Blood Lead Levels and Death from Cardiovascular Disease and Cancer
Blood Lead Levels and Death from Cardiovascular Disease and Cancer
Background: Analyses of mortality data for participants examined in 1976-1980 in the second National Health and Nutrition Examination Survey (NHANES II) suggested an increased risk of mortality at blood lead levels > 20 µg/dL. Blood lead levels have decreased markedly since the late 1970s. In NHANES III, conducted during 1988-1994, few adults had levels > 20 µg/dL.
Objective: Our objective in this study was to determine the risk of mortality in relation to lower blood lead levels observed for adult participants of NHANES III.
Methods: We analyzed mortality information for 9,757 participants who had a blood lead measurement and who were ≥ 40 years of age at the baseline examination. Using blood lead levels categorized as < 5, 5 to < 10, and ≥ 10 µg/dL, we determined the relative risk of mortality from all causes, cancer, and cardiovascular disease through Cox proportional hazard regression analysis.
Results: Using blood lead levels < 5 µg/dL as the referent, we determined that the relative risk of mortality from all causes was 1.24 [95% confidence interval (CI) , 1.05-1.48] for those with blood levels of 5-9 µg/dL and 1.59 (95% CI, 1.28-1.98) for those with blood levels ≥ 10 µg/dL (p for trend < 0.001) . The magnitude of risk was similar for deaths due to cardiovascular disease and cancer, and tests for trend were statistically significant (p < 0.01) for both causes of death.
Conclusion: In a nationally representative sample of the U.S. population, blood lead levels as low as 5-9 µg/dL were associated with an increased risk of death from all causes, cardiovascular disease, and cancer.
Toxic effects of exposure to high levels of lead among adults in occupational settings and from poisonings include neurologic and renal impairment as well as effects on other organ systems [Agency for Toxic Substances and Disease Registry (ATSDR) 1999]. Environmental exposure to lead-exposure much lower than that found in occupational settings-is associated with long-term adverse effects, particularly on blood pressure (Cheng et al. 2001; Glenn et al. 2003; Hertz-Picciotto and Croft 1992; Hu et al. 1996; Moller and Kristensen 1992; Nash et al. 2003), renal function (Kim et al. 1996; Muntner et al. 2003; Payton et al. 1994; Staessen et al. 1992; Tsaih et al. 2004), and cognition (Payton et al. 1998; Weisskopf et al. 2004; Wright et al. 2003). Recent reports suggest that even blood lead levels that are currently typical in the U.S. population are associated with renal dysfunction (Muntner et al. 2005) and peripheral arterial disease (Muntner et al. 2005; Navas-Acien et al. 2004). Lead and lead compounds are reasonably anticipated to be human carcinogens based on evidence from occupational mortality and animal studies [National Toxicology Program (NTP) 2005].
Lead exposure declined dramatically beginning in the late 1970s largely because of mandated removal of lead from gasoline, from paint, and to a lesser extent, from solder used in cans (Annest et al. 1983; Pirkle et al. 1994). Blood lead measurements from the National Health and Nutrition Examination Surveys (NHANES) have provided documentation of lead exposure in the U.S. population beginning with data from NHANES II conducted during 1976-1980. Among person 1-74 years of age, the geometric mean of blood lead level dropped from 12.8 µg/dL in 1976-1980 to 2.8 µg/dL in 1988-1991 (Annest et al. 1983), and to 2.3 µg/dL in 1991-1994 [Centers for Disease Control and Prevention (CDC) 1997].
Analyses of mortality follow-up data for participants of NHANES II suggested an increased risk of mortality at blood lead levels > 20 µg/dL (Jemal et al. 2002; Lustberg and Silbergeld 2002). Mortality follow-up through the year 2000 is now available for NHANES III participants. The purpose of our study was to examine the risk of mortality from all causes, cardiovascular disease, and cancer in relation to blood lead levels observed for adult participants of NHANES III.
Background: Analyses of mortality data for participants examined in 1976-1980 in the second National Health and Nutrition Examination Survey (NHANES II) suggested an increased risk of mortality at blood lead levels > 20 µg/dL. Blood lead levels have decreased markedly since the late 1970s. In NHANES III, conducted during 1988-1994, few adults had levels > 20 µg/dL.
Objective: Our objective in this study was to determine the risk of mortality in relation to lower blood lead levels observed for adult participants of NHANES III.
Methods: We analyzed mortality information for 9,757 participants who had a blood lead measurement and who were ≥ 40 years of age at the baseline examination. Using blood lead levels categorized as < 5, 5 to < 10, and ≥ 10 µg/dL, we determined the relative risk of mortality from all causes, cancer, and cardiovascular disease through Cox proportional hazard regression analysis.
Results: Using blood lead levels < 5 µg/dL as the referent, we determined that the relative risk of mortality from all causes was 1.24 [95% confidence interval (CI) , 1.05-1.48] for those with blood levels of 5-9 µg/dL and 1.59 (95% CI, 1.28-1.98) for those with blood levels ≥ 10 µg/dL (p for trend < 0.001) . The magnitude of risk was similar for deaths due to cardiovascular disease and cancer, and tests for trend were statistically significant (p < 0.01) for both causes of death.
Conclusion: In a nationally representative sample of the U.S. population, blood lead levels as low as 5-9 µg/dL were associated with an increased risk of death from all causes, cardiovascular disease, and cancer.
Toxic effects of exposure to high levels of lead among adults in occupational settings and from poisonings include neurologic and renal impairment as well as effects on other organ systems [Agency for Toxic Substances and Disease Registry (ATSDR) 1999]. Environmental exposure to lead-exposure much lower than that found in occupational settings-is associated with long-term adverse effects, particularly on blood pressure (Cheng et al. 2001; Glenn et al. 2003; Hertz-Picciotto and Croft 1992; Hu et al. 1996; Moller and Kristensen 1992; Nash et al. 2003), renal function (Kim et al. 1996; Muntner et al. 2003; Payton et al. 1994; Staessen et al. 1992; Tsaih et al. 2004), and cognition (Payton et al. 1998; Weisskopf et al. 2004; Wright et al. 2003). Recent reports suggest that even blood lead levels that are currently typical in the U.S. population are associated with renal dysfunction (Muntner et al. 2005) and peripheral arterial disease (Muntner et al. 2005; Navas-Acien et al. 2004). Lead and lead compounds are reasonably anticipated to be human carcinogens based on evidence from occupational mortality and animal studies [National Toxicology Program (NTP) 2005].
Lead exposure declined dramatically beginning in the late 1970s largely because of mandated removal of lead from gasoline, from paint, and to a lesser extent, from solder used in cans (Annest et al. 1983; Pirkle et al. 1994). Blood lead measurements from the National Health and Nutrition Examination Surveys (NHANES) have provided documentation of lead exposure in the U.S. population beginning with data from NHANES II conducted during 1976-1980. Among person 1-74 years of age, the geometric mean of blood lead level dropped from 12.8 µg/dL in 1976-1980 to 2.8 µg/dL in 1988-1991 (Annest et al. 1983), and to 2.3 µg/dL in 1991-1994 [Centers for Disease Control and Prevention (CDC) 1997].
Analyses of mortality follow-up data for participants of NHANES II suggested an increased risk of mortality at blood lead levels > 20 µg/dL (Jemal et al. 2002; Lustberg and Silbergeld 2002). Mortality follow-up through the year 2000 is now available for NHANES III participants. The purpose of our study was to examine the risk of mortality from all causes, cardiovascular disease, and cancer in relation to blood lead levels observed for adult participants of NHANES III.
