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(Hypertension. 2003;41:463.)
© 2003 American Heart Association, Inc.

Scientific Contributions

Blood Lead Level Is Associated With Elevated Blood Pressure in Blacks

Suma Vupputuri; Jiang He; Paul Muntner; Lydia A. Bazzano; Paul K. Whelton; Vecihi Batuman

From the Epidemiology Branch, National Institute of Environmental Health Sciences (S.V.), Research Triangle Park, NC; the Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine (J.H., P.M., L.A.B., P.K.W.), and the Department of Medicine, Tulane University School of Medicine (J.H., V.B., P.K.W.), New Orleans, La; and the VA Medical Center (V.B.), New Orleans, La.

Reprint requests to Jiang He, MD, PhD, Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, 1430 Tulane Ave SL18, New Orleans, LA 70112. E-mail jhe{at}tulane.edu

	Abstract

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Chronic lead exposure has been associated with elevated blood pressure in epidemiological studies. It is not known whether the previously observed relation between blood lead and hypertension persists after significant reductions have been made in environmental lead contamination. We examined the relation between blood lead levels and blood pressure in a representative sample of 14 952 whites and blacks aged 18 years or older who participated in the Third National Health and Nutrition Examination Survey. Blood lead was measured by atomic absorption spectrophotometry and blood pressure by standard sphygmomanometry. Mean blood lead levels were significantly higher for black men and women (5.4 and 3.4 µg/dL, respectively) compared with white men and women (4.4 and 3.0 µg/dL, respectively). After multivariate adjustment for important covariables, each standard deviation higher blood lead (3.3 µg/dL) was associated with a 0.82 (95% confidence interval [CI], 0.19 to 1.44) mm Hg and a 1.55 (95% CI, 0.47 to 2.64) mm Hg higher systolic blood pressure among black men and women, respectively. In contrast, blood lead level was not associated with blood pressure among white men or women. The multivariate-adjusted odds ratio (95% CI) of hypertension associated with a 1-SD higher level of blood lead was 1.08 (95% CI, 0.99 to 1.19) for black men and 1.39 (95% CI, 1.21 to 1.61) for black women. These findings suggest that increased levels of blood lead remain an important environmental risk factor for elevated blood pressure in blacks.

Key Words: blood pressure • ethnic groups • blood lead • blacks • epidemiology

	Introduction

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Most,^1–10 but not all,^11–16 studies have indicated that environmental exposure to lead is associated with an increased risk of hypertension and renal disease. A strong association between blood lead level and prevalence of hypertension was noted in the Second National Health and Nutrition Examination Survey (NHANES II).^4,17,18 The NHANES II was conducted during 1976 and 1980, when many of the current environmental measures, such as reduction in use of leaded gasoline, had not been adopted or had not been in place long enough to have a measurable effect on lead pollution.^17–19 In recent years, a strong secular trend toward decreasing blood lead concentrations has been noted in the general population. For example, among the US population aged 1 to 74 years, mean blood lead concentrations dropped by 78%, from 12.8 µg/dL to 2.8 µg/dL between 1976 to 1980 (NHANES II) and 1988 to 1991 (the first phase of the Third National Health and Nutrition Examination Survey [NHANES III]).^8,19–21 Whether the relation between blood lead level and blood pressure (BP) is still present after this marked decline in environmental lead exposure is unknown. The present study examined the relation between blood lead level and BP in a large representative sample of blacks and whites who participated in NHANES III.

	Methods

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Study Participants
The NHANES III was conducted by the National Center for Health Statistics between 1988 and 1994. Details of the NHANES III study participants and methods have been published elsewhere.²² In brief, a stratified multistage probability design was used to obtain a representative sample of the civilian noninstitutionalized US general population. To improve the precision of estimates in certain subgroups, the design included oversampling of the very young, the elderly, blacks, and Mexican-Americans. A total of 19 618 participants 18 years of age and older were included in NHANES III. Participants were excluded from the current analysis when their self-reported race was not white or black (n=635) or when data on blood lead (n=3936) or BP (n=95) were missing. A total of 10 548 whites and 4404 blacks were included in the main analysis where hypertension was the outcome of interest. Participants who were taking antihypertensive medications (n=2496) were excluded from the linear regression analysis examining BP as a continuous variable.

