Case study of Parkinson’s disease from firefighting.
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The tire fire in Spencer MA in 1986.
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Article about contamination from tire fire in Spencer MA in 1986.
Testing reveal contamination!
By Kim Ring TELEGRAM & GAZETTE STAFF
Posted Sep 25, 2007 at 2:04 AM
More than two decades after a massive five-day fire burned several million tires on Northwest Road, selectmen have approved a study of the site that could help them decide whether to take a tax title to the property.
The board approved a plan for Weston & Sampson, a Peabody engineering company, to begin looking at what contamination might remain on the site and how best to clean it. The $30,000 study will be funded by a grant secured through the combined efforts of the Pioneer Valley Planning Commission in West Springfield and the Central Massachusetts Regional Planning Commission in Worcester.
George D. Naslas, Weston & Sampson project manager, told selectmen last night that monitoring wells installed a decade ago will most likely be used to help determine if there is contamination in the ground water. He said a pit would be dug to sample soil, as well.
The study is the second phase of an Environmental Site Assessment. The first phase included developing a history of the property, including results of other testing, a review of available records and, in some cases, interviews with neighbors and local officials, Pioneer Valley Planning Commission Senior Planner Christopher J. Dunphy said.
“What I hope phase two will give us ... is a good cost estimate,” Mr. Naslas said.
Weston & Sampson has found piles of tires at the abandoned property. A house -- in disrepair -- still stands at the site where metal and other debris is still scattered.
In 1990, tests showed “residual contamination” in the soil and groundwater. Arsenic, cadmium, lead and zinc were found in the soil. The water showed arsenic, chromium and lead in excess of state guidelines, although water at nearby homes had not been affected beyond what the guidelines allow, according to Mr. Naslas’ report.
Whether the contamination remains or has changed will be determined by the study.
Rosemary Scrivens, transportation planner for the Central Massachusetts Regional Planning Commission, said she is hopeful that next year her agency will be helping the town to seek funding to clean up the site.
The 1986 fire is still remembered by those who battled the blaze. Firefighters were trucked in from miles away to relieve exhausted local crews. Acrid smoke from the fire could be seen for miles. For many years, firefighters might be spotted wearing commemorative T-shirts indicating they had helped to extinguish the legendary blaze.
In 2001 a local man had hoped to buy and clean the junkyard land for use as an auto repair shop, but at that time there was no clear title to the property and such a use would have violated zoning bylaws. The owner, Joseph Wozniak, had died in 1989.
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Document presents connection between toxins and Parkinson’s disease!
Chronic Lead Exposure Increases Risk of Parkinson Disease
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May 21, 2009
ARTICLE IN BRIEF
A new study found that risk for Parkinson disease increased with increasing tibial lead.
SEATTLE—Cumulative exposure to lead increases the risk of Parkinson disease (PD) in a case-control study reported at the AAN annual meeting here in April.
“In vitro studies have shown that lead can be neurotoxic to dopamine cells and impede dopaminergic neurotransmission. Few epidemiologic studies have assessed the role of lead in PD. We wanted to explore the association between lead in tibial bone — a biomarker of cumulative lead exposure — and PD,” said lead author Marc Weisskopf, PhD, ScD, assistant professor in the departments of environmental health and epidemiology at Harvard School of Public Health in Boston, MA.
According to a 1997 report in Neurology, epidemiological studies at the Henry Ford Health System found that more than 20 years of occupational exposure to lead plus copper or lead plus iron increased the risk of developing PD. Occupational exposure to lead was estimated by an industrial hygienist based on occupational histories. A subsequent study by the same group found that an estimated lifetime exposure to lead alone — using occupational history, blood lead, and tibial and calcaneal lead — was also associated with increased risk of PD. A suggestive increase in risk was also observed with increasing tibial bone lead alone, but it was not statistically significant, Dr. Weisskopf explained.
In study by Dr. Weisskopf and colleagues, a non-invasive imaging technique called K-shell X-ray Fluorescence (KXRF) was used to measure tibia bone lead.
“KXRF of tibial bone is a better biomarker for lead than blood is for case-control studies, because it averages exposure over a long time, including prior to PD diagnosis. Just one measurement can assess cumulative lead exposure over the long term,” he commented.
STUDY PROTOCOLS, FINDINGS
The authors recruited 330 patients with PD from four movement disorder clinics in the Boston area and intended to recruit age-matched controls from relatives of the PD patients. Cases and controls were also recruited from the Boston-based Normative Aging Study (NAS). However, the investigators could recruit only 166 controls from these sites, so they broadened recruiting efforts to participants in the Harvard Cooperative Program on Aging, as well as the general community, and attained a total of 354 controls (including the 166 recruited at the four movement disorder clinics and the NAS).
PD patients in the highest quartile of tibial bone lead levels had an approximately two-fold higher risk of PD compared with those in the lowest quartile. This was true when the analysis included all cases and controls, cases and controls from the movement disorder clinics and NAS only, or cases and controls from only the movement disorder clinics.
“A concern of ours was that the varied means of recruiting controls could introduce bias. However, results were similar regardless of which controls were included in the analysis,” Dr. Weisskopf explained.
No association was found between tibial bone lead level and duration of PD, Dr. Weisskopf said. “We don't know whether lead exposure could cause a more rapid course of Parkinson disease. This is an important question. The lack of an association between lead exposure and PD in this study suggests that lead is related to risk of developing the disease, not the time course.”
The statistical analysis adjusted for age, cigarette smoking, sex, education, and race, as well as recruitment site. As expected, cigarette smoking was associated with a decreased risk of PD. “We saw the classic picture showing that people who never smoked were at greater risk of developing PD,” Dr. Weisskopf commented.
The next step will be to determine whether any genetic polymorphisms among cases are associated with vulnerability to PD. The investigators will also look at associations with pesticide exposure.
MOUNTING EVIDENCE
“Lead neurotoxicity was recognized by the ancient Romans, but only in recent years has an association between lead and PD been investigated,” explained Caroline D. Tanner, MD, director of Research at the Parkinson's Institute and Clinical Center in Sunnyvale, CA.
The work at Henry Ford Hospital in Detroit (cited by Dr. Weisskopf) suggested that lead exposure may be a risk factor for PD, she continued. “The study by Weisskopf and colleagues reported remarkably similar results. Risk of PD increased with increasing tibial lead, and persons in the highest exposure group had almost twice the risk as those in the lowest exposure group,” Dr. Tanner continued.
She called the use of controls drawn from two different populations “a unique feature” of the study. One control population was drawn from the same clinics as the cases, and the second was drawn from a community population. “The results were similar when PD cases were compared to either control group. This increases confidence in the results and suggests that the changes are likely to be associated with PD, not with some other difference between cases and controls,” she said.
“Lead exposure is a common problem worldwide. Increased focus on the role of lead in future laboratory and clinical studies may provide important new insights into the cause of PD,” Dr. Tanner said.
REFERENCES
• Gorell JM, Johson CC, Richardson RJ, et al. Occupational exposure to metals as risk factors for Parkinson's disease. Neurology 1997;48:650–658.
• Coon S, Stark A, Gorell J, et al. Whole-body lifetime occupational lead exposure and risk of Parkinson's disease. Environ Health Perspect 2006;114:1872–1876.
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Actual results! At least four fire fighters who fought the tire fire in 1986 have Parkinson’s disease.
Tim MacMillan
Paul MacMillan (Deceased)
Dave Ramsey (Deceased)
Neil Blodgett