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ScienceWeek
PUBLIC HEALTH: LEAD EXPOSURE AND CATARACT
The following points are made by D.A. Schaumberg et al (J. Am. Med. Assoc. 2004 292:2750):
1) Although lead toxicity in humans has been recognized for centuries, the 20th century has left a legacy of unprecedented lead levels spread throughout the environment. Lead continues to pose a significant public health problem in spite of substantial reductions in lead exposure in the US in the recent past. Moreover, exposure has not been totally eliminated and most adults continue to have substantial body burdens of lead.[1]
2) Much of the lead taken into the body is incorporated into bone where it constantly interchanges with other tissues.[2] Recent studies suggest that accumulated lead exposure is related to several chronic disorders of aging including hypertension and cognitive decline,[1] disorders that have been associated with oxidative stress.[3-4] Several lines of evidence suggest that accumulated lead exposure could also increase the risk of another oxidative-stress-related disorder of aging, age-related cataract -- the leading cause of blindness and visual impairment worldwide.[5]
3) The authors tested whether bone lead levels measured in both the tibia and patella were associated with age-related cataract in an ongoing study of men from the US who were drawn from the general population surrounding Boston. Participants were drawn from the Normative Aging Study (NAS), a longitudinal study of 2280 healthy male volunteers, begun in Boston in the 1960s. At the time of their initial enrollment, all NAS participants were free of heart disease, hypertension, diabetes mellitus, cancer, peptic ulcer, gout, recurrent asthma, bronchitis, or sinusitis. Study participants were predominantly white, and ranged in age from 48 to 93 years at the time of bone lead measurement. Every 3 to 5 years, participants underwent an extensive physical examination that included a standard ocular evaluation, not always including a dilated fundus examination, with notation of any abnormalities in the lens, optic nerve, and macula. Beginning in 1991 and continuing through 1999, NAS participants were invited to undergo bone and blood lead measurements.[2] At the time the present study was initiated, 795 (68%) of the 1171 NAS participants who were still being monitored had completed bone lead measurements.
4) Cataract assessment was done while masked to the lead level results. A participant was considered to have cataract if there was documentation for either eye of cataract surgery or a cataract graded clinically as 3+ or higher on a 4-point scale. The mean age of the study participants was 69 years and cataract was identified in 122 men.
5) The authors conclude these epidemiological data suggest that accumulated lead exposure, such as that commonly experienced by adults in the US, may be an important unrecognized risk factor for cataract. The authors suggest the research indicates that reduction of lead exposure could help decrease the global burden of cataract.
References (abridged):
1. Vig EK, Hu H. Lead toxicity in older adults. J Am Geriatr Soc. 2000;48:1501-1506
2. Hu H, Rabinowitz M, Smith D. Bone lead as a biological marker in epidemiologic studies of chronic toxicity. Environ Health Perspect. 1998;106:1-8
3. Romero-Alvira D, Roche E. High blood pressure, oxygen radicals and antioxidants: etiological relationships. Med Hypotheses. 1996;46:414-420
4. Mecocci P, Mariani E, Cornacchiola V, Polidori MC. Antioxidants for the treatment of mild cognitive impairment. Neurol Res. 2004;26:598-602
5. Thylefors B, Negrel AD, Pararajasegaram R, Dadzie KY. Global data on blindness. Bull World Health Organ. 1995;73:115-121
J. Am. Med. Assoc. http://www.jama.com
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Related Material:
MEDICAL BIOLOGY: BLOOD LEAD AND INTELLECTUAL IMPAIRMENT
The following points are made by R.L. Canfield et al (New Engl. J. Med. 2003 348:1517):
1) Lead is neurotoxic, and young children are at particular risk for exposure. Numerous studies indicate that blood lead concentrations above 10 micro-g per deciliter (0.483 micro-mol per liter) are associated with adverse outcomes on measures of intellectual functioning and social behavioral conduct. Such studies led to the identification of a blood lead concentration of 10 micro-g per deciliter or higher as a "level of concern" by the Centers for Disease Control and Prevention (CDC) and the World Health Organization.
2) It remains unclear whether lead-associated cognitive deficits occur at concentrations below 10 micro-g per deciliter. The CDC and WHO recognized that no evidence of a threshold existed for lead-associated deficits but noted an absence of research on the possible effects of blood lead concentrations below 10 micro-g per deciliter. Although some studies in which the average blood lead concentration was below 10 micro-g per deciliter have reported associations between the blood lead concentration and cognitive deficits, the analyses did not focus specifically on children whose concentrations remained below 10 micro-g per deciliter throughout life. Other evidence suggesting lead-related deficits at concentrations below 10 micro-g per deciliter relied on linear extrapolation or on data unadjusted for important potential confounders such as maternal intelligence and the quality of caregiving.
3) The authors examined associations between low-level exposure to lead and children's performance on intelligence tests at the ages of three and five years in a population that included many children whose blood lead concentrations remained below 10 micro-g per deciliter.
