Osteoporosis, lead, and baby boomers: When time gets the lead out.

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Recent research indicates that lead accumulated in young skeletons can re-emerge in later life. Health effects can result. Who is at risk?

One aspect of the demographic bulge called the baby boom is often overlooked: This very large population group was born and matured during a period of rapid changes in the environment. In many ways, this generation differs from both preceding and succeeding generations in the types and amounts of environmental exposures it has received.

One common exposure for youthful baby boomers was to lead: The boomers grew up during the peak years of the modern love affair with the automobile. Increased automotive traffic required increased use of automotive fuels, which, for most of the period, contained lead. This fuel use in turn resulted in extensive deposition of lead in the environment.

Moreover, this same time period saw unprecedented expansion in housing stocks in the US-- all of which needed to be painted, and many of which were painted with lead-based paint. Some of the same buildings had lead-soldered plumbing, which leached lead into drinking water. Some families replace home canned foods with commercial foods in lead soldered cans.

 

Baby boom lead exposures -- the contribution of leaded gas

Most people are familiar by now with the idea that lead-based paint is a primary source for lead exposure. Less well known is that automotive fuel deposited as much lead in the environment in 60 years as lead paint did in over a century. The paint was used throughout the country in and on all kinds of structures, and its use peaked in the 1920's, when the US economy was primarily rural, and relied on rail transport. In contrast, lead from automotive fuel, was deposited in the environment disproportionately in urban areas, as a result of automotive traffic in and out of urban centers. The lead from automotive exhaust was deposited primarily as dust.

Researchers estimate that there are 4 to 5 million metric tons of lead in the environment as the result of automotive fuel use. Leaded gasoline was used between 1929 and 1989; peak use occurred in the early 1970s. Most of the gasoline lead was emitted from automobile exhaust pipes as a fine lead dust. The remainder wound up in car motor oil or was trapped on internal surfaces of the engine and exhaust system. The lead dust is mobile in the environment, capable of being tracked into buildings, released by horticultural, gardening, and building activities, washed into water supplies, and other incidents that mobilize soil and dust.

By the time the boomers' skeletons were at their maximum mineral density (early adulthood), they had had ample opportunities to absorb and retain lead in their bones. Absorption of lead through inhalation might have occurred through exposure to automotive exhaust, or by handling gasoline in the course of fueling vehicles or doing household chores. Lead could have been ingested by drinking water from lead-soldered plumbing, or eating foods from lead soldered cans. Exposures to lead from paint could have happened in several ways. One is handling or being exposed to lead -based paints removed from or applied to homes, schools, and other buildings during renovations. Children could have absorbed lead through either inhalation of fumes and dusts, or through deliberate or inadvertent ingestion of lead paint chips, fragments, and dusts.

 

Everything has to be somewhere: Lead in bone

This is due to lead's behavior in the body. Lead competes with calcium for the same sites in the body, including the skeleton. It can mimic calcium in various body processes, and when it does, it can disrupt the very processes in which it is involved. Thus when lead is substituted for calcium in the nervous system, the transmission processes of the nervous system are derailed. If this occurs during the formation of the nervous system, the effects can be life-long. Similarly, if lead fills in for calcium during bone formation, it becomes part of the bone structure, where it remains until it is released.

At the time of lead exposure, if sufficient calcium and other nutrients are not present in the body, ingested lead can be easily absorbed into the body, and become incorporated into the body's tissues. Adults absorb about 10% of the lead they ingest, while children absorb about 50%.

"Absorbed lead enters the blood and reaches the bones and soft tissues of the body, including the liver, from which it is gradually excreted. . . .Lead is not excreted at the same rate as it is absorbed,. . .[but] continually accumulates in the body tissues with age," according to researcher Marjorie Peraza. Regardless of where lead comes from, once inside the body, it can be delivered to the skeleton and incorporated in new cells produced in bone tissue. Lead in blood and other soft tissues has a half-life of 35 days; but lead in bone has a half-life of 5 to 20 years.

