Carpal tunnel syndrome among grocery store workers.

The California Department of Health Services evaluated carpal tunnel syndrome (CTS), a median nerve entrapment condition associated with forceful and repetitive wrist motion, among grocery store workers at a large California supermarket where a CTS cluster had been reported. Forceful and repetitive wrist motion was measured, in three exposure levels, through a job classification scheme based upon type of work tasks and average time per week spent performing these tasks. A medical questionnaire and measurements of median sensory nerve conduction were used to measure CTS. CTS prevalence was 23% based upon a sample of 56 participants drawn from a workforce of 69 employees. A relative risk of 8.3 (95% confidence interval 2.6-26.4) for a history of CTS-like symptoms between the high and low exposure level groups held up after adjustment for the potential confounders of age, sex, alcohol consumption, and high-risk medical history. It was concluded that the basic principles of good ergonomic design should be used to prevent or diminish the risk of musculoskeletal injury in the workplace.

Neurotoxicological evaluation of hospital sterilizer workers exposed to ethylene oxide.

Ethylene oxide is now frequently used to chemically sterilize heat-sensitive materials in the hospital setting. Previous reports of neurotoxic effects of ethylene oxide have been described in animals and humans. Recent reports suggest that cognitive deficits may be associated with chronic low-level ethylene oxide exposure. We undertook this study of hospital workers with chronic ethylene oxide exposure and compared them with a non-exposed control group in an attempt to detect neurological and neuropsychological abnormalities. Ethylene oxide breathing zone levels of up to 250 ppm in exposed subjects were reported. All evaluations were done without examiners' knowledge of exposure status of the subjects. The exposed group was found to have a statistically significant lower P300 amplitude, bilaterally hypoactive distal deep tendon reflexes and poorer performance on neuropsychological tests involving psychomotor speed. Exposed subjects acknowledged more symptoms and higher levels of depression and anxiety. Nerve conduction velocities and EEG spectral analysis were similar in both exposed and control groups as were scores on most psychological tests. Based upon this information and prior reports, ethylene oxide should be considered in a differential diagnosis of neuropsychological, peripheral and central nervous system dysfunction in workplace settings associated with ethylene oxide exposure.

Prolongation of the P-300 latency associated with hydrogen sulfide exposure.

Three patients exposed to hydrogen sulfide developed persistent cognitive impairment, as suggested by the P-300 event-related potential and measured by neuropsychological testing. Routine neurological and physical examinations were unremarkable, although the patients were sufficiently impaired so as to be unable to work. The P-300 event-related potential and neuropsychological testing proved to be important in the detection of cognitive dysfunction following acute hydrogen sulfide exposure. The three patients with neurocognitive dysfunction were acutely exposed to hydrogen sulfide. The incidents occurred independently and under different circumstances. Each patient was evaluated at the Northern California Occupational Health Clinic, San Francisco, examined neurologically and neuropsychologically, and evaluated with a P-300 event-related potential. Each patient had persistent neurological symptoms, neuropsychological deficit, and abnormally prolonged P-300 latencies.

Cross-sectional neurotoxicology study of lead-exposed cohort.

Although the toxic effects of lead have been known for centuries, lead intoxication is still widespread in the United States. Without baseline tests of neuropsychological, neurobehavioral and neurophysiological testing it may be difficult to detect subtle changes in neurological function after lead exposure. This may be further confounded by partial chelation treatment and exposure to neurotoxic mixtures or inability to quantitate alcohol consumption. We undertook a cross-sectional study to address these problems in 24 exposed and 29 control subjects in a plant that manufactured electrical components using fritted leaded glass to coat capacitors and transistors. Potentially exposed workers had blood lead levels ranging between 3 micrograms/dL to 135 micrograms/dL. Industrial hygiene monitoring revealed the plant's air lead levels ranged from 61 micrograms/m3 to 1,700 micrograms/m3 in excess of OSHA permissible exposure limits of 40 micrograms/m3/10 hr day. Using a specially designed battery of neurophysiological, neurobehavioral and neuropsychological screening tests, we demonstrated a significant difference from controls in measures of psychomotor speed, motor strength and verbal memory. Although limited by the cross-sectional design, these findings support the hypothesis that the battery of neurophysiological, neuropsychological and neurobehavioral tests can detect a significant inter-group differences between lead-exposed and control subjects.

The P-300 event-related potential in experimental nitrous oxide exposure.

