Bones link long-term lead exposure to increased risk of Parkinson's disease.
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Weisskopf, MG, J Weuve, H Nie, M-H Saint-Hilaire, L Sudarsky, DK Simon, B Hersh, J Schwartz, RO Wright and H Hu. 2010. Association of cumulative lead exposure with Parkinson's disease. Environmental Health Perspectives http://dx.doi.org/10.1289/ehp.1002339. |
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More evidence suggests lead is a risk factor for Parkinson's disease.
In one of the first comprehensive studies to explore the possible impact of long-term lead exposure on risk of Parkinson's, researchers report that higher lifetime lead exposure was associated with a three-fold increase in risk of developing Parkinson's.
Context
Parkinson's disease is a chronic, degenerative disease of the brain that affects approximately one in 100 older adults, usually over the age of 50. The disease results from cell death in certain regions of the brain. This cell loss reduces the levels of certain brain chemicals – particularly dopamine. Dopamine is partly responsible for the brain signals that control movements.
Parkinson's symptoms can be physical and cognitive, although cognitive symptoms are rare at onset. The symptoms generally worsen as the disease progresses.
The major physical symptoms include trembling in hands, arms, legs, jaw and face; stiffness of the limbs and trunk; slow movements; and unstable or impaired balance and coordination. Walking, talking, dressing, swallowing and other ordinary tasks may be difficult for those with the debilitating condition.
About half of all Parkinson's patients have some cognitive decline over the course of the disease, according to the National Parkinson Foundation. Thinking and memory problems can include trouble with words, loss of concentration and slowed thoughts. Sufferers can also become depressed, have sleep disruptions and experience emotional problems.
Yet, Parkinson's affects people differently, with varying symptoms and severities. There is no cure but medications and newer brain stimulation devices can control symptoms.
While no one knows the cause of Parkinson's disease, environmental exposures have long been suspected in its development. Particularly, studies show pesticides and heavy metals – such as lead – may contribute. Most prior research with heavy metals relied on surveys and blood lead levels, which indicate only very recent exposures. Because lead circulates in the blood and is deposited in bones as they grow and regenerate, certain bone types can hold a long and accurate record of the heavy metal exposure.
Lead is a heavy metal commonly found in the environment. Burning waste, mining and other industrial activities can release the metal into the air and water. It was widely used in consumer products until the latter part of the 20th century – most notably in paint and gasoline – and still contaminates some products, such as jewelry. Leaded paint in older homes and businesses and contaminated soils are major sources of exposure to lead.
Early childhood exposures to even low amounts of lead can increase risks for behavior and neurodevelopmental issues, including mental retardation, violence, and lower IQ. However, recent studies show lead can also affect adults, including changes in brain function.
What did they do?
In this case-control study, bone lead levels in 330 patients diagnosed with Parkinson's disease were compared to levels in 308 individuals without the disease. Bone lead levels were calculated from 30 minute measurements taken of the kneecap (patella) and a leg bone (tibia) with a special x-ray machine.
Because lead deposits into bone, measuring bone lead levels gives a good estimate of long-term, cumulative expsoures. The kneecap bone renews itself in about 8 years; the tibia takes about 20 years to turn over. Kneecap measurements, then, are useful for shorter exposure periods while tibia lead levels reflect lifetime exposure to the metal.
The patient population was recruited from movement disorder clinics in and around Boston, Mass., and from participants in the Normative Aging Study (a Boston-based study of aging in men that was established in 1963). The control group was recruited from participants in the Harvard Cooperative Program on Aging, community advertisements, and spouses, in-laws, and friends of the patients.
Participants were asked for information on their smoking history, education, age and race. These factors were used as part of the statistical analysis analysis of the data. Smoking history was important because earlier studies have shown a protective effect of smoking on risks of certain types of Parkinson's disease.
What did they find?
This large study showed that chronic lifetime exposures to lead increased the risk of Parkinson's disease. That is, more patients had higher bone lead levels than did the controls. People with the highest lead levels were three times more likely to have Parkinson's.