 

Bone and lead dynamics

Most people are aware of bone changes associated with old age-- brittle bones, shrinking stature, osteoporosis, and hip fracture. However, bone tissue is dynamic and undergoes changes throughout life. Very rapid growth in infancy, and 'spurts' of growth during youth, involve dramatic changes in the skeleton, including accumulations of minerals (and toxic heavy metals like lead, if exposures occur during these periods). Once incorporated into the skeleton, lead becomes a source of "endogenous" exposure-- exposures arising from within the body. Such exposures can occurat different stages of life, and for a variety of reasons. For instance:

  • Pregnancy and lactation are periods of significant changes in bone, which releases large quantities of calcium into the bloodstream in response to hormonal signals. The released calcium serves to support the pregnancy, and later, milk production. Researchers have found that lead accumulated in maternal bone during growth can be released along with the calcium during pregnancy and lactation, resulting in exposures to both the mother and the child.. Maternal blood lead levels fluctuate during pregnancy, with lead levels increasing in the second half of pregnancy. This is the period during which the fetal skeleton undergoes rapid mineralization, and hormonal changes in the mother favor mineral turnover in her skeleton at the same time, a process that can liberate lead stored in the mother's bone. [See Rothenberg in Sources, below.] Researchers have been able to determine that lead in the blood of pregnant and lactating mothers derived from bone stores of lead, not diet at the time of pregnancy and lactation. [See Gulson in Sources.] "Mobilization of lead from skeletal stores during pregnancy and lactation may constitute a potential threat to the fetus during critical stages of organ development," according to researcher R.A. Goyer.
  • At any stage of life, bone mass loss can occur if conditions warrant it: Endocrine, liver, and kidney disease can cause bone loss, as can certain cancers and some metabolic disorders. Long-term use of steroids like prednisone can cause bone loss, as can heparin, and some anti-epilepsy drugs. Alcohol use can contribute to osteoporosis, as can dietary deficiencies due to alcoholism. Nutritional deficiencies arising from insufficient food intake, eating disorders, 'fad' weight loss diets, and medical conditions that interfere with food intake can all promote bone loss. Immobilization from illness or injury causes bone to lose density. Astronauts have experienced bone thinning due to weightlessness.
  • Some bone loss is related to the passage of time, and it starts long before the familiar "old age" signs are present: After age 40, both men and women lose about 5% to 10% of their bone mass each decade. In women after menopauset different stages of life, and for a variety of reasons. For instance: [not undergoing estrogen replacement therapy], bone mass loss speeds up five to seven fold until about age 70, when the rate of bone loss returns to the premenopausal 5% to 10% rate per decade.

Regardless of the cause, when bone mass is lost, lead stored in the skeleton can be released along with the bone's minerals. For boomers who stockpiled lead in their bones during early exposures, lead may present a dual risk: People may be at increased risk for osteoporosis if they have lead in their bones; and people who release lead from their bones may suffer effects from the released lead.

 

Lead and osteoporosis

ead is a risk factor for osteoporosis both because it is stored in the skeleton, and because bone is a target tissue for lead toxicity, according to researcher R.A. Goyer. As lead, a non-bone material incorporated into bone, is released into the body during normal body processes, it accelerates the process whereby bone mass diminishes. Lead also has direct, complex toxic effects on bone cell function, and may indirectly alter how bone cells develop, and how they function. These effects appear to occur partly because lead alters critical hormone levels in the body. Lead may also alter bone cell function by disturbing the ability of bone cells to respond to hormonal stimuli; even if circulating levels of the hormones in the body are within normal range, the bone cells may not respond to them normally. Lead may also disrupt normal processes that control the activities of bone cells. It may inhibit enzymes that affect bone cell functions. In all these ways, lead in bone may threaten bone health and structural integrity.

 

Health effects of lead

Most people have an image of lead poisoning: an infant eating lead paint chips, and suffering brain damage. This image is correct, but it is partial: If the infant's mother released large quantities of lead during pregnancy and nursing, the baby was exposed before birth-- long before paint chips posed a direct threat to him. And the baby's brain may not have been the only organ damaged by lead: Lead exposure causes injury to many of the body's systems. "Lead causes many adverse health effects, including toxicity of the nervous, hematopoietic [blood], renal [kidney], endocrine and skeletal systems, with the [central nervous system]CNS as the primary target organ," according to researcher Marjorie Peraza.

Another way in which the popular image of lead poisoning is misleading is age-related: Although infants and their nervous systems are particularly vulnerable, "people can suffer lead-related health effects throughout life. Toxicity, which is both age and lead dose dependent, occurs from low-level exposures from various environmental sources, including air, food and water. . . . [In adults,] physiologic conditions associated with bone resorption, including pregnancy, lactation and aging, can also potentiate CNS effects of lead and enhance exposure," according to Peraza.

