ABSTRACT
OBJECTIVES: The aim of this study is to determine the association between length of time in the USA with blood lead (BPb). DESIGN: Population-based cross-sectional study using data from the 2013-2016 National Health and Nutrition Examination Survey. SETTING: USA. PARTICIPANTS: 5933 men and women (≥15 years); subgroups of men only (n=2867), women only (n=3064) and women of childbearing age (15-45 years) (n=1580). PRIMARY AND SECONDARY OUTCOMES: The primary outcome was BPb concentration. The main exposure variable was self-reported number of years spent in the USA, categorised as: born in the USA; 0-4 years; 5-9 years; 10-19 years and ≥20 years. We used linear regression models adjusted for race/ethnicity, education, blood cotinine, age, sex (as appropriate) and accounted for complex survey design. RESULTS: Women of childbearing age who have lived 0-4 years in the USA have, on average, a 54% (95% CI 36% to 75%) higher BPb compared with women born in the USA. Corresponding results for all women, men and the entire population were 49% (95% CI 34% to 66%), 49% (95% CI 28% to 75%) and 49% (95% CI 33% to 66%), respectively. Similar, statistically significant, results were observed for other time periods (5-9 years, 10-19 years and ≥20 years); the magnitude of the association decreased with increasing time in the USA. CONCLUSIONS: This study provides additional evidence that newcomers to the USA may be a population at higher risk of elevated BPb.
Subject(s)
Lead Poisoning/blood , Lead/blood , Nutrition Surveys/methods , Self Report , Adolescent , Adult , Child , Child, Preschool , Cross-Sectional Studies , Female , Humans , Incidence , Infant , Infant, Newborn , Lead Poisoning/epidemiology , Male , Mass Spectrometry , Middle Aged , Retrospective Studies , Time Factors , United States/epidemiology , Young AdultABSTRACT
BACKGROUND: Previous studies suggest that cumulative lead exposure is associated with cognitive decline, but its relation with Alzheimer's disease (AD) remains unclear. Therefore, this study investigated the longitudinal association between blood lead level (BLL) and AD mortality. METHODS: This study included 8,080 elders (60 years or older) with BLL data from the 1999 to 2008 US National Health and Nutrition Examination Survey. Mortality was determined from linked 1999-2014 National Death Index data. A causal diagram presented causal assumptions and identified a sufficient set of confounders: age, sex, poverty, race/ethnicity, and smoking. Cox proportional hazard models were used to determine the association between BLL and subsequent AD mortality. Impacts of competing risks and design effect were also assessed. Adjusted hazard rate ratio (HRR) and 95% confidence interval (CI) were reported. RESULTS: Follow-up ranged from <1 to 152 months (median, 74). Eighty-one participants died from AD over 632,075 total person-months at risk. An increase in BLL was associated with an increase in AD mortality after adjusting for identified confounders. We estimated that those with BLL of 1.5 and 5 µg/dl had 1.2 (95% CI = 0.70, 2.1) and 1.4 (95% CI = 0.54, 3.8) times the rate of AD mortality compared to those with BLL of 0.3 µg/dl, respectively, after accounting for competing risks. Adjusted HRRs were 1.5 (95% CI = 0.81, 2.9) and 2.1 (95% CI = 0.70, 6.3), respectively, after considering design effect. CONCLUSIONS: This longitudinal study demonstrated a positive, albeit not statistically significant, association between BLL and AD mortality after adjustment for competing risks or design effect.