Without the availability of objective measures of central neurologic dysfunction, neuroepidemiologic investigations of individuals exposed to psychoactive drugs and potential environmental and occupational neurotoxins are extraordinarily difficult, particularly when the central nervous system manifestations are subtle, diffuse, and limited to cognitive deficits. In an attempt to assess and quantitate psychomotor dysfunction, P-300 event-related potentials, Symbol Digit Test, Continuous Performance Test, and Finger Tapping Test were obtained from six subjects sequentially exposed to nitrous oxide at 0%, 10%, 20%, and 40%. With increasing concentration of N2O, there was prolongation of P-300 latency and worsening of Continuous Performance Test and Symbol Digit Test performance; P-300 amplitude and Finger Tapping Test performance were decreased by exposure to N2O. This study demonstrates a dose-dependent reduction in P-300 amplitude and prolongation of P-300 latency in subjects in whom psychomotor impairment was induced by the acute administration of N2O.

Evidence of neurologic dysfunction related to long-term ethylene oxide exposure.

Eight hospital workers with chronic ethylene oxide exposure were age-sex matched with eight nonexposed controls with no significant differences in educational backgrounds and vocabulary scores. The exposed group performed more poorly on all eight measures of cognition, memory, attention, and coordination, with 71.3% less accuracy on the Hand-Eye Coordination Test. There was a dose-response relationship between exposure and the following: Continuous Performance Test and sural velocity. These findings suggest that neurologic dysfunction may result from long-term low-dose exposure to ethylene oxide, and that these effects may occur at exposure levels common in hospital sterilizer operations.

Alcoholic cerebellar degeneration is not a dose-dependent phenomenon.

Eleven alcoholics with cerebellar degeneration (eight with computerized tomography confirmation of cerebellar atrophy) were matched with nonataxic alcoholics and nonalcoholics. There were no laboratory or physiological markers for ataxia, including hemoglobin A1a + b, red blood cell transketolase, liver function enzymes, and measures of reaction time and hand-eye coordination. Acetaldehyde-modified hemoglobin levels (as hemoglobin A1a + b) did not, as previously reported, distinguish between alcoholics and nonalcoholics. There was 24% less annual alcohol consumption in ataxic alcoholics compared with nonataxic alcoholics, 9% less lifetime consumption in ataxic alcoholics, and 33% less maximal daily intake. The finding that ataxic alcoholics do not have higher alcohol consumption than nonataxic alcoholics suggests that alcoholic cerebellar degeneration is not a dose-dependent phenomenon, and that alcoholics with cerebellar degeneration may have an idiosyncratic sensitivity to the neuronal effects of alcohol.

Basal and adenosine receptor-stimulated levels of cAMP are reduced in lymphocytes from alcoholic patients.

Alcoholism causes serious neurologic disease that may be due, in part, to the ability of ethanol to interact with neural cell membranes and change neuronal function. Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the brain. Human lymphocytes also have adenosine receptors, and their activation causes increases in cAMP levels. To test the hypothesis that basal and adenosine receptor-stimulated cAMP levels in lymphocytes might be abnormal in alcoholism, we studied lymphocytes from 10 alcoholic subjects, 10 age- and sex-matched normal individuals, and 10 patients with nonalcoholic liver disease. Basal and adenosine receptor-stimulated cAMP levels were reduced 75% in lymphocytes from alcoholic subjects. Also, there was a 76% reduction in ethanol stimulation of cAMP accumulation in lymphocytes from alcoholics. Similar results were demonstrable in isolated T cells. Unlike other laboratory tests examined, these measurements appeared to distinguish alcoholics from normal subjects and from patients with nonalcoholic liver disease. Reduced basal and adenosine receptor-stimulated levels of cAMP in lymphocytes from alcoholics may reflect a change in cell membranes due either to chronic alcohol abuse or to a genetic predisposition unique to alcoholic subjects.

Amyotrophic lateral sclerosis in dizygotic twins.

A pair of dizygotic twins developed typical amyotrophic lateral sclerosis during adulthood. The concordance for this disease in these two patients of nonconsanguineous parentage with no family history of the disorder suggests the possibility of sublethal intrauterine injury to anterior horn cells. Infectious or toxic exposure during the twins' intimately shared milieu in the prenatal period could have resulted in a neuronal "abiotrophy" that would not have become clinically apparent until decades later. If such a prenatal neuronal injury plays a role in the pathogenesis of amyotrophic lateral sclerosis, it becomes clear that attempts at experimental animal transmission of the disease from affected adults would fail even if the offending agent were viral.