 

Acute symptoms

Symptoms of acute lead poisoning are well known. In children, onset is usually sudden, with vomiting, altered gait, seizures and alterations of consciousness. In severe cases the seizures may become intractable, and coma may follow. In retrospect, parents may realize that in the days or weeks prior to the onset of these symptoms, the child had been irritable and uninterested in play. Clinically, the child may be anemic and may experience kidney damage. Death can occur at very high levels.

In adults, acute lead poisoning symptoms may develop over several weeks. There may be personality changes, a metallic taste in the mouth, headache and loss of appetite with abdominal discomfort. Then vomiting, constipation and crampy, colicky pain ensue. Except at very high levels, adults usually do not have alterations in consciousness, seizures or coma as the result of lead poisoning. The exception to this rule is lead poisoning induced by inhaling lead from gasoline: this can produce toxic psychosis. Clinically, high levels of lead can produce damage in the peripheral nervous system, kidney damage, and in men, decreased fertility. Production of red blood cells may be reduced, and anemia may result. Very high levels of exposure can cause death.

 

Chronic symptoms

Chronic lead poisoning may produce subtle alterations in health. People affected by these changes may not even experience symptoms, or realize that they symptoms they do have are related to lead. In children, low levels of lead can inhibit growth, affect hearing, and cause small but significant reductions in IQ. Higher levels can produce more developmental toxicity, as well as alterations in blood cells and in the nervous system. Still higher levels can inhibit metabolism of vitamin D (essential for bone growth and health). Children experiencing these effects may not seem ill, but rather appear to have behavioral or attention problems. Most clinicians are aware that children may suffer these effects as the result of lead exposure, may screen affected children for blood lead levels, and recommend steps to remove the child from further exposure to lead.

In adults, chronic lead poisoning may be, or appear to be, silent. Increased hypertension may be present at low levels of lead, but may not be attributed to lead. Both men and women experience reductions in a blood component, erythrocyte protoporphyrin, but women experience this effect at lower levels than do men. Reduced hearing and increased hypertension are seen at higher levels. At yet higher levels, symptoms of acute poisoning intervene. At levels below those required to induce acute symptoms, health effects from lead may be attributed to aging, heredity or lifestyle. Health effects may be treated symptomatically, and lead exposures (either environmental or arising from bone metabolism) may be overlooked.

 

Nutrition and lead absorption

Inadequate diet can promote lead absorption-- and adequate diet can protection against it. A recent review [see M. Peraza in Sources] of the interactions of diet and metal absorption noted the following about lead:

Lead competes with calcium in the body, and calcium deficiency can promote lead absorption. Studies have indicated that adequate calcium in the diet can inhibit lead absorption, but that amounts of calcium in excess of normal requirements does not have a proportionally protective effect-- more is not particularly better.

  • Adequate dietary phosphorus also inhibits lead absorption. In diets deficient in both calcium and phosphorus, the two deficiencies have an additive effect, increasing lead absorption.
  • Vitamin D plays a key role in absorbing calcium, phosphorus, and other nutrient minerals, as well as absorption of metals like lead. In people with diets deficient in calcium, a vitamin D hormone is produced in the intestinal tract. This hormone enhances absorption of calcium, but it also facilitates absorption of lead.
  • Iron deficiency promotes lead absorption, particularly in children.
  • Zinc intake inhibits lead absorption.
  • Diets adequate in total food intake, including fats, inhibit lead absorption. Frequency of meals also inhibits lead absorption.
  • Attention to diet during critical periods of growth and development can protect against lead absorption and its effects. Pregnant women, infants and children represent one group that can benefit from adequate diet. However, the need for adequate nutrition continues throughout life. Women may not become aware of the need for adequate dietary calcium until they approach menopause. But researcher R. A. Goyer notes that "The level of dietary calcium during the third decade of life [is]... important in determining bone density and risk of osteoporosis later in life." Some women may not be aware of the need for calcium until twenty years later, by which time bone density loss has been under way for a decade. Goyer also notes, " Dietary sodium increases urinary calcium loss. Smoking and alcohol abuse also decrease bone mineral content. Estrogen is an important determinant of bone density and calcium and other supplementation cannot repair other nutrient deficiencies, offset estrogen deprivation, or neutralize the untoward effects of unhealthy habits."

