Document Eq58Gp9214RXrMoLqNvjZMJn0

Vol. 35/No. 8 MMWR 113 Leading Work-Related Diseases and Injuries --United States The National Institute for Occupational Safety and Health (NIOSH) has developed a list of J O leading work-related diseases and injuries. The first six categories have been described pre viously (1 -6); a discussion of the seventh category. Neurotoxic Disorders, appears below. NEUROTOXIC DISORDERS Background. Diseases of the nervous system resulting from toxic exposures in the work place were known as early as the first century A.D.. when Pliny identified palsy as a manifesta tion of lead poisoning among workers exposed to lead dust (7). in 1557, Jean Feme! linked gingival pigmentation, tremor, and behavioral changes to occupational mercury poisoning (SI; in the nineteenth century, Delpech recognized rubber processing as the cause of the bizarre psychoses occurring among French workers who manufactured condoms and balloons in small cottage industries. Later, carbon disulfide was implicated as the specific neurotoxic agent (9). Industrial hygiene practices have improved in the twentieth century, and some animal models of neurotoxic disease have been developed. In addition, workers who become ill often draw attention to outbreaks of neurotoxic diseases. Despite the prior identification of acryla mide as neurotoxic in animals, its neurotoxicity in humans was first recognized in the 1950s. when several Japanese workers involved in a pilot production project developed peripheral neuropathy (10). During the 1960s and early 1970s, dozens of cases of neuropathy occurred among Japanese and Italian workers exposed to solutions containing n-hexane during the manufacture of shoes {ID. Subsequently, high doses of n-hexane were found to be neuro toxic in exposed animals. In the past 15 years alone, outbreaks of serious human neurotoxicity occurred among workers exposed to three substances not previously known to be neurotoxic: the chlorinated hydrocarbon, chlordecone, which caused opsoclonus, tremor, disturbances of gait, and changes in personality (12); and two hexacarbons, methyl-n-butyl ketone and 2t-butylazo-2-hydroxy-5-methylhexane, both of which caused a predominantly peripheral neuropathy (13,14). Nature of Neurotoxic Disorders. Neurotoxic disorders are on the NIOSH list of Ten Lead ing Work-Related Diseases and Injuries (1) because of their potential severity--as exemplified by the neurotoxicity of chlordecone--and because of the large number of workers potentially at risk. A conservative estimate of the workers exposed full time to one or more neurotoxic agents is 7.7 million (15). The number of potentially neurotoxic chemicals found in the work place exceeds 850; an abbreviated list of the more commonly used of these chemicals is shown in Table 3 (76). Clinically, symptoms and signs of neurotoxicity can be diverse. Depending on the intensity of exposure^ the molecular configuration of the agent, and the mechanism of toxicity, either central or peripheral neurologic effects may predominate. Most neurotoxic chemicals, howev er, affect both the central and peripheral nervous systems. Because the symptoms of peripheral neuropathy are more specific and the nerves themselves more directly accessible to precise diagnostic examinations, the effects of neurotoxic agents on the peripheral nervous system are usually more easily identified than effects on the central nervous system (CNSI. Early symptoms of peripheral neuropathy may include numbness, tingling, or pain in the feet or hands. As the disease progresses, clumsiness or incoordination due to both sensory and motor changes may develop. Production workers may find their ability to do usual work par tially or fully impaired. Chemicals used extensively in industry, which cause peripheral neu- UCC 008229 114 MMWR February 28,1986 Work-Related Diseases and Injuries -- Continued ropathy when present in sufficiently high and persistent concentrations, include: lead, nhexane, acrylamide, carbon disulfide, mercury, and methyl bromide it 7,18) (Table 4). Several chemicals are known to cause selective impairment of cranial-nerve function, including dys function of the fifth cranial nerve (trichloroethylene) (18). The effects of neurotoxic agents on the CNS present a far wider range of disturbances (16,18,19) (Table 5). At times, the most striking effects are changes in mood and personality (20). High levels of exposure to manganese or carbon disulfide produce psychoses and suici dal