Several patients with Parkinson’ s disease (PD) reveal an history of chronic exposure to hydrocarbon-solvents.
Chronic exposure to hydrocarbon-solvents has been proposed as a risk factor for more severe forms of PD with earlier onset
of symptoms and reduced response to dopaminergic therapy. A direct correlation between disease severity and exposure degree
has been previously shown. Seven exposed PD patients (two with low degree exposure and five with high degree exposure), 10
unexposed PD patients matched for sex, age and Hoehn and Yahr scale (=3 in the “on” phase), and 10 unexposed PD
patients matched for sex, age and l-dopa daily intake instead of disease severity (Hoehn and Yahr scale = 3.5 in the “on”
phase) were studied.
Twenty normal subjects without previous exposure to hydrocarbon-solvents and matched for age and sex with HPD patients
were studied for comparison. The purpose of the study was to assess neuronal degeneration in the striatum of exposed vs unexposed
PD patients. The authors investigated whether neuronal damage/loss was detectable in the lentiform nucleus measuring N-acetylaspartate
(NAA) levels by 1-H MRS. Multiple single voxel MRS water-suppressed spectra were obtained also from the white matter and the
occipital lobe.
NAA was normal in the lentiform nucleus of patients with low exposure as well as in patients with no exposure whereas
it was decreased in PD patients with high degree exposure. White matter and occipital lobe NAA content was normal both in
exposed and unexposed PD patients. Clinical expression is more severe in PD patients with previous high degree solvent exposure
because of the associated post-synaptic damage of the nigro-striatal pathway.
PLEASE READ UCLA scientists have discovered how chronic exposure to low levels of carbon
monoxide (CO) damages the inner ear of young rats, resulting in permanent hearing loss. At the Ca/OSHA's exposure limit of
0.0025 percent -- or 25 parts per million CO in the air -- the gas creates oxidative stress, a condition that damages the
cochlear cells, leading to impairment of the auditory nerves.
CONTEXT: Tobacco smoke, gas heaters, stoves and ovens all emit CO, which can
rise to high concentrations in poorly ventilated homes. Infants and children are particularly vulnerable to CO exposure because
they spend a great deal of time in the home. No policies exist to regulate CO in the home. Many commercial home monitors sound
an alarm only 20 minutes after CO concentrations reaches 70 parts per million -- nearly three times the 25 parts per million
limit set by Cal/OSHA.
IMPACT: This
is the first time that inhaled CO has been linked to oxidative stress, a known risk factor in many disorders, including Alzheimer's,
Parkinson's, multiple sclerosis, Lou Gherig's disease and cardiovascular disease.
Tobacco smoke, which contains CO, aggravates
many of these diseases. The UCLA findings highlight the need for policy makers to reexamine the regulation of car exhaust,
tobacco smoke, smog, and heating and cooking appliances.
AUTHORS: John Edmond, Ph.D., professor of biological chemistry; Ivan Lopez, Ph.D.,
assistant professor of head and neck surgery; and Douglas Webber, Ph.D., postdoctoral fellow; at the David Geffen School of
Medicine at UCLA, are available for interviews.
