Ning Ding1, Xin Wang1, Katherine L Tucker2, Marc G Weisskopf3, David Sparrow4, Howard Hu5, Sung Kyun Park6. 1. Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA. 2. Department of Clinical Laboratory and Nutritional Sciences, University of Massachusetts at Lowell, Lowell, MA, USA. 3. Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA. 4. Normative Aging Study, Veterans Affairs Boston Healthcare System, and Department of Medicine, Boston University School of Medicine, Boston, MA, USA. 5. School of Public Health, University of Washington, Seattle, WA, USA. 6. Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA; Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA. Electronic address: sungkyun@umich.edu.
Abstract
BACKGROUND: Most absorbed lead ends up in the bone, where it can be measured as a biomarker of cumulative exposure, elevations of which have been shown to predict a higher risk of coronary heart disease (CHD). Knowledge about the role of dietary patterns is critical to the development of effective interventions for the cardiovascular toxicity of cumulative lead exposure. METHODS: 594 men, free of CHD at baseline, were followed from August 1991 to June 2011 in the Normative Aging Study. Bone lead concentrations were measured by K-shell-X-ray fluorescence. Dietary patterns were identified using principal components analysis. Two dietary patterns were identified: a 'prudent' pattern characterized by high intake of fruit, vegetables, legumes, tomatoes, poultry, and seafood; and a 'Western' pattern, with high intake of red meat, processed meat, refined grains, high-fat dairy products, high-energy drinks, fries, butter and eggs. Cox proportional hazard models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CHD. Effect modification on the multiplicative scale was examined through cross-product interaction terms. RESULTS: 137 men developed incident CHD events during 5071 person-years of follow-up. After adjusting for age, body mass index, total energy intake, smoking status, total cholesterol to high-density lipoprotein ratio, education and occupation, an HR of incident CHD was 1.64 (95% CI: 1.27-2.11) with each doubling in patella lead concentration in the low prudent diet group (< median prudent score); and the HR decreased to 1.07 (95% CI: 0.86-1.34) in the high prudent diet (≥ median prudent score) (p-for-interaction = 0.01), suggesting protective effects of prudent diet against lead-related CHD. By contrast, the association between tibia lead and CHD was non-significantly larger in the low Western diet group (HR = 1.43, 95% CI: 1.14-1.80) compared with the high Western diet group (HR = 1.08, 95% CI: 0.86-1.34) (p-for-interaction = 0.06). No significant effect modifications were detected by Western diet in the patella lead-CHD association and by prudent diet in the tibia lead-CHD association. CONCLUSIONS: Prudent diet may reduce the risk of development of CHD in relation to patella lead. However, these findings need to be interpreted with caution, given the modest sample size.
BACKGROUND: Most absorbed lead ends up in the bone, where it can be measured as a biomarker of cumulative exposure, elevations of which have been shown to predict a higher risk of coronary heart disease (CHD). Knowledge about the role of dietary patterns is critical to the development of effective interventions for the cardiovascular toxicity of cumulative lead exposure. METHODS: 594 men, free of CHD at baseline, were followed from August 1991 to June 2011 in the Normative Aging Study. Bone lead concentrations were measured by K-shell-X-ray fluorescence. Dietary patterns were identified using principal components analysis. Two dietary patterns were identified: a 'prudent' pattern characterized by high intake of fruit, vegetables, legumes, tomatoes, poultry, and seafood; and a 'Western' pattern, with high intake of red meat, processed meat, refined grains, high-fat dairy products, high-energy drinks, fries, butter and eggs. Cox proportional hazard models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CHD. Effect modification on the multiplicative scale was examined through cross-product interaction terms. RESULTS: 137 men developed incident CHD events during 5071 person-years of follow-up. After adjusting for age, body mass index, total energy intake, smoking status, total cholesterol to high-density lipoprotein ratio, education and occupation, an HR of incident CHD was 1.64 (95% CI: 1.27-2.11) with each doubling in patella lead concentration in the low prudent diet group (< median prudent score); and the HR decreased to 1.07 (95% CI: 0.86-1.34) in the high prudent diet (≥ median prudent score) (p-for-interaction = 0.01), suggesting protective effects of prudent diet against lead-related CHD. By contrast, the association between tibia lead and CHD was non-significantly larger in the low Western diet group (HR = 1.43, 95% CI: 1.14-1.80) compared with the high Western diet group (HR = 1.08, 95% CI: 0.86-1.34) (p-for-interaction = 0.06). No significant effect modifications were detected by Western diet in the patella lead-CHD association and by prudent diet in the tibia lead-CHD association. CONCLUSIONS: Prudent diet may reduce the risk of development of CHD in relation to patella lead. However, these findings need to be interpreted with caution, given the modest sample size.
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