4) The authors conclude: "Blood lead concentrations, even those below 10 micro-g per deciliter, are inversely associated with children's IQ scores at three and five years of age, and associated declines in IQ are greater at these concentrations than at higher concentrations. These findings suggest that more U.S. children may be adversely affected by environmental lead than previously estimated."
New Engl. J. Med. http://www.nejm.org
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Related Material:
ON LEAD AS AN ENVIRONMENTAL POLLUTANT
The following points are made by Vincent T. Breslin (J. Chem. Educ. 2001 78:1647):
1) Despite the ban on lead-based paints and leaded gasoline in the US in the 1970s and 1980s, 4.4 percent of American children aged 1 to 5 years still have blood lead levels high enough to cause irreversible damage to the developing nervous system. In addition, almost 12 percent of children in older housing in large urban areas have elevated blood lead levels, and African-American children living in the major US inner cities are affected disproportionately (approximately 22 percent). Lead exposure in young children results primarily from ingestion or inhalation of soil particles, drinking water, paint, and dust particles in and around the home and play areas.
2) Lead was used extensively as a corrosion inhibitor and pigment in both interior and exterior oil-based paints prior to 1978, and some paints were manufactured with lead concentrations of 50 percent by weight. Therefore, weathering of lead-based exterior paint and deposition of paint chips and dust on soils remains a significant source of lead to soils surrounding homes. Soil lead concentration at or above 500 micrograms per gram will result in a 1 to 5 percent probability that a child will have a blood lead concentration that equals or exceeds 10 micrograms per deciliter.
3) Drinking water is another source of ingested lead. Household plumbing fixtures, including metal pipes, faucets, and soldered joints, are possible sources of lead in drinking water. The lower the pH of the water and the lower the concentration of dissolved salts in the water, the greater is the solubility of lead in the water. Leaching of lead from plastic pipes has also been documented and has been attributed to the use of lead stearate, a stabilizer used in the manufacture of polyvinyl plastics.
J. Chemical Education http://jchemed.chem.wisc.edu
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A DANGEROUS NEW SOURCE OF ENVIRONMENTAL LEAD
The following points are made by Howard W. Mielke (American Scientist 1999 87:62):
1) Since the 1920s, millions of US children have been quietly poisoned by lead, and thousands of deaths are attributed to this over the long term.
2) Although childhood lead exposure in the US has diminished during the past 2 decades, the problem has not been solved. Instead, the demographics has shifted.
3) Over 50 percent (and perhaps even 70 percent) of children living in the inner city of New Orleans and Philadelphia have blood lead levels above the current guideline of 10 micrograms per deciliter [*Note #2]. In contrast, in the concrete "jungle" of Manhattan, where very little of the soil is exposed and almost all apartments and housing contain lead-based paints, only between 5 and 7 percent of children under the age of 6 have been reported to have blood-lead levels of 10 micrograms per deciliter or higher. It is of significance that in Brooklyn, across the river from Manhattan, where yards containing soil are common, the percentage of affected children is several times higher than in Manhattan.
4) The serious of the problem has been recognized by the US Centers for Disease Control and Prevention since the early 1990s, which has called pediatric lead poisoning "entirely preventable".
5) The author suggests that effective prevention assumes an accurate identification of the environmental reservoirs of lead, and that current policies to reduce lead exposure are based on the assumption that the greatest lead hazard comes from lead-based paints [*Note #3]. Most lead-based have now been removed from the market, and parents have been instructed to guard their children from eating paint flakes. However, for children, paint is now neither the most abundant nor the most accessible source of lead. The common problem is lead dust in the environment, with the soil a giant reservoir of tiny particles of lead. The greatest risk for exposure of inner city children is in the yards around houses and to a lesser extent in public playgrounds.
6) The author suggests that an accurate and complete appreciation of the distribution of lead in the environment can help shape policies that more effectively protect the health of children. The author concludes: "It took nearly 10 decades for lead to accumulate to its current levels in urban areas. With judicious planning, the problem can be resolved in much less time."
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Notes by ScienceWeek:
Note #1: There is much data concerning certain syndromes, e.g., fetal alcohol syndrome, lead poisoning, etc. One research problem is that effects of low levels of environmental toxins on the developing nervous system can be subtle and not detected unless specific rather than general behavioral measures are applied.
Note #2: There is hardly a consensus concerning acceptable levels of lead in the whole blood of children. Some clinicians consider the danger point to be in the region of 50 micrograms per deciliter whole blood; other clinicians consider anything above 10 micrograms per deciliter as a cause for alarm. In terms of low-level effects on the developing central nervous system, general concentration cut-off points are perhaps arbitrary, since there is considerable individual variation in toxic susceptibility.
Note #3: In the US, lead was used in residential paint between 1884 and 1978, and leaded paint remains on the walls of many old buildings.
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