From the publishers of The New England Journal of Medicine
December 7, 2006
Past Lead Exposure and Brain Lesions
A dose-response relation was found between past lead exposure and brain
lesions on MRI scans.
Despite decades of research on lead poisoning, few data are available on the
effects of occupational exposures on brain structures. In 532 former
organolead workers (mean age, 56; mean time since last exposure, 18 years),
researchers evaluated the associations between cumulative lead dose and MRI
measures of white matter lesions and of total and region-specific brain
volumes. They measured tibia lead levels, which reflect long-term stores but
decline over time after exposure ends. They estimated peak tibia level (PTL)
from the time since last exposure.
PTL was significantly associated with both the prevalence and the severity
of white matter lesions. Higher PTL was significantly related to reduced
volumes in 6 of 20 areas measured: total brain, total gray matter, parietal
white matter, frontal gray matter, insula, and cingulate gyrus. Final models
were adjusted for age, education level, APOE genotype, and height, although
numerous other potential confounders were considered, including smoking,
alcohol use, and race. The authors conclude that past exposures to lead
resulted in persistent global and region-specific brain lesions, perhaps
mediating the progressive decline that they had previously observed in the
workers on tests of verbal memory and learning, visual memory, and executive
function.
Comment: Accumulating data suggest that lead exposure contributes to
age-related cognitive decline and neurodegeneration. Among the relevant
pathogenetic processes in which lead has been implicated are mitochondrial
dysfunction, oxidative stress, deregulation of protein turnover, and brain
inflammation. Limited evidence suggests that the APOE 4 allele increases
susceptibility to lead neurotoxicity (Environ Health Perspect 2002;
110:501), and elevated brain lead levels have been found in patients with
diffuse neurofibrillary tangles with calcification (Neuroreport 2001;
12:3887). In rodents and primates, developmental lead exposure produces
delayed overexpression of the amyloid precursor protein and aggregated
beta-amyloid peptides (Rev Neurosci 2005; 16:325). To date, most attention
has focused on the effects of lead on children. Apparently, much remains to
be learned about the effects of lead on our aging population.
- David C. Bellinger, PhD
Dr. Bellinger is Senior Research Associate in Neurology, Children's
Hospital; Professor, Department of Environmental Health, Harvard School of
Public Health; and Professor of Neurology, Harvard Medical School, Boston.
Published in Journal Watch Neurology December 5, 2006
Citation(s):
Stewart WF et al. Past adult lead exposure is linked to neurodegeneration
measured by brain MRI. Neurology 2006 May 23; 66:1476-84.
[Original article][Medline abstract]
--------------------------------------...
Multiple Sclerosis and the Petrochemical industry have been linked in many
studies -- and as our gasoline used to contain lead, and my first symptoms
started when I was cleaning out the Gulf oil refinery in North Burnaby in
1974, just a little numbness in my right hand' s fingertips, I thought that
perhaps there are other people who could connect their MS with
petrochemicals.
The gunk I was cleaning out, the sludge at the bottom of those huge white
tanks you see in refineries, contained lead and a lot of other toxic
chemicals that were added to gasoline in the 1970s.
There are a lot of other symptoms which I have that are connected, or could
be connected, with toxic chemicals particularly lead.
I had my blood level lead analyzed recently -- and it's okay now. And I
haven't progressed for at least six years -- all the lead has been flushed
out by now. But the damage remains.
And just because they eliminated lead in gasoline, doesn't mean that they've
rid our environment of environmental poisons -- in fact they've probably
added more than they've taken out!
A friend of a friend of mine, suffers from MCS -- Multiple Chemical
Sensitivity -- he really does, it's been confirmed by the UBC neurology
clinic, well anyways, he says that Febreeze was derived from Agent Orange of
the Vietnam era -- and he confronted, via telephone, the lab that had
developed Febreeze and asked why???
"Why are you doing this when you know it's dangerous???"
And the answer was a mumbled explanation that "The consumers wanted a
product like Febreeze."
We've come a long way in the last 50 years -- but for every gain, there are
sacrifices.
As an afterthought, I think Multiple Sclerosis should be renamed
"demyelination of unknown etiology" -- but I don't think I'll get anywhere.
__________________
richardlong@telus.net
Vancouver, BC, Canada
Telephone: 604 301 1606
Tags: