Cumulative lead exposure and prospective change in cognition among elderly men: the VA Normative Aging Study

Lead exposure has been found to affect cognitive function in several different populations. Whether chronic low-level environmental exposure to lead results in cognitive decline among adults has not been examined. The authors assessed the relation between biomarkers of lead exposure and change in Mini-Mental State Examination (MMSE) scores in the Normative Aging Study, a cohort of elderly US men. Bone lead was measured with K-shell x-ray fluorescence. A total of 466 men aged 67.4 (standard deviation, 6.6) years took the MMSE on two occasions that were an average of 3.5 (standard deviation, 1.1) years apart during the period 1993-2001 and had bone lead concentrations measured during the period 1991-2002. A one-interquartile range (20 microg/g of bone mineral) higher patella bone lead concentration was associated with a change in MMSE score of -0.24 (95% confidence interval: -0.44, -0.05) after adjustment for age, education, smoking, alcohol intake, and time between MMSE tests. This effect is approximately equivalent to that of aging 5 years in relation to the baseline MMSE score in study data. The association with tibia lead was weaker and that with blood lead was absent. The data suggest that higher patella bone lead levels, a marker of mobilizable accumulated lead burden, are associated with a steeper decline over time in performance on the MMSE test among nonoccupationally exposed elderly men.     

Total homocysteine and cognitive decline in a community-based sample of elderly subjects: the Rotterdam Study.

Homocysteine has been associated with an increased risk of cardiovascular disease. Cardiovascular diseases have been related to cognitive decline. The authors investigated the association of homocysteine with concurrent cognitive impairment and subsequent cognitive decline in a random sample of 702 community-dwelling respondents aged 55 years or over to the prospective Rotterdam Study in 1990-1994. Multiple logistic regression was used to calculate odds ratios and 95 percent confidence intervals for the association between total homocysteine levels and cognitive impairment (Mini-Mental State Examination (MMSE) score <26) and cognitive decline (drop in MMSE score of >1 point/year). Mean duration of follow-up was 2.7 years. After adjustment for age, sex, and education, there was no relation between total homocysteine and cognitive impairment (highest vs. lowest tertile: odds ratio (OR) = 1.30, 95% confidence interval (CI): 0.50, 3.38) or cognitive decline (middle vs. lowest tertile: OR = 1.14, 95% CI: 0.67, 1.93; highest vs. lowest tertile: OR = 0.91, 95% CI: 0.52, 1.58). Subjects who were lost to follow-up due to death or nonresponse had slightly higher age-adjusted homocysteine levels and lower MMSE scores at baseline. Sensitivity analyses showed that selective loss to follow-up was not a likely explanation for the absence of an association in the participants. Although a relation between homocysteine and reduced cognitive function is biologically plausible, this study suggests no such association in a community-based sample of the elderly.     

Modifying effects of the HFE polymorphisms on the association between lead burden and cognitive decline

BACKGROUND: As iron and lead promote oxidative damage, and hemochromatosis (HFE) gene polymorphisms increase body iron burden, HFE variant alleles may modify the lead burden and cognitive decline relationship. OBJECTIVE: Our goal was to assess the modifying effects of HFE variants on the lead burden and cognitive decline relation in older adults. METHODS: We measured tibia and patella lead using K-X-ray fluorescence (1991-1999) among participants of the Normative Aging Study, a longitudinal study of community-dwelling men from greater Boston. We assessed cognitive function with the Mini-Mental State Examination (MMSE) twice (1993-1998 and 1995-2000) and genotyped participants for HFE polymorphisms. We estimated the adjusted mean differences in lead-associated annual cognitive decline across HFE genotype groups (n = 358). RESULTS: Higher tibia lead was associated with steeper cognitive decline among participants with at least one HFE variant allele compared with men with only wild-type alleles (p interaction = 0.03), such that a 15 microg/g increase in tibia lead was associated with a 0.2 point annual decrement in MMSE score among HFE variant allele carriers. This difference in scores among men with at least one variant allele was comparable to the difference in baseline MMSE scores that we observed among men who were 4 years apart in age. Moreover, the deleterious association between tibia lead and cognitive decline appeared progressively worse in participants with increasingly more copies of HFE variant alleles (p-trend = 0.008). Results for patella lead were similar. CONCLUSION: Our findings suggest that HFE polymorphisms greatly enhance susceptibility to lead-related cognitive impairment in a pattern consistent with allelelic dose.     