 

Some highlights of nutritional needs throughout life

Rapidly growing children and adolescents are at risk for incorporation of lead into growing bone, which can later serve as a source of internal exposure to lead. Teenage girls may be at particular risk, as their age predisposes them to weight loss regimens (and even eating disorders) that may result in inadequate intake of protective nutrients. Teenagers who take control of their food intake without guidance about what makes a diet adequate to protect health may make poor choices that have lasting effects on health in general, and on bone health in particular. In addition, this is the period of life when eating patterns and habits tend to become established. Habits acquired at this period can have effects on lifelong health.

With the onset of middle age, many people gain weight. Activity levels may decline, while caloric intake may remain the same as it was during more active youth. Some people may be encouraged by their physicians to lose weight, and virtually everyone in the US is under considerable pressure to conform to the ideal of slim "youthfulness." Weight loss programs that do not provide adequate nutrient intake can facilitate the bone density loss that is already under way in people in their 40s. In postmenopausal women there may be pressure to lose weight at the very time when their bone density loss has speeded up many fold from pre-menopausal levels. Most people in this age group are now aware that calcium intake is important to bone health, but they may not be aware of other nutrients that are important to bone health. They may assume that taking calcium supplements may provide all the protection necessary-- and they may be wrong.

Increasing age brings additional risks to nutritional adequacy. Declines in dental health and visual acuity may affect food choices, and increasing frailty may affect food preparation techniques and thus food choices. Increased medication intake can increase nutritional needs, and elderly patients may be unaware of these increased requirements. In addition, advancing age brings on the symptoms of frank osteoporosis, and increasing bone fragility may inhibit activities that can protect general health, and thus foster increased bone mineral loss.

 

Where does this leave the baby boomers? Some speculations.

High lead exposures, and risk factors that predispose absorption of lead, may have put this generation at risk for late life re-exposure to lead stored in bone. Consider the following:

  • The baby boomers potentially were exposed to increasingly high levels of lead from automotive exhaust, and from lead paint, almost from conception. At the time, the chronic effects of low level lead exposure were unknown, and attempts to avoid exposure were not made.
  • The boomers were perhaps the first generation to benefit from a rapidly increasing and improving food supply, but they were also the first generation to view weight loss as desirable for both looks and health. The sheer availability of food during boomer childhood and youth may not have resulted in corresponding health benefits, if food preferences and weight loss goals were primary determinants in food choices.
  • The phenomenon of popular fast foods high in protein, fat and sugar occurred during boomer adolescence-- a period when nutritional adequacy is particularly important for future health. The popularity of soft drinks in the same period may have displaced the intake of milk products for many during the same period.
  • Smoking reached an all time high among boomers in the 1960s and 70s, during adolescence and late youth. Women in particular took up smoking in this period in unprecedented numbers. The combination of smoking and inadequate diet may have facilitated lead absorption during this period, and set the stage for later osteoporosis.
  • Although lead was phased out of gasoline through the late 1970s and 1980s, the lead dust it left in the environment persisted. Health and weight conscious runners and joggers along busy streets could have been exposed to this dust. If dietary intake was inadequate at the same time, lead absorption was possible.
  • Young adult boomers who redecorated or renovated housing during the 1970s and 1980s may have unwittingly exposed themselves and their families to lead dust from old painted surfaces. This is particularly true in inner city areas where 'gentrification' took place, in which deteriorating housing stocks containing lead based paint were taken over from the urban poor, and restored by middle and upper class owners. However, lead based paint existed (and still exists) in suburban housing built during the post World War 2 housing boom. In urban areas, lead exposures from outdoor lead dusts could have been precipitated by landscaping and gardening activities as well as building renovations.
  • At the same time housing-related lead exposures were potentially common, many boomers were starting their families. Pregnant women exposed to lead in their home and neighborhood environments could have absorbed significant quantities of lead, some of which was incorporated into their bones, and some of which was passed on to their fetuses. Nursing mothers were also at increased risk for absorbing lead and passing it on to their infants, as well as incorporating it into their own skeletons.
  • Attempts to battle middle age weight gain may have both increased the capacity of boomers to absorb lead, and to promote its release from their aging skeletons. Inadequate information about nutrition and osteoporosis may have caused aging boomers to make poor food choices during there 30s.
  • Now that the boomers are facing retirement age, they are well informed about osteoporosis, but they may not be as well informed about nutrition, or about the risks posed by releases of lead from their bones. They may dread the onset of age related neurological disorders, like Alzheimer's disease. But they may not be aware of the following: Lead exposure may induce autoimmune responses to the body's own nervous system tissues, and thus may be implicated in neurological diseases that have an immune system component. Such diseases include autoimmune encephalomyelitis, multiple sclerosis, Lyme neuroborreliosis, and Alzheimer's disease. "Because of the presence of autoantibodies against nervous system proteins in several neurological disorders and because of the suspected involvement of environmental pollutants in the pathogenesis of neurological diseases it is reasonable to propose a mechanism whereby metal alteration of neural proteins leads to autoantibody production against neural structures, causing progressive degeneration in the nervous system," says researcher S.J. Waterman.

