^ a b c Feldman, Robert G.; Marcia Hillary Ratner; Thomas Ptak (May 1999). "Chronic Toxic Encephalopathy in a Painter Exposed to Mixed Solvents". Environmental Health Perspectives 107: 417–422.  
  5. ^ a b c d e van Valen, Evelien; Ellie Wekking; Gert van der Laan; Mirjam Sprangers; Frank van Dijk (June 3, 2009). "The course of chronic solvent induced encephalopathy: A systematic review". NeuroToxicology: 1172–1186. 
  6. ^ a b c d Krstev, Srmena; Bogoljub Perunicic; Boris Farkic; Radmila Banicevic (Oct 30, 2002). "Neuropsychiatric Effects in Workers with Occupational Exposure to Carbon Disulfide". Journal of Occupational Health 45: 81–87.  
  7. ^ a b van der Hoek, Joffrey; Maarten M. Verberk; Gerard Hageman (December 27, 1999). "Criteria for solvent-induced chronic toxic encephalopathy: a systematic review". International Archive of Occupational and Environmental Health 73: 362–368.  
  8. ^ a b c Baker, Edward L. (June 2, 1992). "A Review of Recent Research on Health Effects of Human Occupational Exposure to Organic Solvents: A Critical Review". Journal of Occupational Medicine 36: 1079–1092.  
  9. ^ Maizlish, N A; L J Fine; J W Albers; L Whitehead; G D Langold (March 17, 1986). "A neurological evaluation of workers exposed to mixtures of organic solvents". British Journal of Industrial Medicine 44: 14–25.  
  10. ^ a b Furu, Heidi; Markku Sainio; Hanna Kaisa Hyvarinen; Ritva Akila; Beatrice Back; Sanni Uuksulainen; Ari Kaukiainen (2012). "Detecting chronic solvent encephalopathy in occupations at risk". NeuroToxicology. 
  11. ^ Cherry, Nicola; Helen Hutchins; T Pace; H A Waldron (October 12, 1984). "Neurobehavioral effects of repeated occupational exposure to toluene and paint solvents". British Journal of Industrial Medicine 42: 291–300.  


Occupations that have been found to have higher risk of causing CSE are painters, printers, industrial cleaners, and paint or glue manufacturer.[5] Of them, painters have been found to have the highest recorded incidence of CSE. Spray painters in particular have higher exposure intensities than other painters.[3] Studies of instances of CSE have specifically been carried out in naval dockyards, mineral fiber manufacturing companies, and rayon viscose plants.[11]

Though movements to reduce CSE have been successful, CSE still poses an issue to many workers that are at occupational risk. Statistics published in 2012 by Nicole Cherry et al. claim that at least 20% of employees in Finland still encounter organic solvents at the workplace, and 10% of them experience some form of disadvantage from the exposure. In Norway, 11% of the male population of workers and 7% of female workers are still exposed to solvents daily and as of 2006, the country has the highest rate of diagnosed CSE in Europe.[2][10] Furthermore, due to the complexity of screening for CSE, there is still a high likelihood of a population of undiagnosed cases.[1]

To reduce cases of CSE in the workforce, a diagnostic criterion for CSE appeared on information notices in occupational disease records in the European Commission. Following, from 1998 to 2004, was a health surveillance program for CSE cases among construction painters in the Netherlands. By 2000, a ban was put into action against using solvent-based paints indoors, which resulted in a considerable reduction of solvent exposure to painters. As a result, the number of CSE cases dropped substantially after 2002. In 2005–2007, no new CSE cases were diagnosed among construction painters in the Netherlands, and no occupational CSE has been encountered in workers under thirty years of age in Finland since 1995.[1][10]

Cases of CSE have been studied predominantly in northern Europe, though documented cases have been found in other countries such as the United States, France, and China. The first documented evidence for CSE was in the early 1960s from a paper published by Helena Hanninen, a Finnish neuropsychologist. Her paper described a case of workers suffering from


Like diagnosis, treating CSE is difficult due to how vaguely defined it is, as well as lack of data on the mechanism of CSE effects on neural tissue. There is no existing treatment that is effective at completely recovering any neurological or physical function lost due to CSE. This is believed to be because of the limited regeneration capabilities in the central nervous system. Furthermore, existing symptoms of CSE can potentially worsen with age. Some symptoms of CSE, such as depression and sleep issues, can be treated separately, and therapy is available to help patients adjust to any disabilities. Current treatment for CSE involves treating accompanying psychopathology, symptoms, and preventing further deterioration.[3][5]


Brain imaging techniques that have been explored in research have shown little promise as alternative methods to diagnose CSE. Neuroradiology and functional imaging have shown mild cortical atrophy, and effects in dopamine-mediated frontostriatal circuits in some cases.[1] Examinations of regional cerebral blood flow in some imaging techniques have also shown some cerebrovascular abnormalities in patients with CSE, but the data were not different enough from healthy patients to be considered significant.[6] The most promising brain imaging technique being studied currently is functional magnetic resonance imaging (fMRI) but as of now, no specific brain imaging techniques are available to reliably diagnose CSE.[1][5]

Furthermore, CSE must be diagnosed "by exclusion". This means that all other possible causes of the patient’s symptoms must first be ruled out beforehand. Because screening and assessing for CSE is a complex and time consuming procedure requiring several specialists of multiple fields, few cases of CSE are formally diagnosed in the medical field. This may, in part, be a reason for the syndrome’s lack of recognition. The solvents responsible for neurological effects dissipate quickly after an exposure, leaving only indirect evidence of their presence, in the form of temporary or permanent impairments.

Due to its non-specific nature, diagnosing CSE requires a multidisciplinary "Solvent Team" typically consisting of a neurologist, occupational physician, occupational hygienist, neuropsychologist, and sometimes a psychiatrist or toxicologist. Together, the team of specialists together assesses the patient's history of exposure, symptoms, and course of symptom development relative to the amount and duration of exposure, presence of neurological signs, and any existing neuropsychological impairment.[1]


Psychological symptoms of CSE that have been reported include mood swings, increased irritability, depression, a lack of initiative, uncontrollable and intense displays of emotion such as spontaneous laughing or crying, and a severe lack of interest in sex.[1][2][6][8] Some psychological symptoms are believed to be linked to frustration with other symptoms, neurological, or pathophysiological symptoms of CSE. A case study of a painter diagnosed with CSE reported that the patient frequently felt defensive, irritable, and depressed because of his memory deficiencies.[4]


[8] A common


The mechanism behind these symptoms beyond solvent molecules crossing the blood-brain barrier is currently unknown. [8][6]

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