Measurements
The NHANES III data collection included a standardized home interview followed by a detailed physical examination in a mobile examination center or the participant’s home. Information on a wide variety of sociodemographic, medical history, nutritional history, and family history questions, such as self-reported age, race/ethnicity, gender, years of education completed, usual level of physical activity, history of smoking, hypertension, diabetes, alcohol intake, and 24-hour dietary recall, were obtained at the home interview.²²

BP was measured 3 times during the home interview and another 3 times at the mobile examination center. BP for individual participants was calculated as the average of all available systolic and diastolic readings. Hypertension was defined as the presence of a mean systolic BP 140 mm Hg and/or diastolic BP 90 mm Hg and/or taking antihypertensive medication. Body weight and height were measured according to a standard protocol, and body mass index was calculated as an index for obesity.

A blood sample was collected by venipuncture during the physical examination. Blood lead concentration was measured at the National Center for Environmental Health of the Centers for Disease Control and Prevention in Atlanta, Ga, by graphite furnace atomic absorption spectrophotometry.^23,24

Statistical Analyses
Baseline characteristics were calculated as means and SEs for continuous variables and percentages for categorical variables by race and gender. Next, interactions between lead and race and lead and gender were examined. Age- and multivariate-adjusted linear regression models were used to examine the association of blood lead level with systolic and diastolic BPs stratified by race and gender. Multivariate models were adjusted for age, high school education, body mass index, alcohol consumption, leisure-time physical activity (any versus none), and dietary intake of sodium, potassium, and total energy. Race- and gender-specific age-adjusted and multivariate-adjusted logistic regression models were used to assess the association of blood lead level with hypertension. Additional linear and logistic regression models were used to examine the effects of high blood lead level (defined as blood lead 5 µg) on BP and hypertension, respectively.

All analyses were weighted to account for the complex sampling methodology of NHANES III by using Stata statistical software (Stata Corp, release 7.0).

	Results

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Characteristics of the study participants by race and gender are presented in Table 1. Black participants were younger than their white counterparts and were less likely to have a high school education. Mean body mass index was higher among black women compared with black men, white men, or white women. Whites and black men were more likely to have reported consumption of alcohol at least 12 times during the preceding year than black women. Dietary sodium, potassium, and total energy intake were higher among men compared with women, and dietary potassium intake was higher among whites than among blacks. Systolic and diastolic BP levels were higher in blacks compared with whites and higher in men compared with women. Blood lead levels were higher for blacks compared with whites and for men compared with women.

View this table: [in this window] [in a new window]   TABLE 1. Characteristics of 10 548 White and 4404 Black Participants in the Third National Health and Nutrition Examination Survey, 1988–1994

Tests for interaction terms (lead-race and lead-gender) in multivariate logistic and linear regression models revealed that the relation between blood lead level and BP differed significantly by race as well as gender (each P<0.001).

In age-adjusted linear regression analyses (Table 2), blood lead level was not associated with systolic BP among white men and women but was significantly and positively associated among black men and women. After multivariate adjustment for important covariables, each SD higher blood lead (3.3 µg/dL) was associated with a 0.82 (95% confidence interval [CI], 0.19 to 1.44) mm Hg and a 1.55 (95% CI, 0.47 to 2.64) mm Hg higher systolic BP among black men and women, respectively. Furthermore, in age-adjusted models, blood lead level was significantly associated with diastolic BP only among black women. After further controlling for education, body mass index, alcohol consumption, leisure-time physical activity, dietary intake of sodium, potassium, and total energy, higher blood lead was statistically significantly associated with higher diastolic BP for black men and women but not whites.