tendencies. Delusions and hallucinations may result from exposure to high concentrations of solvents, such as methylene chloride. Manifestations of cognitive dysfunction, such as re duced attention span, lack of alertness, and memory loss, are prominent neurotoxic effects that may occur in addition to personality changes after exposure to many solvents and to asphyxiants, such as carbon monoxide. Other neurologic effects occur under certain restricted conditions of exposure to unique chemical substances (Table 6). Although research into the neurobehavioral effects of industrial chemicals is relatively new, early results suggest that occupational neurotoxicity may be a larger problem than pre viously suspected. Sensitive methods for evaluating subtle losses in cognitive function have only recently been applied to the evaluation of exposed workers. Because of the complexity of the nervous system and the variety of potentially neurotoxic exposures, the true scope of this health hazard in the workplace is unknown. Reported by Div of Biomedical and Behaviorel Science, Div of Surveillance, Hazard Evaluations, and Field Studies. National institute for Occupational Safety end Health, COC. Editorial Note: Studies of the neurotoxicity of workplace chemicals demonstrate the prob lems encountered in recognizing occupational disease in general. Despite occasional large and dramatic outbreaks of neurotoxic disorders, such as those mentioned above, more often small numbers of workers in many workplaces are chronically exposed to neurotoxic agents TABLE 3. Commonly used industrial chemicals recognized as neurotoxic Acetyl ethyl tetramethyl tetretin Acetyl pyridine Acrylamide Adiponitrile Alkyl phosphates Aluminum Aniline Arsenic, inorganic Arsine Aryl phosphates Azide Barium Benzene Boron p-Bcomophenyl acetylurea Cadmium Carbon disulfide Carbon monoxide Carbon tetrachloride Chlordane Chlordecone Chloroprene Cobalt Cuprizone Cyanide 2.4-OicWorophenoxy acetic Bcid (2,4-Di Dichlorodiphenyt tri chloroethane (otm Diethyl ether Diisopropyl fluorophosphate (DPPi Dimethyl sulphate Ethylene dichloride H exa chlo ro ph ene n- Hexane Hydroquinone Lead Lead, tetraethyl Leptophos Maloni trite Manganese Mercury Methanol Methyl bromide Methyl chloride Methyl />-butyt ketone Nickel (carbonyl) Nitrogen trichloride Organochtorine insecticides Organophosphate esters Organotins Uriethyttin) Paraquat Phenol Phenyl mercury Phthalate esters Potybromineted biphenyls (PBB's) Selenium Styrene Sulfur dioxide Tetrachlorobipheny! Thallium Toluene Trichloroethylene Triorthocresyiphosphate (TOCP) Vanadium, inorganic salt Zinc Zinc pyridinethione UCC 008230 Vol. 35/No. 8 MMWR 115 Work-Related Diseases and Injuries -- Continued that subtly and slowly alter nervous-system functions. Several neurotoxic syndromes mimic diseases of nonoccupational and "idiopathic" etiology, e g., the toxic axonopathy associated with exposure to various metals and solvents, the parkinsonian syndrome of chronic intoxica tion with manganese, and the organic brain syndrome of chronic solvent intoxication. Because of these similarities to other nonoccupational diseases, such cases are frequently not identi fied as occupational in origin. In addition, many physicians are not trained to take an adequate occupational medical history (21). For these reasons, the prevalence of occupational neuro logic disease is unknown, and important causal relationships between chemicals and disease remain obscure. The prevention of neurotoxicity among workers will require strategies such as those sug gested in the 1990 objectives for improving the nation's health (22), developed by the U.S. Public Health Service: (II analyses of structural analogues of known neurotoxic agents in an effort to predict the neurotoxicity of untested chemicals: (2) continuing search for animal models of disease; (3) ongoing research in establishing an acceptable human exposure level for identified neurotoxic agents; (4) epidemiologic evaluations of suspected neurotoxicity; (5) development of simple screening tools for use on asymptomatic populations exposed to known neurotoxic agents; and (6) premanufacture and premarket testing of new chemicals as required by the Toxic Substances Control Act (23). As in the prevention of other work-related diseases, however, the most direct and effective method for preventing neurotoxic illness will continue to be the environmental control of exposures to neurologic chemicals. Such efforts as the substitution of less toxic substances where possible, engineering controls, teaching ap propriate work practices, and educating workers about the potential neurotoxicity of chemi cals will aid a comprehensive prevention effort. References 1. COC. Leading work-related diseases and injuries--United States. MMWR 1983;32:24-6, 32. 