studies and seven cross-sectional studies published through 2007. The mean tibia lead concentrations ranged from 4.2 μg/g (a study of childhood lead exposure in a lead-smelter cohort in Silver Valley, Idaho, and a nonexposed cohort in Spokane, Washington) (Gerr et al. 2002) to 38.4 μg/g (a study of Korean lead workers) (Glenn et al. 2006), and mean patella lead concentrations ranged from 17.3 μg/g (Boston Nurses Health Study) (Korrick et al. 1999) to 32.1 μg/g (Normative Aging Study) (Hu et al. 1996). The combined summary estimates of SBP and DBP for a 10-μg/g increase in tibia lead were 0.26 mm Hg (95% CI: 0.02, 0.50) and 0.02 mm Hg (95% CI: -0.15, 0.19), respectively. The overall ORs for hypertension were 1.04 (95% CI: 1.01, 1.07) for tibia lead and 1.04 (95% CI: 0.96, 1.12) for patella lead.

Additional individual studies support a possible association of BLL over 10 μg/dL and 40 μg/dL and lower with higher blood pressure. A study in China compared 120 female crystal-toy workers (BLLs of 22.5-99.4 μg/dL) with 70 nonexposed controls (sewing workers, BLLs under 11.4 μg/dL) (Nomiyama et al. 2002). They found that workers who had BLLs of 60 μg/dL or higher had SBP, DBP, and pulse pressure 7.5 mm Hg (95% CI: 3.0, 12.0), 6.3 mm Hg (95% CI: 3.4, 9.1), and 3.4 mm Hg (95% CI: 0.5, 6.2), respectively, higher than those in the control group (BLLs under 11.4 μg/dL).

Glenn et al. (2006) explored whether the association between lead and blood pressure could be an acute response to lead or a long-term cumulative effect of lead. Their cohort consisted of 575 lead-exposed workers in South Korea with a baseline mean (standard deviation [SD]) BLL and tibia bone lead concentration of 31.4 (14.2) μg/dL and 38.4 (42.9) μg/g, respectively. They found that every increase of 10 μg/dL per year in concurrent BLL, as assessed with a longitudinal difference in BLL between visits, was associated with an average annual increase of 0.9 mm Hg (95% CI: 0.1, 1.6) in SBP during the 3-year followup. Tibia lead, however, was nonsignificantly inversely associated with a change in SBP. The authors suggested that SBP might be more responsive to circulating lead (as reflected by BLL), whereas lifetime cumulative dose may influence the risk of hypertension through other biologic pathways. Weaver et al. (2008) also examined the same cohort and observed a statistically significant cross-sectional association of SBP with concurrent BLL but not with patella lead. The significant association remained even after controlling for patella lead. There was no association of DBP or hypertension prevalence with either lead measure. A community-based cohort study conducted in the Baltimore, Maryland, area (Baltimore Memory Study) found that BLL was associated with blood pressure, whereas tibia lead was associated with hypertension; this suggested that “lead has an acute effect on blood pressure via recent dose and a chronic effect on hypertension risk via cumulative dose” (Martin et al. 2006).

Two studies examined BLL and blood pressure by using data from NHANES II. Sorel et al. (1991) reported age-adjusted BLLs of 13.2 μg/dL in black females, 12.1 μg/dL in white females, 20.1 μg/dL in black males, and 16.8 μg/dL in white males. They fitted linear BLL, but Schwartz (1991) constructed a log-linear model (natural log-transformation). Linear BLL was significantly associated with DBP only in males (β = 0.13 mm Hg; 95% CI: 0.04, 0.21, for every 1 μg/dL) (Sorel et al. 1991), whereas log-linear BLL was significantly



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