View this table: [in this window] [in a new window]   TABLE 2. Differences and 95% Confidence Interval of Blood Pressures Associated With a 1-SD Higher Level of Blood Lead Concentration Among NHANES III Participants by Race and Gender

The age-adjusted prevalence of hypertension was higher among blacks compared with whites. In age-adjusted logistic regression analysis, blood lead levels were positively related with increased odds of hypertension for black women (Table 3). After multivariate adjustment for important covariables, blood lead level was significantly associated with the odds of hypertension among white women (odds ratio [OR]=1.32; 95%CI, 1.14 to 1.52) and black women (OR=1.39; 95%CI, 1.21 to 1.61), marginally significantly associated with hypertension among black men (OR=1.08; 95%CI, 0.99 to 1.19; P=0.08), and not associated with hypertension among white men (OR=1.04; 95% CI, 0.93 to 1.16).

View this table: [in this window] [in a new window]   TABLE 3. Odds Ratios and 95% Confidence Intervals of Hypertension Associated With a 1-SD Higher Level of Blood Lead Concentration Among NHANES III Participants by Race and Gender

In multivariate-adjustment models, a blood lead concentration 5 µg/dL was associated with higher systolic and diastolic BP among blacks but not whites (Figure). Compared with their counterparts with a blood lead <5 µg/dL, systolic and diastolic BP was 1.67 and 1.68 mm Hg higher, respectively, among black men and 2.48 and 2.22 mm Hg higher, respectively, among black women with a blood lead concentration 5 µg/dL (each P<0.05). Also, the multivariate-adjusted OR (95% CI) of hypertension associated with a blood lead concentration 5 µg/dL was 1.06 (0.81 to 1.38) for white men, 1.48 (1.13 to 1.93) for white women, 1.22 (0.93 to 1.60) for black men, and 1.73 (1.24 to 2.43) for black women.

View larger version (17K): [in this window] [in a new window]   Multivariate-adjusted differences in systolic and diastolic blood pressure for persons with a blood lead concentration 5 µg/dL compared with those with a blood lead concentration <5 µg/dL by race and gender. Data were adjusted for age, education, body mass index, use of alcohol, physical activity, sodium, potassium, and total calories. *P<0.05; **P<0.01

	Discussion

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Our study shows that, in addition to having higher mean blood lead levels, blacks demonstrated consistent, significant associations between blood lead level and systolic and diastolic BPs. In contrast, blood lead level was not significantly associated with BP among whites. Furthermore, blacks with blood lead levels 5 µg had a significant increase in mean BP (systolic BP of 1.66 mm Hg and 2.48 mm Hg in men and women, respectively). The association of blood lead with hypertension in this study was significant in black women but only of borderline significance in black men.

It is important to distinguish between the implications of individual and population changes in BP. For an individual, the increases in BP that we observed were slight (systolic BP of 0.82 mm Hg and 1.55 mm Hg in black men and women, respectively) and have limited importance. However, at the population level, even a small downward shift in BP would be expected to result in a substantial reduction in cardiovascular disease.²⁵ It is estimated that a population-wide reduction in diastolic BP of as little as 2 mm Hg would result in a 17% reduction in the prevalence of hypertension as well as a 15% reduction in the risk of stroke and transient ischemic attacks and a 6% reduction in the risk of coronary heart disease.²⁵

Our findings are consistent with the experience in a majority of other studies suggesting that exposure to lead (including low-level exposure) is significantly and positively associated with an elevated BP level and risk of hypertension.^{4–7,9,17,18,26–44} Furthermore, our findings are similar to those of others who identified higher blood lead levels in blacks and a stronger association between blood lead and hypertension in blacks, compared with whites.^36,41

The biological mechanisms for the observed racial differences in the association between blood lead level and elevated BP are not entirely clear. Our results suggest that blacks have a higher mean blood lead level compared with whites. In addition, different patterns of exposure in different environments, ie, inner city tenements, where blacks are disproportionately represented, may have divergent consequences. Epidemiological studies also indicate that blacks are more likely to be exposed to lead in an occupational setting.⁴¹ Furthermore, racial differences in bone metabolism and, specifically, in bone handling of lead may contribute to this apparent discrepancy in the association between blood lead level and elevated BP.⁴⁵ Blacks might also be more sensitive to the effects of lead exposure on BP owing to environmental and genetic factors. Residual confounding due to factors related to social-economic status might also contribute to a stronger association among blacks.