The link between lead exposure and Parkinson's was found with lead levels only in the tibia bone. As lead levels in the tibia increased, so did the risk for developing Parkinson's. The association was strongest – and statistically significant – in those with the highest measured levels of tibia bone lead (more than 19 micrograms of lead per gram (μg/g) of bone mineral).
Little association was found between patella lead levels and the risk of developing Parkinson's disease. Also, no link was found between lead levels and how long someone had the disease. These findings confirm that chronic exposure to lead is a key risk factor for Parkinson's disease.
The overall mean and standard deviation for patella and tibia bone lead concentrations were 13.6 (15.9) and 10.7 (12.1) μg/g bone mineral. A previous population-based study of bone lead levels – that was unrelated to Parkinson's disease – found mean levels within this same range.
When specific characteristics such as age, sex, race, education and smoking were used in the analysis of the data they did not change the relationship between tibia lead and risk of Parkinson's disease. This means that the link between elevated lifetime lead level and increased risk of Parkinson's disease does not depend on any of these characteristics.
What does it mean?
Higher exposure to lead during a lifetime is associated with an increased risk of developing Parkinson's disease. Those individuals with the highest lead measured in tibia bone were three times as likely to have Parkinson's disease.
The higher bone lead levels observed in Parkinson's patients is difficult to relate to exposures. The levels are likely due to elevated exposures during an individual's lifetime; however, there are likely genetic differences in bone turnover that would skew the observed bone lead levels.
The results of this study are the first to show a conclusive link between long-term exposure to lead and this degenerative neurological disease. It suggests that earlier and consistent lifetime exposures can impact health later on.
The study also builds on prior studies that suggest lead is a risk factor for Parkinson's disease. The importance here is that researchers measured and compared lead levels in two types of bone – the tibia and the patella – rather than blood lead levels, which measure only short-term exposures. Most of the prior studies have relied on patient exposure histories and/or blood lead levels to estimate lead exposures.
This study is also better designed, larger and more conclusive than a prior but smaller study that measured bone lead levels in relation to Parkinson's disease. The two studies found similar associations and report similar concentrations of bone lead in the participants.
No one is sure what causes Parkinson's disease, but most researchers agree it is likely a combination of genetic and environmental factors. Some studies show an association between pesticide exposure and increased risks of developing Parkinson's. This is the first to provide solid evidence of an association with lead exposure.
Lead is a neurotoxicant that can affect brain development and function. The authors suggest lead may interfere with dopamine, affecting its levels and how it is used by the brain. Lead can also harm cells by altering free oxygen, leading to oxidative stress, which can injure or kill the cells.
Bone lead levels are a more accurate measure of long-term lead exposure than blood lead levels. Even though the lead level was measured in the study's participants after the disease was diagnosed, the data reflect decades old exposures – those that occurred before disease onset.
These results give weight for monitoring lifetime exposures to lead, not only levels in children. Current regulations focus on childhood exposures, but reducing the risks for chronic, degenerative diseases that effect adults has obvious implications for improving overall health.
ResourcesCoon, S, A Stark, E Peterson, A Gloi, G Kortsha, J Pounds, D Chettle and J Gorell. 2006. Whole-body lifetime occupational lead exposure and risk of Parkinson’s disease. Environmental Health Perspectives.114: 1872–1876. Lead in paint, dust and soil. U.S. Environmental Protection Agency. Lin, C, R Kim, S-W Tsaih, D Sparrow and H Hu. 2004. Determinants of bone and blood lead levels among minorities living in the Boston area. Environmental Health Perspectives 112:1147-1151. Parkinson's disease information. National Institute of Neurological Disorders and Stroke, National Institutes of Health. Parkinson's disease overview. National Parkinson Foundation. Skeie, GO, B Muller, K Haugarvoll, JP Larsen and OB Tysnes. 2010. Differential effect of environmental risk factors on postural instability gait difficulties and tremor dominant Parkinson's disease. Movement Disorders 25(12):1847–1852. Vlajinac HD, SB Sipetic, JM Maksimovic, JM Marinkovic, ED Dzolijic, IS Ratkov and VS Kostic. 2010. Environmental factors and Parkinson's disease: a case-control study in Belgrade, Serbia. International Journal of Neuroscience http://dx.doi.org/10.3109/00207451003668374. |
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