Jury is still out on PCBs' aging effects
For years, nutritionists have been extolling the virtues of fish and their heart-healthy oils. But fish often carry some unwanted toxicological baggage -- such as polychlorinated biphenyls (PCBs) and other organic pollutants that can be picked up while traversing less than pristine waters.
Most concern over dietary intake of PCBs has focused on risks to children, because a growing body of data indicate that these and certain related dioxinlike compounds can impair development, including our ability to think and learn (see
Banned pollutant’s legacy: Lower IQs ). However, neurologists observe, there’s no reason to think adults might not also suffer.Indeed, animal studies by Susan L. Schantz of the University of Illinois Institute for Environmental Studies, in Urbana, and by others have found that PCB exposures can impair not only cognition, but also the production of dopamine, an important communications molecule in the brain.
Both adult exposures to PCBs and the natural process of aging can diminish brain dopamine levels. "What we’ve sort of predicted," Schantz says, "is that with PCB exposures, you might eventually see effects that resemble Parkinson’s disease" -- a disorder characterized by too little dopamine, by problems with motor function, and by memory or reasoning impairments.
In scouting populations at risk for such problems, neurotoxicologists like Schantz have been focusing on fish-eating communities around the Great Lakes, where local waters have sustained significant PCB contamination since the 1940s. Though concentrations of PCBs in fish have been falling since the 1970s -- when most uses for these compounds were banned -- EPA notes that within the Great Lakes, there remains "a reservoir of PCBs in the sediments that will continue to release PCBs into the lakes at significant rates for decades to come."
People who haven’t visited the region may have a difficult time picturing how massive the affected area is. Not only does this five-lake system cover 94,000 square miles -- an area roughly equal to the state of Oregon -- but it also holds some 18 percent of the world’s surface supply of fresh water (only the polar ice caps contain more).
One in four Canadians and one in 10 U.S. residents live within this watershed, which is home to some of the most concentrated industrial and agricultural activity on the planet. Both spew massive concentrations of pollutants into the environment. Eventually, much of this pollution settles into the water where it can be taken up by fish.
As with many other organochlorine pollutants, PCBs settle into body fat and resist degradation. Indeed, that’s what allows them to continue to move throughout the food chain almost 2 decades after most of their uses have been banned (see
Because we eat PCBs... ). Already, some states have issued health advisories over PCBs, warning residents to limit their consumption of locally caught fish.Moreover, many people alive today consumed large quantities of Great Lakes fish during the period that their aquatic environment was most contaminated. One study that was initiated in 1974, for instance, found that on average, Michigan sport fishermen ate an average of 32 pounds of Great Lakes fish each year -- and some as much as 262 pounds annually.
Chinook salmon from the Great Lakes, a relatively robust source of dietary PCBs.
Credit: EPAMany of these fish aficionados are now approaching old age, a period that may make them especially vulnerable to PCBs’ toxicity.
Aging and vulnerability"Aged populations are more susceptible to incremental declines in mentation and resistance to disease," observes Joan Cranmer of the University of Arkansas for Medical Sciences, in Little Rock. As such, "Exposures become more important as they continue over a greater proportion of a lifetime," she says -- "especially as lifespan increases."
Neurotoxicologist Bernard Weiss of the University of Rochester, N.Y., agrees. For most of our lives, the brain tends to be a very "redundant organ," he notes, with more than enough cells to carry on normal function. However, every year, some brain cells die, eroding the compensatory mechanisms that might have held any damaged or diseased tissue in check.
As people routinely begin to live into their 80s and 90s and even beyond 100, Weiss notes, its easy to outlive that redundancy, or "functional reserve."
The functional-reserve loss that normally accompanies aging can lead to thinking more slowly and less clearly, he says. However, "you can make the argument that if an organ’s original capacity has been diminished by some toxicant, then with age you’ll see an earlier onset of whatever infirmities are normally produced by damage to that organ."
In effect, he says, they may produce an accelerated or premature aging.
Unlike cancer or heart disease, which can produce damage that becomes visible using X-rays, ultrasound, or magnetic resonance imaging, damage to the brain may leave no visible trace. So to find it, he says, "You may have to look for changes in neuronal connectivity, do an assay on brain chemistry, or study behavior."
Further impeding the identification of this type of "silent" toxicity, he argues, is the long delay between the potential damage by toxicants -- which could occur at any time from the womb to middle adulthood -- and its expression in old age. Finally, he notes that any neurotoxicity may fail to stand out because its manifestations, such as impaired sensory acuity, can "mimic the natural course of aging."
For instance, Weiss notes, "there seems to be cell loss throughout life in the basal ganglia of the brain," particularly in an area called the substantia nigra. "You could speculate that if you live long enough, you’ll get Parkinson’s disease," he says, "because it’s the loss of cells in that area that leads to the clinical syndrome."
However, some chemical agents -- certain drugs or nerve gas, for instance -- can also lead over time to the development of Parkinson’s. So Parkinson’s-like tremors and diminished production of dopamine may reflect normal aging or toxicity.