Although we observed no significant association between blood lead level and systolic or diastolic BP in white women, we did find a significant association between blood lead and hypertension among both white and black women. Several other studies have suggested that blood lead is more strongly related to elevated BP and hypertension in women compared with men.^{6,28,33,36,45,46}

Both environmental and occupational exposure to lead has long been associated with hypertension and renal disease.^{1,4,17,18,47,48} Animal studies suggest that even low levels of exposure to lead can result in hypertension.⁴⁴ Blood lead levels have dramatically declined in the US general population since efforts to reduce environmental lead exposure were emphasized in the 1970s. The virtual disappearance of overt lead poisoning may have caused complacency towards the hazards of low-level asymptomatic lead poisoning. Many believe that the lead-abatement interventions have all but eliminated the major health consequences of lead poisoning, and the association between low-level lead poisoning and hypertension has become increasingly controversial. Several studies have disputed the presence of a relation between low-level lead exposure and hypertension.^{10,12,13,16,21,49–58} Staessen and colleagues¹⁰ identified a significant association between blood lead levels and impairment of renal function in the general population in the Cadmibel study but failed to recognize a significant relation between blood lead and hypertension. Although it is possible that the latter does not exist, the findings in the Cadmibel study are consistent with the hypothesis that renal microvascular disease caused by lead precedes the occurrence of hypertension.^14,57–59

Since NHANES II, there has been a significant reduction in the mean blood lead concentration in the general population.^19,60–62 With more stringent exposure guidelines in the workplace and environmental measures, such as reducing lead content in gasoline and house paint, the average blood lead concentration has declined dramatically in the general population, and symptomatic overt lead poisoning has become a rare event.^1,8,20 Although the overall lowering of blood lead levels in the United States may represent a public health success in primary prevention efforts, disturbing disparities in exposure to environmental lead continue to be noted. Higher blood lead levels are still being seen in older versus younger adults, males versus females, inner-city residents versus non–inner-city residents, and blacks versus whites.⁸ In addition, higher-than-average blood lead levels are being noted in those with a low income, low educational attainment, and residence in the northeastern United States.⁸

The possibility that environmental lead exposure may be a contributing factor in the occurrence of hypertension among blacks is very important. This may explain, in part, the unusually high burden of illness due to hypertension and renal disease among blacks. Hypertension is more common, more severe, and usually appears earlier in life in blacks.⁶³ The higher blood lead levels and associated higher BP levels in blacks raises the possibility that chronic exposure to environmental lead is partially responsible for the strikingly higher incidence of both hypertension and renal disease in this population.

A continued diligent effort to eliminate lead pollution in the United States, especially targeting high-risk black communities, is crucial. Unfortunately, the cost of lead abatement is high, and the number of properly trained lead-abatement professionals is low. Many interventions that have been implemented to reduce environmental lead exposure have focused on secondary prevention, targeting homes with children who already have elevated blood lead levels. However, the number of these children with elevated blood lead levels has decreased rapidly, and the focus can, appropriately, be placed on primary prevention strategies with continuing efforts to adequately remove lead pollutants (such as leaded paint) in high-risk communities.

Our study has a number of important strengths. Because NHANES III surveyed a large probability sample of the general population, our findings can be generalized to US adults. This study also provides the opportunity to reevaluate the association of blood lead level and BP after lead-abatement procedures were put in place since NHANES II. Additionally, the large sample size of NHANES III provided ample power to detect a small but important association between blood lead level and elevated BP. A limitation of the present study is the use of a cross-sectional study design. Although this restricts the inferences that can be made based on our findings, there are numerous prospective studies that support the causal role of lead exposure in raising BP.

Another limitation of our study is that blood lead concentration is not an optimal biomarker and may underestimate the internal dose of lead. Current evidence points to bone lead as the most valuable measure of internal dose because it represents a cumulative exposure, and thus it can accurately assess persons who are exposed to chronic low-level environmental lead pollutants. However, currently, the most effective way to measure bone lead involves in vivo K x-ray fluorescence, which is expensive, time-intensive, and thus impractical for large-scale population studies. Furthermore, blood lead is a good measure of recent exposure to environmental lead and has been shown to be strongly associated with bone lead.^64,65 Therefore, although bone lead is a more sensitive marker for environmental lead exposure, the majority of epidemiological studies to date have assessed lead exposure by means of blood lead concentration measurements.

