Respiratory symptom reporting error in occupational surveillance of older farmers.

OBJECTIVE: Agricultural health studies often use respiratory symptom report as a surrogate measure of disease and exposure; little data exists on the accuracy of symptom report in a work-motivated population. METHODS: Screening spirometry and telephone survey data for Kentucky male farmers >55 year (n = 134) in the NIOSH Farm Family Health and Hazard Surveillance Project were compared to investigate the accuracy of symptom report as a measure of respiratory disease risk in older farmers. RESULTS: The prevalence of reported obstructive respiratory symptoms was 0.24 (95% CI = 0.17 to 0.31); objective measures increased prevalence to 0.35 (95% CI = 0.27 to 0.43). Customary symptom questions did not reliably reflect objective indicators of respiratory impairment. CONCLUSIONS: Older farmers may not accurately report respiratory symptoms. Whether by intention or misinterpretation of physical cues, self-reporting errors in this population may introduce misclassification bias.

Trichloroethylene: Parkinsonism and complex 1 mitochondrial neurotoxicity.

OBJECTIVE: To analyze a cluster of 30 industrial coworkers with Parkinson's disease and parkinsonism subjected to long-term (8-33 years) chronic exposure to trichloroethylene. METHODS: Neurological evaluations were conducted on the 30 coworkers, including a general physical and neurological examination and the Unified Parkinson's Disease Rating Scale. In addition, fine motor speed was quantified and an occupational history survey was administered. Next, animal studies were conducted to determine whether trichloroethylene exposure is neurotoxic to the nigrostriatal dopamine system that degenerates in Parkinson's disease. The experiments specifically analyzed complex 1 mitochondrial neurotoxicity because this is a mechanism of action of other known environmental dopaminergic neurotoxins. RESULTS: The three workers with workstations adjacent to the trichloroethylene source and subjected to chronic inhalation and dermal exposure from handling trichloroethylene-soaked metal parts had Parkinson's disease. Coworkers more distant from the trichloroethylene source, receiving chronic respiratory exposure, displayed many features of parkinsonism, including significant motor slowing. Neurotoxic actions of trichloroethylene were demonstrated in accompanying animal studies showing that oral administration of trichloroethylene for 6 weeks instigated selective complex 1 mitochondrial impairment in the midbrain with concomitant striatonigral fiber degeneration and loss of dopamine neurons. INTERPRETATION: Trichloroethylene, used extensively in industry and the military and a common environmental contaminant, joins other mitochondrial neurotoxins, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and some pesticides, as a risk factor for parkinsonism.