Good news...
An ongoing study to investigate any neurodegenerative synergy between PCBs and aging was launched in Michigan about 4 years ago. It’s monitoring the functioning of nerves -- through tests of cognition and motor function -- in 188 aging residents of 11 counties along the western shores of Lake Michigan. Roughly half of these volunteers had been heavy consumers of local fish, eating at least 26 pounds per year when first surveyed by the State of Michigan in 1980. The remainder, defined as not being fish eaters, ate 6 pounds or less of this fish annually.
Why focus on fish? Though trace quantities of PCBs lace many foods, fish from cool, contaminated waterways have proven an especially rich dietary source because of their fat. Indeed, studies conducted in Michigan, Wisconsin, and Minnesota have found evidence that body stores of PCBs tend to be highest in people who eat lots of Great Lakes fish.
As a rule, organochlorines accumulate in fat. Because animals higher in the food chain tend to be fattier -- especially when their environment is cold -- they can accumulate proportionately more organochlorines than leaner animals.
For example, while microscopic plants in the Great Lakes, known collectively as phytoplankton, may contain 0.025 parts per million PCBs, the tiny animals that feed on them will build up concentrations that are about four times higher. Each step up the food chain has the potential to further increase the PCB loading, to where smelt may contain 1 ppm, lake trout almost 5 ppm, and the fat-rich eggs of herring gulls more than 120 ppm.
Not surprisingly, then, more PCBs will be ingested while eating a single meal of lake trout from Lake Michigan "than in a lifetime of drinking water from the lake," notes the Environmental Protection Agency in its Great Lakes Atlas.
The good news: Despite her concern about the risk of Parkinson’s symptoms from PCBs in fish, Schantz and her colleagues found that people who had consumed large amounts of Great Lakes fish were no more likely to suffer from tremor than those who ate little or none. She reported her preliminary data in Montreal on May 14, at a meeting known as Health Conference 97: Great Lakes/St. Lawrence.
In a second test, Schantz’s group asked the Michigan volunteers to place grooved pegs into a board with notched holes. Because the placement of the notch varied from hole to hole, the challenge was orienting the groove on each peg so that it would slide into the hole. While persons who had had the fishiest diets proved somewhat less competent at this task, the difference in the performance of the two groups was not statistically significant.
"While that would indicate that there’s probably no effect, we saw enough of a trend [in the pegboard test] that I want to be conservative before I say there’s no problem," Schantz told Science News Online. "So we’re testing each person a second time, 3 years from when they were originally assessed. I think that how much a person declines over that period will be a more sensitive measure than just comparing [people of the same age]."
...and a caution
Though these early data show no solid evidence that adult consumption of large amounts of Great Lakes fish causes neurological harm, Schantz cautions against interpreting this to mean that PCBs pose no risks to the elderly -- at least, not yet.
Besides being somewhat troubled by the negative-trend data in the pegboard test, she observes that her group has yet to finish crunching the numbers for any of the remaining 9 tests that they administered to this population. These additional assays focus on learning and memory, executive function (such as attention and planning), and visual and spatial function (for example, mentally assembling a simple puzzle).
Finally, Schantz points out that many of the people she’s studying may have to become older still before enough of them exhaust any functional reserve that might be masking subtle but functionally important damage.
References:
Schantz, S.L., et al. 1996. Neuropsychological assessment of an aging population of Great Lakes fisheaters. Toxicology and Industrial Health 12:403.
Related Reading:
Environment Canada and U.S. Environmental Protection Agency. Great Lakes concerns today, in The Great Lakes Atlas. (http://www.epa.gov/glnpo/atlas/).
Raloff, J. 1997. A new world of pollutant effects. Science News 151(March 1):S19.
Raloff, J. 1996. Banned pollutant’s legacy: Lower IQs. Science News 150(Sept. 14):165.
Raloff, J. 1996. Because we eat PCBs... Science News Online (Sept. 14).
Raloff, J. 1995. PCBs’ legacy can affect next generation. Science News 148(Nov. 11):310.
U.S. Environmental Protection Agency and Agency for Toxic Substances and Disease Registry. 1996. The effects of Great Lakes contaminants on human health: A report to Congress. (http://www.epa.gov/glnpo/health/atsdr.htm).
Weiss, B. 1990. Risk assessment: The insidious nature of neurotoxicity and the aging brain. NeuroToxicology 11:305.
Sources:
Joan M. Cranmer
Department of Pediatrics
University of Arkansas for Medical Sciences
4301 W. Markham
Mail #512
Little Rock, AR 72205-7199
USASusan L. Schantz
Institute for Environmental Studies
University of Illinois
1101 W. Peabody Dr.
Urbana, IL 61801
USABernard Weiss
Department of Environmental Medicine
University of Rochester School of Medicine and Dentistry
Rochester, NY 14642
USAThis week's Food for Thought has been prepared by Janet Raloff, senior editor of Science News.
Food for Thought Archives
copyright 1997 ScienceService