Perspectives
Despite major overall reductions in the United States, blood lead level remains significantly and positively related to elevated BP and hypertension among blacks, who continue to have higher blood lead concentrations compared with whites. This observation suggests that continuous efforts to reduce environmental lead exposure in the US general population, especially among blacks, may be an important approach to prevent hypertension in the community.

	Acknowledgments

 
This study was supported in part by grant R01HL60300 from the National Heart, Lung, and Blood Institute of the National Institutes of Health, Bethesda, Md.

Received August 15, 2002; first decision September 6, 2002; accepted December 18, 2002.

	References

Top Abstract Introduction Methods Results Discussion References

 
1. Batuman V. Lead nephropathy, gout, and hypertension. Am J Med Sci. 1993; 305: 241–247.[Medline] [Order article via Infotrieve]

2. Bost L, Primatesta P, Dong W, Poulter N. Blood lead and blood pressure: evidence from the Health Survey for England 1995. J Hum Hypertens. 1999; 13: 123–128.[CrossRef][Medline] [Order article via Infotrieve]

3. Cheng Y, Schwartz J, Sparrow D, Aro A, Weiss ST, Hu H. Bone lead and blood lead levels in relation to baseline blood pressure and the prospective development of hypertension: the Normative Aging Study. Am J Epidemiol. 2001; 153: 164–171.[Abstract/Free Full Text]

4. Harlan WR. The relationship of blood lead levels to blood pressure in the US population. Environ Health Perspect. 1988; 78: 9–13.[Medline] [Order article via Infotrieve]

5. Kim R, Rotnitsky A, Sparrow D, Weiss S, Wager C, Hu H. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. JAMA. 1996; 275: 1177–1181.[Abstract/Free Full Text]

6. Korrick SA, Hunter DJ, Rotnitzky A, Hu H, Speizer FE. Lead and hypertension in a sample of middle-aged women. Am J Public Health. 1999; 89: 330–335.[Abstract/Free Full Text]

7. Menditto A, Morisi G, Spagnolo A, Menotti A. Association of blood lead to blood pressure in men aged 55 to 75 years: effect of selected social and biochemical confounders: NFR Study Group. Environ Health Perspect. 1994; 102 (suppl 9): 107–111.

8. Pirkle JL, Kaufmann RB, Brody DJ, Hickman T, Gunter EW, Paschal DC. Exposure of the US population to lead, 1991–1994. Environ Health Perspect. 1998; 106: 745–750.[Medline] [Order article via Infotrieve]

9. Sharp DS, Osterloh J, Becker CE, Bernard B, Smith AH, Fisher JM, Syme SL, Holman BL, Johnston T. Blood pressure and blood lead concentration in bus drivers. Environ Health Perspect. 1988; 78: 131–137.[Medline] [Order article via Infotrieve]

10. Staessen JA, Lauwerys RR, Buchet JP, Bulpitt CJ, Rondia D, Vanrenterghem Y, Amery A. Impairment of renal function with increasing blood lead concentrations in the general population: the Cadmibel Study Group. N Engl J Med. 1992; 327: 151–156.[Abstract]

11. Chu NF, Liou SH, Wu TN, Chang PY. Reappraisal of the relation between blood lead concentration and blood pressure among the general population in Taiwan. Occup Environ Med. 1999; 56: 30–33.[Abstract/Free Full Text]

12. Micciolo R, Canal L, Maranelli G, Apostoli P. Non-occupational lead exposure and hypertension in northern Italy. Int J Epidemiol. 1994; 23: 312–320.[Abstract/Free Full Text]

13. Pocock SJ, Shaper AG, Ashby D, Delves T, Whitehead TP. Blood lead concentration, blood pressure, and renal function. BMJ (Clin Res Ed). 1984; 289: 872–874.[Abstract/Free Full Text]