 

Conclusion

The health risks associated with lead released from the skeleton are not known. In children, toxic effects of lead on the central nervous system have been shown to occur at relatively low exposures, and there is still no established lower threshold for lead toxicity. Unfortunately, no similar data have been produced for populations prone to increased bone mineral loss, such as the elderly," says researcher D.R. Smith. However, he says his research indicates: [P]previously accumulated lead stores within the skeletons of. . . exposed subjects are serving as important sources of lead by contributing 40 - 70% of the lead in the circulation.

Other research indicates support for this concern. Blood lead levels have been decreasing in response to environmental measures that restrict emissions of lead. However, some evidence suggests that elevated exposure to lead may continue for many years, even after exposure to environmental sources has been reduced. This may occur primarily due to the mobilization of endogenous bone lead store. The skeleton is the primary site of storage for about 95% of lead in the adult human body. [See M. Hernandez-Avila et al. in Sources] ".

"With regard to adults, low to moderate levels of lead in the blood have been associated with increases in blood pressure as well as decreased creatinine clearance [a measure of kidney function]. These studies suggest that the prevalence of subclinical lead toxicity in. . . adults is far more prevalent than commonly recognized," says researcher Howard Hu. He continues: " Post-menopausal women had significantly higher blood lead levels than premenopausal women, even after controlling for age, race, income, alcohol consumption and other variables."

"Historically regarded as an inert sink for lead, the skeleton is now recognized to be as important in the kinetic behavior of lead as are the influences of exposures, absorption and elimination. The skeleton is the predominant. . . endogenous storage site for lead. The bulk of that lead is contained within long-lived compartments of . . . bone, with comparatively small amounts of lead in [other tissues]. . . . Because lead is qualitatively a biologic analog to calcium, its uptake and release from the skeleton are, in part, controlled by many of the mechanisms that regulate calcium and bone mineral homeostasis.. . . . [T]he skeleton may serve as an endogenous source of lead to the circulation. This has been suggested to occur during normal homeostasis, after the cessation of chronic occupational exposures, during periods of accelerated bone turnover and mineral loss, such as in osteoporosis, pregnancy and lactation, and under conditions of thyroid and parathyroid hormone imbalances," D. R. Smith notes.

 

SOURCES:

