Lead has a half-life of 27 days in the blood (according to Environmental Health Perspective 1995; 103:988-999). Therefore, chronic exposure will not adequately show up in blood tests, so performing these tests and documenting their results will not properly diagnose chronic heavy metal toxicity. In chronic exposure cases, the blood does not carry the heavy metals, but rather the metals are stored in body tissue and can only be released to be measured with a chelating agent. The source of chronic exposure is difficult, if not impossible, to determine.
There are several recent documentations of the fact that blood tests do not reveal the chronic levels of heavy metals that disrupt organ function. For example, an article in the Journal of American Society of Nephrology, 2004; 15:1016-1022, Environmental Exposure to Lead and Progression of Chronic Renal Diseases: A Four-Year Prospective Longitudinal Study, links environmental exposure to lead with chronic renal disease. According to the article, in reference to studies comparing lead levels with renal disorder, “most of these studies measured BLL [blood lead level] as an indicator of lead exposure. However, the BLL reflects recent lead exposure rather than the actual body lead burden (BLB). Calcium disodium EDTA mobilization tests and bone x-ray fluorescence studies are the most reliable methods for measuring the BLB. …The authors’ previous studies, using EDTA-mobilization tests to assess the BLB, suggested that low-level environmental lead exposure may be associated with the progression of renal insufficiency in patients without known lead exposure. Our recent work further established that repeated chelation therapy to reduce the BLB may slow the progression of renal insufficiency in a 27-month clinical trial.” Taking this further, the importance of improving renal function can be seen by the conclusion of “Relation between Renal Dysfunction and Cardiovascular Outcomes after Myocardial Infarction” from The New England Journal of Medicine 2004; 351:1285-1295. It states, “Even mild renal disease, as assessed by the estimated GFR, should be considered a major risk factor for cardiovascular complications after a myocardial infarction.”
Another article proving the effects of chronic lead toxicity, even without elevated blood lead levels, from the New England Journal of Medicine 2003; 348:1517-1526, Intellectual Impairment in Children with Blood Lead Concentrations below 10 μg per Deciliter, states that “blood lead concentrations, even those below 10 μg per deciliter, are inversely associated with children’s IQ scores at three and five years of age, and associated decline 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.”
Another related article on blood lead level, found in JAMA 2003; 289:1523-1532, Blood Lead, Blood Pressure, and Hypertension in Permenopausal and Postmenopausal Women, states that “at levels well below the current US occupational exposure limit guidelines (40 μg/dL), lead level is positively associated with both systolic and diastolic blood pressure and risks of both systolic and diastolic hypertension among women aged 40 to 59 years. The relationship between blood lead levels and systolic and diastolic hypertension is most pronounced in postmenopausal women. These relationships provide support for continued efforts to reduce lead levels in the general population.”
An article entitled “Lead, Cadmium, Smoking, and Increased Risk of Peripheral Arterial Disease” found in Circulation 2004; 109:3196-3201 corroborated the evidence that blood lead levels within safety standards can still be harmful. “Blood lead and cadmium, at levels well below current safety standards, was associated with an increased prevalence of peripheral arterial disease in the general US population. Cadmium may partially mediate the effect of smoking on peripheral arterial disease.”
One last example of lead toxicity with blood lead levels within normal range is found in the American Journal of Epidemiology 2004; 160(9):901-911, entitled “Bone Density-related Predictors of Blood Lead Level among Peri- and Postmenopausal women in the United States”. The article states: “Because of the long half-life of lead stored in bone (years), skeletal lead stores may be a source of endogenous lead exposure during periods of increased bone demineralization, such as menopause. …Bone mineral density was significantly inversely related to blood lead levels in log-linear multivariate models that adjusted for age, race/ethnicity, smoking, education, household income, alcohol use, and residence (urban/rural).”