14. Staessen JA, Bulpitt CJ, Fagard R, Lauwerys RR, Roels H, Thijs L, Amery A. Hypertension caused by low-level lead exposure: myth or fact? J Cardiovasc Risk. 1994; 1: 87–97.[CrossRef][Medline] [Order article via Infotrieve]

15. Staessen JA, Roels H, Lauwerys RR, Amery A. Low-level lead exposure and blood pressure. J Hum Hypertens. 1995; 9: 303–328.[Medline] [Order article via Infotrieve]

16. Wu TN, Shen CY, Ko KN, Guu CF, Gau HJ, Lai JS, Chen CJ, Chang PY. Occupational lead exposure and blood pressure. Int J Epidemiol. 1996; 25: 791–796.[Abstract/Free Full Text]

17. Harlan WR, Landis JR, Schmouder RL, Goldstein NG, Harlan LC. Blood lead and blood pressure: relationship in the adolescent and adult US population. JAMA. 1985; 253: 530–534.[Abstract/Free Full Text]

18. Pirkle JL, Schwartz J, Landis JR, Harlan WR. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. Am J Epidemiol. 1985; 121: 246–258.[Abstract/Free Full Text]

19. Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG. Chronological trend in blood lead levels between 1976 and 1980. N Engl J Med. 1983; 308: 1373–1377.[Abstract]

20. Pirkle JL, Brody DJ, Gunter EW, Kramer RA, Paschal DC, Flegal KM, Matte TD. The decline in blood lead levels in the United States: the National Health and Nutrition Examination Surveys (NHANES) JAMA. 1994; 272: 284–291.[Abstract/Free Full Text]

21. Brody DJ, Pirkle JL, Kramer RA, Flegal KM, Matte TD, Gunter EW, Paschal DC. Blood lead levels in the US population: phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991). JAMA. 1994; 272: 277–283.[Abstract/Free Full Text]

22. National Center for Health Statistics. Plan, and operation of the Third National Health and Nutrition Examination Survey, 1988–1994. Series 1: programs and collection procedures. Vital Health Stat 1. 1994; 32: 1–407.

23. Gunter EW, Lewis BL, Koncikowski SM. Laboratory Methods Used for the Third National Health and Nutrition Examination Survey (NHANES III), 1984–1994. Hyattsville, Md: Centers for Disease Control and Prevention; 1996.

24. Miller DT, Paschal DC, Gunter EW, Stroud PE, D’Angelo J. Determination of lead in blood using electrothermal atomisation atomic absorption spectrometry with a L’vov platform and matrix modifier. Analyst. 1987; 112: 1701–1704.[Medline] [Order article via Infotrieve]

25. Mulrow PJ. Hypertension—A Worldwide Epidemic. Dallas, Tex: American Heart Association, Council on High Blood Pressure Research; 1999.

26. Hu H, Aro A, Payton M, Korrick S, Sparrow D, Weiss ST, Rotnitzky A. The relationship of bone and blood lead to hypertension: the Normative Aging Study. JAMA. 1996; 275: 1171–1176.[Abstract/Free Full Text]

27. de Kort WL, Verschoor MA, Wibowo AA, van Hemmen JJ. Occupational exposure to lead and blood pressure: a study in 105 workers. Am J Ind Med. 1987; 11: 145–156.[Medline] [Order article via Infotrieve]

28. Houston DK, Johnson MA. Lead as a risk factor for hypertension in women. Nutr Rev. 1999; 57: 277–279.[Medline] [Order article via Infotrieve]

29. Kirkby H, Gyntelberg F. Blood pressure and other cardiovascular risk factors of long-term exposure to lead. Scand J Work Environ Health. 1985; 11: 15–19.[Medline] [Order article via Infotrieve]

30. Kopp SJ, Barron JT, Tow JP. Cardiovascular actions of lead and relationship to hypertension: a review. Environ Health Perspect. 1988; 78: 91–99.[Medline] [Order article via Infotrieve]

31. Maheswaran R, Gill JS, Beevers DG. Blood pressure and industrial lead exposure. Am J Epidemiol. 1993; 137: 645–653.[Abstract/Free Full Text]