  • Agency for Toxic Substances and Disease Registry, Case Studies in Environmental Medicine: Lead Toxicity. USDHHS, PHS, ATSDR , September 1992.
  • Berkow, R. (ed in chief), The Merck Manual of Diagnosis and Therapy 16th edition. Rahway NJ: Merck and Co., Inc. 1992.
  • Clarkson, T. , Health effects of metals. Environmental Health Perspectives 101 (Supp. 1):9-12. February 1995.
  • Goyer, R.A. et al., Environmental risk factors for osteoporosis [meeting report. Environmental Health Perspectives 102(4):390-394. April 1994.
  • Greene, H.L. et al. (eds), Introduction of Clinical Medicine. Philadelphia et al.: B.C. Decker Inc. 1991.
  • Gulson, B.L. et al., Impact of diet on lead in blood and urine in female adults and relevant to mobilization of lead from bone stores. Environmental Health Perspectives 107(4):257-263. April 1999.
  • Hernandez-Avila, M. et al., The influence of bone and blood lead on plasma blood levels in environmental exposed adults. Environmental Health Perspectives 106(8):473-477. August 1998.
  • Hu, H et al., Bone lead as a biological marker in epidemiologic studies of chronic toxicity: conceptual paradigms. Research review. Environmental Health Perspectives 106:1-8. January 1998.
  • Hickler, R.B. and Lynn Li, Geriatric medicine: physiologic alterations of aging. In Greene.
  • Legget, R. An age-specific kinetic model on lead metabolism in humans. Environ Health Perspect 101:598-616. 1993. In Smith.
  • Manton, W.I., Total contribution of airborne lead to blood lead. Br. J Ind Med 42:168-72. In Smith.
  • Marcus, A., Multicompartment kinetic models for lead, bone diffusion models for long-term retention. Environ Res 36:441-458. 1985. In Smith.
  • Mielke, H.W. and P.L. Reagan, Soil in an important pathway of human lead exposure. Environmental Health Perspectives 106 Supplement 1:217-229. February 1998.
  • National Academy of Sciences, Measuring Lead Exposure in Infants Children and Other Sensitive Populations. Washing DC: National Academy of Sciences Press, 1993. In Mielke.
  • Nilsson, U. et al., Kinetics of lead in bone and blood after end of occupational exposures. Pharmacol. Toxicol. 69:477-484; 1991. In Rothenberg.
  • O'Flaherty, E.J., Physiologically based models for bone-seeking elements. kinetics of lead disposition in humans. Toxicol Appl Pharmacol 118:16-29. 1993. In Smith.
  • Peraza, M.A. et al., Effects of micronutrients on metal toxicity. Environmental Health Perspectives 106(Supplement 1):203-216. February 1998.
  • Rothenberg, S.J. et al., Changes in serial blood levels during pregnancy. Environmental Health Perspectives 102(10):876-880; 1994.
  • Silbergeld, E.K. et al., Lead and osteoporosis: Mobilization of lead from bone in post-menopausal women. Environ. Res 47:79-94. 1988. In Hu.
  • Silbergeld, E.K., Lead in bone: implications for toxicology during pregnancy and lactation. Env Hea Perspect 91:62-70. 1991. In Smith.
  • Smith, D.R. et al., Use of endogenous stable lead isotopes to determine release of lead from the skeleton. Environmental Health Perspectives 104(1):60-66. January 1996.
  • Symanski, E et al., Blood lead levels in relation to menopause, smoking and pregnancy history. Am J. Epidemiol 141:1047-1058. 1995. In Hu.
  • Waterman, S.J. et al., Lead alters the immunogenicity of two neural proteins: a potential mechanism for the progression of lead-induced neurotoxicity. Environmental Health Perspectives 102(12):1052-1056. December 1994.
  • Webber, C.E. et al., hormone replacement therapy may reduce the return of endogenous lead from bone to the circulation. Environ Health Perspect 103:1150-1153. 1995 In Peraza.
  • Xinteras, C. Analysis paper: Impact of lead contaminated soil on public health. Atlanta: ATSDR. 1992 In Mielke.

 

Lead and osteoporosis on the web

For more information about lead, see the following sites:

  • EPA's OPPT Lead Page
  • National Safety Council's Environmental Health Center
  • Centers for Disease Control and Prevention Lead Fact Sheet
  • The Lead Page
  • For more information about osteoporosis, including treatment and research, see the following sites:
  • Centers for Disease Control and Prevention brochure
  • National Osteoporosis Foundation

 

At a glance: Osteoporosis-- facts and figures c. 1998-1999

People at risk for osteoporosis:

  • Post menopausal women
  • Men over age 50
  • People with Cushings Disease
  • People with high or low thyroid levels
  • People who are immobilized
  • People with bone cancer
  • People with genetic predisposition toward thinning bones
  • People with eating disorders
  • People who smoke
  • People who use steroid hormones (licit or illicit)
  • People who consume alcohol heavily

--Encyclopedia at Adam

 

Women and osteoporosis

"Nearly one of two women over 50 will experience an osteoporotic fracture in her lifetime."

National Osteoporosis Foundation

  • Post-menopausal women in the US.................................................38.2 million
  • Estimated number of women over 50 who have osteoporosis...........25%
  • Estimated number of women over 50 who have low bone density....40%-56%
  • Percent who have had bone density tests..........................................20

 

Not for Caucasians only: Minority women and osteoporosis

Some figures from screenings of 130,000 women screened for osteoporosis:

  • Asian....................65.1% had low bone density; 8.2% had full-blown osteoporosis
  • Native American..58.9% had low bone density; 9.5% had full blown osteoporosis
  • Hispanic...............55.5% had low bone density; 4.3% had full blown osteoporosis
  • Caucasian.............50.5% had low bone density, 5.2% had full-blown osteoporosis

--Dr. Ethel Seris, Columbia Presbyterian Medical Center, in a presentation to a joint meeting of the American Society of Bone and Mineral Research and the International Bone and Mineral Society, December 1998.