Hazardous waste and neurobehavioral effects: a developmental perspective.

This paper summarizes the findings gleaned from detailed clinical examinations of three groups of residents who were exposed to trichloroethylene in well water. Also summarized are diagnostic findings for peripheral neuropathy. A detailed description of the neuropsychological test results is included, as well as a summary of domain-specific findings and diagnostic outcomes. A high rate of cognitive deficits of the type seen in patients with central nervous system dysfunction attributable to solvent exposure was seen. In addition, there was a clear developmental trend: subjects who were younger at the time of TCE exposure showed deficits in a larger variety of cognitive realms than did subjects who had already reached adulthood by the time of exposure. In particular, language deficits were seen in the younger, but not older, exposed subjects.

Occupational lead neurotoxicity: a behavioural and electrophysiological evaluation. Study design and year one results.

To evaluate the effects of chronic lead exposure on the nervous system in adults, a set of neurobehavioural and electrophysiological tests was administered to 99 lead exposed foundry employees and 61 unexposed workers. Current and past blood lead concentrations were used to estimate the degree of lead absorption; all previous blood lead concentrations had been less than or equal to 90 micrograms/100 ml. Characteristic signs (such as wrist extensor weakness) or symptoms (such as colic) of lead poisoning were not seen. Sensory conduction in the sural nerve was not affected. By contrast, various neurobehavioural functions deteriorated with increasing lead burden. Workers with blood lead concentrations between 40 and 60 micrograms/100 ml showed impaired performance on tests of verbal concept formation, visual/motor performance, memory, and mood. Thus impairment in central nervous system function in lead exposed adults occurred in the absence of peripheral nervous system derangement and increased in severity with increasing lead dose.

Neurologic evaluation of a population exposed to arsenic in Alaskan well water.

One hundred forty-seven persons exposed to arsenic from well water were evaluated by neurologic examination and nerve conduction studies. Total arsenic concentrations in well water ranged from 1 to 4781 micrograms/L and from 6 to 4964 micrograms/L in urine; a calculated index of arsenic ingestion ranged from 1 to 4521 micrograms/day. No dose-response relationship existed between arsenic ingestion and symptoms or physical findings compatible with peripheral neuropathy. Five of six persons with symptoms or physical findings suggestive of sensory neuropathy had normal nerve conduction velocities. Thirteen persons with elevated arsenic ingestion but no signs or symptoms of neuropathy had one or more abnormal nerve conduction velocities. No dose-response relationship, however, existed between arsenic ingestion and nerve conduction velocities. The authors concluded that arsenic ingestion from well water at the concentrations found in this Alaskan community did not result in clinical or subclinical neuropathy.

Follow-up studies of workers with bladder neuropathy caused by exposure to dimethylaminopropionitrile.

Following a 1978 outbreak of bladder neuropathy among workers exposed to dimethyl-aminopropionitrile (DMAPN), follow-up studies were performed 2 a after the original epidemic to evaluate the persistence of symptoms among a small group of initially affected workers. Although the overall prevalence of urologic and neurological symptoms fell for the 11 persons interviewed, significantly high rates of persistent symptoms were seen. Of particular concern was the increase in the prevalence of symptoms of sexual dysfunction. Physical examination identified one individual with sensorimotor neuropathy which was initially detected 2 a earlier. Three individuals who had similar neuropathic findings in 1978 were normal 2 a later. Objective neurophysiological and urologic testing revealed evidence of persistent abnormalities in several workers, but most of the objective findings had improved over the 2-a period. The follow-up of residual effects of occupational exposure to neurotoxic substances is essential to the understanding of the course of occupational illnesses.

Neurological dysfunction of the bladder in workers exposed to dimethylaminopropionitrile.

Neurogenic bladder dysfunction, characterized by hesitancy, need to strain, decreased stream, and increased duration of urination, developed in 104 (63%) of 166 employees working in the manufacture of polyurethane foam. Highest rates of illness (69%) occurred in production workers, and no illness occurred in office or warehouse workers. Onset of the epidemic coincided with introduction of a catalyst, dimethylaminopropionitrile (DMAPN), and monthly case incidence rates increased as DMAPN use increased. Outbreak ceased abruptly when DMAPN use was stopped. Of eight patients who underwent neurourologic testing during recovery, seven lacked either detrusor reflex or normal sensation of bladder filling; seven had a subclinical sensory abnormality; three had prolonged sacral-evoked responses; and two of these three had limb motor neuropathies. Dimethylaminopropionitrile is unique among known neurotoxins in producing urinary symptoms more frequently than limb nerve symptoms.

Peripheral neuropathy in arsenic smelter workers.

We conducted a double-blind controlled study of individuals exposed to arsenic trioxide in a copper-smelting factory. Subjects fell into three categories of peripheral neuropathy: none, subclinical, and clinical. The subclinical group had no symptoms or signs of numbness or reduced reflexes, but did have reduced nerve conduction velocity and amplitude measurements. Clinical neuropathy groups had signs and symptoms of neuropathy and electrophysiologic abnormalities. The clinical and subclinical groups correlated with increased content of arsenic in urine, hair and nails. The incidence of subclinical and clinical neuropathy was greater in arsenic workers than in unexposed controls.