32. Inglis JA, Henderson DA, Emmerson BT. The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland. J Pathol. 1978; 124: 65–76.[CrossRef][Medline] [Order article via Infotrieve]

33. Rabinowitz M, Bellinger D, Leviton A, Needleman H, Schoenbaum S. Pregnancy hypertension, blood pressure during labor, and blood lead levels. Hypertension. 1987; 10: 447–451.[Abstract/Free Full Text]

34. Sanchez-Fructuoso AI, Torralbo A, Arroyo M, Luque M, Ruilope LM, Santos JL, Cruceyra A, Barrientos A. Occult lead intoxication as a cause of hypertension and renal failure. Nephrol Dial Transplant. 1996; 11: 1775–1780.[Abstract/Free Full Text]

35. Schwartz J. The relationship between blood lead and blood pressure in the NHANES II survey. Environ Health Perspect. 1988; 78: 15–22.[Medline] [Order article via Infotrieve]

36. Schwartz J. Lead, blood pressure, and cardiovascular disease in men and women. Environ Health Perspect. 1991; 91: 71–75.[Medline] [Order article via Infotrieve]

37. Schwartz BS, Stewart WF. Different associations of blood lead, meso 2,3-dimercaptosuccinic acid (DMSA)-chelatable lead, and tibial lead levels with blood pressure in 543 former organolead manufacturing workers. Arch Environ Health. 2000; 55: 85–92.[Medline] [Order article via Infotrieve]

38. Scherrer M. Air burden and respiratory and vascular diseases. Schweiz Med Wochenschr. 1985; 115: 1042–1048.[Medline] [Order article via Infotrieve]

39. Sharp DS, Becker CE, Smith AH. Chronic low-level lead exposure: its role in the pathogenesis of hypertension. Med Toxicol. 1987; 2: 210–232.[Medline] [Order article via Infotrieve]

40. Sharp DS, Osterloh J, Becker CE, Smith AH, Holman BL, Fisher JM. Elevated blood pressure in treated hypertensives with low-level lead accumulation. Arch Environ Health. 1989; 44: 18–22.[Medline] [Order article via Infotrieve]

41. Sorel JE, Heiss G, Tyroler HA, Davis WB, Wing SB, Ragland DR. Black-white differences in blood pressure among participants in NHANES II: the contribution of blood lead. Epidemiology. 1991; 2: 348–352.[Medline] [Order article via Infotrieve]

42. Wedeen RP, Malik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med. 1979; 139: 53–57.[Abstract/Free Full Text]

43. Wedeen RP, Van de Vyver FL, D’Haese PC, Visser WJ, Elseviers MM, Knippenberg LJ, Lamberts LV, De Broe ME, Batuman V, Schidlovsky G, et al. Bone lead and the diagnosis of lead nephropathy. Contr Nephrol. 1988; 64: 102–108.

44. Khalil-Manesh F, Gonick HC, Weiler EW, Prins B, Weber MA, Purdy RE. Lead-induced hypertension: possible role of endothelial factors. Am J Hypertens. 1993; 6: 723–729.[Medline] [Order article via Infotrieve]

45. Rothenberg SJ, Manalo M, Jiang J, Cuellar R, Reyes S, Sanchez M, Diaz M, Khan F, Aguilar A, Reynoso B, Juaregui M, Acosta S, Johnson C. Blood lead level and blood pressure during pregnancy in South Central Los Angeles. Arch Environ Health. 1999; 54: 382–389.[Medline] [Order article via Infotrieve]

46. Dawson EB, Evans DR, Kelly R, Van Hook JW. Blood cell lead, calcium, and magnesium levels associated with pregnancy-induced hypertension and preeclampsia. Biol Trace Elem Res. 2000; 74: 107–116.[CrossRef][Medline] [Order article via Infotrieve]

47. Beevers DG, Erskine E, Robertson M, Beattie AD, Campbell BC, Goldberg A, Moore MR, Hawthorne VM. Blood-lead and hypertension. Lancet. 1976; 2: 1–3.[CrossRef][Medline] [Order article via Infotrieve]

