Environmental Factor, April 2008, National Institute of Environmental Health Sciences
Extramural Papers of the Month
By Jerry Phelps
- Black Carbon Air Pollution May Lower IQ
- Mitochondrial Protein Mortalin and the Progression of Parkinson's Disease
- Identical Twins: Are They Really Identical?
- Flaxseed Improves Outcome from Lung Injury
Black Carbon Air Pollution May Lower IQ
Children who live in neighborhoods heavily polluted by automobile traffic typically have lower IQs and score worse on other intelligence and memory tests than children in healthier environments, according to a new study by NIEHS supported researchers. While the respiratory and cardiovascular effects of air pollution are well documented, this study is one of the few that have explored the possible neurodegenerative effects of air pollution.
Researchers reported dramatic differences in the 202 children eight to eleven years old from the Boston, Mass. area in the study. The more heavily exposed children were to black carbon, the lower their scores on several intelligence tests. For example, the average IQ of the most heavily exposed children was 3.4 points less than children with low exposure. When the researchers adjusted for the effects of parents' education, birth weight and exposure to tobacco smoke, the associations remained. The effects were roughly equivalent to those seen in children whose mothers smoked ten cigarettes per day while pregnant.
The researchers speculated that the harmful effects may be caused by the inflammatory and oxidative effects of the black carbon particles. These findings suggest that additional research is warranted to investigate the effects of air pollution on the development of intelligence in children and on cognitive decline for people of all ages.
Citation: Suglia SF, Gryparis A, Wright RO, Schwartz J, Wright RJ. (http://www.ncbi.nlm.nih.gov/pubmed/18006900?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum) 2008. Association of black carbon with cognition among children in a prospective birth cohort study. Am J Epidemiol 167(3):280-286.
Mitochondrial Protein Mortalin and the Progression of Parkinson's Disease
NIEHS-supported researchers employed combined proteomic and labeling techniques to identify a protein, mortalin, that may be involved in the progression of Parkinson's disease. Using brain tissue samples from deceased Parkinson's patients at various stages of the disease and comparing those to samples from age matched controls, they isolated many proteins that had differential expression and found that mortalin was decreased in late stages of the disease.
Parkinson's disease is a progressive neurodegenerative condition that currently afflicts more than one million people in the United States alone and strikes about one percent of all people over the age of 60.
Mortalin is a multifunctional protein involved in mitochondrial energy generation and in protection from oxidative stress. In previous work, these investigators demonstrated that mortalin expression is associated with other proteins thought to be involved in Parkinson's disease including alpha-synuclein.
This study employed a novel proteomic method to study the mechanisms of Parkinson's disease progression. Using pathological samples from diseased Parkinson's patients, the study verified that mortalin is decreased in brain tissue at advanced stages of the disease. Further studies are necessary to determine mortalin's role and mechanism of action in the progression of Parkinson's disease.
Citation: Shi M, Jin J, Wang Y, Beyer RP, Kitsou E, Albin RL, Gearing M, Pan C, Zhang J. (http://www.ncbi.nlm.nih.gov/pubmed/18219256?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum) 2008. Mortalin: a protein associated with progression of Parkinson disease? J Neuropathol Exp Neurol 67(2):117-124.
Identical Twins: Are They Really Identical?
In groundbreaking research, an international team of scientists, including NIEHS-funded investigators, has shown that identical or monozygotic twins are indeed not genetically identical as was previously thought. Until now, environmental factors were thought to be the reason that one twin might develop an illness such as Parkinson's disease while the other remained healthy. The current study suggests that other factors may be in play.
The team studied 19 pairs of monozygotic twins and found subtle differences in their DNA due to copy number variation (CNV). CNV occurs when segments of DNA are missing or when extra copies of segments are inserted in the DNA sequence. Previous research suggested that CNV may play a bigger role in health and disease than previously thought, and one recent study proposed that sequence variation involving CNV may actually be more important than single nucleotide polymorphisms.
DNA differences due to CNV could tell researchers if a missing gene or multiple copies of a gene are implicated in the onset of a disease. If one twin develops a disease and the other doesn't, the region of their genetic sequences that are different could offer a target for further investigation to discover the genetic underpinnings of the disease.
Citation: Bruder CE, Piotrowski A, Gijsbers AA, Andersson R, Erickson S, de StÅhl TD, Menzel U, Sandgren J, von Tell D, Poplawski A, Crowley M, Crasto C, Partridge EC, Tiwari H, Allison DB, Komorowski J, van Ommen GJ, Boomsma DI, Pedersen NL, den Dunnen JT, Wirdefeldt K, Dumanski JP. (http://www.ncbi.nlm.nih.gov/pubmed/18304490?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum) 2008. Phenotypically concordant and discordant monozygotic twins display different DNA copy-number-variation profiles. Am J Hum Genet 82(3):763-771.
Flaxseed Improves Outcome from Lung Injury
NIEHS investigators have determined that flax-seed oil helps to combat the adverse respiratory effects seen in a mouse model of ischemia-reperfusion injury. Mice undergoing experimental ischemia-reperfusion lung injury fed ten percent flax seed in their diets showed improved arterial blood oxygenation, increased levels of protein in bronchoalveolar lavage and lower levels of oxidative lung damage than mice fed diets without flax seed supplementation.
Flax is a blue flowering plant that is grown on the Western Canadian prairies for its oil-rich seeds, one of nature's richest sources of omega-3 fatty acids. Nearly every system in the body can benefit from flax seed oil's natural antioxidant properties, including the cardiovascular, immune, circulatory, reproductive and nervous systems.
This study raises the possibility that flax seed may be a useful antioxidant therapy for treating chronic inflammatory lung diseases. Preliminary studies suggest that human ingestion of just 25 grams of flax seed results in the same blood level of the active ingredients seen in the mouse study. Also, if the bioactive components of flax seed could be isolated and formulated for rapid administration, administering it to both donors and recipients in lung transplantation procedures might reduce the incidence and severity of injury and primary graft failure.
Citation: Lee JC, Bhora F, Sun J, Cheng G, Arguiri E, Solomides CC, Chatterjee S, Christofidou-Solomidou M. (http://www.ncbi.nlm.nih.gov/pubmed/18083772?ordinalpos=36&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum) 2008. Dietary flaxseed enhances antioxidant defenses and is protective in a mouse model of lung ischemia-reperfusion injury. Am J Physiol Lung Cell Mol Physiol 294(2):L255-265.