2. CDC. Leading work-related diseases and injuries--United States. MMWR 1983;32:189-91. TABLE 4. Examples of peripheral neuropathies associated with occupational toxins Type of neuropath y Motor Mixed sensorimotor Toxin Lead Acrylamide Arsenic Carbon disulfide Carbon monoxide DDT /7-Hexane, methyl />Butyl ketone Mercury Comments Wrist extensors primarily involved; wrist and ankle drop are rare. Ataxia; desquamation of hands and soles; sweating of palms. Early distal paresthesias; pain in limbs, especially calves; hyperpathia of feet; weakness prominent in legs. Peripheral neuropathy rather mild; CNS effects more important. After severe intoxication. Only with ingestion. Distal paresthesias, motor weakness; weight loss, fatigue, and muscle cramps. Predominantly distal sensory involvement; more common with alkyl mercury exposure. UCC 008231 716 MMWR February 28,1686 Work-Related Diseases and Injuries -- Continued 3. CDC. tedding work-related diseases, and injuries--United States. MMWR 1984.33:125*6. 4. CDC. Leading work-related diseases and injuries--United States. MMWR 1984:33:213*5. 5. CDC. Leading work-related diseases and injuries--United States. MMWR 1985:34 219-22, 227 6. CDC. Leading work-related diseases and injuries--United States. MMWR 1985:34:537-40. 7. Hunter 0 The diseases of occupations. Sixth edition. London Hodder and Stoughton. 1978*251. 8. Chang LW. Mercury. In: Spencer PS, Schaumburg HH, eds. Experimental and clinical neurDtoxicolo- gy Baltimore. Maryland: Williams & Wilkins, 1980:508-26. 9. Seppdlainen AM, Hattia M. Carbon disulfide. In: Spencer PS, Schaumburg KH, eds. Experimental and clinical neurotoxicology. Baltimore, Maryland: Williams & Wifkins. 1980:356-73. 10. Le Quesne PM. Acrylamide. In: Spencer PS. Schaumburg HH, eds. Experimental and clinical neuro toxicology. Baltimore, Maryland: Williams & Wilkins. 1980 309-25. 11. Spencer PS. Couri D, Schaumburg HH. ivhexane and methyl rvbuiyl ketone. In: Spencer PS, Schaumburg HH, eds. Experimental and clinical neurotoxicology. Baltimore, Maryland: Williams & Wilkins, 1980:456-75. 12. Taylor JR, Selhorst JB, Calabrese VP. Chlordecone. In: Spencer PS, Schaumburg HH, eds. Experi mental and clinical neurotoxicology. Baltimore, Maryland: Williams & Wilkins. 1980:407-21. (Continued on page 121) TABLE t. Summary--cases specified notifiable diseases. United States Disease Acquired Immunodeficiency Syndrome (AIDS! Aseptic meningitis Encephalitis: Primary (Arthropod-borne Cqnonfiu: Hepatitis: a urupecJ Pptt'infectmus Civilian MStary Type A Type8 Non A. Non B Unspecified tegionetlosi* Leprosy Malaria Measles' Tour Indigenous Imported Meningococcal infections: Total Civilian Mumps Mtilerv Pertussis RubeSa (German measles) SyphSis fiNimery & Secondary). CUviJan Military Toxic Shock syndrome TubercUosis Tularemia Typhoid fever Typhus fever, lick-borne IRMSF) Aebos. animal Fab 22. 1366 Bth Week Ending Feb. 23 1985 { Median [ 1981-1985 Cumulative. 8th Week Ending Feb. 22 1986 Fab 23 1985 Median 1981-1985 224 92 N B0 80 73 1.804 633 878 553 N 655 16 . 13.299 398 397 388 53 75 8 13 243 246 3 63 63 . 65 34 3 389 6 4 377 1 7 - S2 19 2 15.233 315 46t 518 87 57 10 11 19 27 27 86 86 102 36 4 607 14 347 3 6 97 19 1 16 561 344 627 479 N 167 N 5 19 28 N N 86 86 99 36 22 669 7 N 416 2 9 109 119 7 117,512 2.272 3.333 3.290 409 747 7B 31 90 399 390 9 444 444 369 290 51 3,470 26 35 2.501 12 31 J 546 120 18 119.548 2.448 3,075 3.533 572 618 99 44 102 112 79 33 447 447 494 189 30 3.772 26 62 2.425 19 39 4 . 609 123 11 141,048 3.829 3,427 3.341 N 1.046 N 34 102 112 N N 489 489 1 603 170 124 4.661 64 N 2.99S 13 60 B 664 TABLE II- Notifiable diseases of low frequency. United States Anthrax Botulism-Foodbome ICe'rf 1) Infant (Calif 1) Other BruceOotis (Mol) Cholera Congenital rubete syndrome CpngenHaf syphilis, ages < > year Diphtheria Corn 1986 3 7 . 6 1 Leptospirosis flows 1} Plague Potkxnytfitis. Paralytic Psittacosis Rabies, human Tetanus (S Dsk. 1} Trichinosis Typhus fever, flea-borne (endemic, munnef Cum 1966 8 4 5 7 'Three Of the 249 reported us lor this wwk wore imported from s foreign country or can be direcity traceable to a Known intentationafly imported case wittnn two generations. UCC 008232