48. Hu H. Exposure to metals. Prim Care. 2000; 27: 983–996.[Medline] [Order article via Infotrieve]

49. Dolenc P, Staessen JA, Lauwerys RR, Amery A. Short report: low-level lead exposure does not increase the blood pressure in the general population: Cadmibel Study Group. J Hypertens. 1993; 11: 589–593.[CrossRef][Medline] [Order article via Infotrieve]

50. Gartside PS. The relationship of blood lead levels and blood pressure in NHANES II: additional calculations. Environ Health Perspect. 1988; 78: 31–34.[Medline] [Order article via Infotrieve]

51. Lilis R, Valciukas JA, Weber JP, Malkin J, Selikoff IJ. Epidemiologic study of renal function in copper smelter workers. Environ Health Perspect. 1984; 54: 181–192.[Medline] [Order article via Infotrieve]

52. Malcolm D, Barnett HA. A mortality study of lead workers 1925–1976. Br J Ind Med. 1982; 39: 404–410.[Medline] [Order article via Infotrieve]

53. Osterloh JD, Selby JV, Bernard BP, Becker CE, Menke DJ, Tepper E, Ordonez JD, Behrens B. Body burdens of lead in hypertensive nephropathy. Arch Environ Health. 1989; 44: 304–310.[Medline] [Order article via Infotrieve]

54. Parkinson DK, Hodgson MJ, Bromet EJ, Dew MA, Connell MM. Occupational lead exposure and blood pressure. Br J Ind Med. 1987; 44: 744–748.[Medline] [Order article via Infotrieve]

55. Pocock SJ, Shaper AG, Ashby D, Delves HT, Clayton BE. The relationship between blood lead, blood pressure, stroke, and heart attacks in middle-aged British men. Environ Health Perspect. 1988; 78: 23–30.[Medline] [Order article via Infotrieve]

56. Staessen J, Yeoman WB, Fletcher AE, Markowe HL, Marmot MG, Rose G, Semmence A, Shipley MJ, Bulpitt CJ. Blood lead concentration, renal function, and blood pressure in London civil servants. Br J Ind Med. 1990; 47: 442–447.[Medline] [Order article via Infotrieve]

57. Staessen JA, Roels H, Fagard R. Lead exposure and conventional and ambulatory blood pressure: a prospective population study: PheeCad Investigators. JAMA. 1996; 275: 1563–1570.[Abstract/Free Full Text]

58. Staessen J. Low-level lead exposure, renal function and blood pressure. Verh K Acad Geneeskd Belg. 1995; 57: 527–574.[Medline] [Order article via Infotrieve]

59. Batuman V, Wedeen RP. Impairment of renal function with increasing blood lead concentrations. N Engl J Med. 1992; 327: 1394–1395.[Medline] [Order article via Infotrieve]

60. Blood lead levels–United States, 1998–1991. MMWR Morb Mortal Wkly Rep. 1994; 43: 545–548.[Medline] [Order article via Infotrieve]

61. Update: Blood lead levels–United States, 1991–1994. MMWR Morb Mortal Wkly Rep. 1997; 46: 141–146.[Medline] [Order article via Infotrieve]

62. Anderson LA Jr. A review of blood lead results from the Third National Health and Nutrition Examination Survey (NHANES III). Am Ind Hyg Assoc J. 1995; 56: 7–8.[Medline] [Order article via Infotrieve]

63. Puschett J, Batuman V. Hypertension and the kidney. Cardiovasc Risk Factors. 1997; 7: 7–16.

64. Todd AC, Lee BK, Lee GS, Ahn KD, Moshier EL, Schwartz BS. Predictors of DMSA chelatable lead, tibial lead, and blood lead in 802 Korean lead workers. Occup Environ Med. 2001; 58: 73–80.[Abstract/Free Full Text]

65. Kamel F, Umbach DM, Munsat TL, Shefner JM, Hu H, Sandler DP. Lead exposure and amyotrophic lateral sclerosis. Epidemiology. 2002; 13: 311–319.[CrossRef][Medline] [Order article via Infotrieve]

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