Comparison of patella lead with blood lead and tibia lead and their associations with neurobehavioral test scores

OBJECTIVE: Lead exposure in adults is associated with worse cognitive function in cross-sectional and longitudinal studies. Previous studies have mainly examined relations with blood lead or cortical bone lead; few have examined trabecular bone lead. METHODS: We performed a cross-sectional analysis of the relations of patella lead and other lead biomarkers with measures of neurobehavioral and peripheral nervous system function in 652 lead workers. RESULTS: Patella lead was found to be associated with worse performance on seven of 19 tests of manual dexterity, sensory vibration threshold, and depressive symptoms. The associations of patella lead with cognitive function were essentially similar to those with blood lead or tibia lead but of somewhat lower magnitude. CONCLUSIONS: In this study, measurement of patella lead did not aid causal inference regarding cognitive effects when compared with blood lead and tibia lead.     

Delta-aminolevulinic acid dehydratase polymorphism and the relation between low level lead exposure and the Mini-Mental Status Examination in older men: the Normative Aging Study

Objective

To determine whether a polymorphism the in δ‐aminolevulinic acid dehydratase (ALAD) gene modifies the neurotoxicity of lead in older adults.

Methods

The authors studied men participating in the Department of Veterans Affairs'' Normative Aging Study, assessing their recent exposure to lead by measuring blood lead (n = 915) at each triennial clinic visit, and, beginning in 1991, assessing their cumulative exposure by measuring lead levels in tibia (n = 722) and patella (n = 720), using K‐shell x ray fluorescence. Starting in 1993 and again at each triennial visit, the authors administered the Mini‐Mental State Examination (MMSE) to assess their cognitive functioning. The relation of the lead biomarkers to MMSE score was evaluated and this association was compared among men who carried the variant allele, ALAD‐2, versus men without the allele.

Results

Sixteen per cent of men carried the ALAD‐2 allele. Median tibia and patella lead levels (first‐third quartile) were 19 (13–28) and 27 (18–39) μg/g. Blood lead levels were consistent with non‐occupational exposure: only 6% of men had levels ⩾10 μg/dl. In multivariable adjusted analyses, higher levels of blood lead were associated with poorer performance on the MMSE. This association was most pronounced among ALAD‐2 carriers, among whom a 3 μg/dl increment in blood lead (the interquartile range) was associated with a 0.26 point lower mean MMSE score (95% CI −0.54 to 0.01), compared with a 0.04 point lower score (95% CI −0.16 to 0.07) among non‐carriers. The modest 0.22 point difference in these associations did not attain statistical significance, however (p_interaction = 0.13). The associations between bone lead levels and MMSE score did not vary by ALAD‐2 status.

Conclusions

Although not statistically significant, these findings suggest that ALAD genotype may modify blood lead''s adverse association with cognition among older men who had community exposures to lead. However, despite a relatively large sample size and the use of sensitive methods for measuring lead burden, the evidence overall was fairly weak.     

Dietary and environmental determinants of blood and bone lead levels in lactating postpartum women living in Mexico City.

Despite the recent declines in environmental lead exposure in the United States and Mexico, the potential for delayed toxicity from bone lead stores remains a significant public health concern. Some evidence indicates that mobilization of lead from bone may be markedly enhanced during the increased bone turnover of pregnancy and lactation, resulting in lead exposure to the fetus and the breast-fed infant. We conducted a cross-sectional investigation of the interrelationships between environmental, dietary, and lifestyle histories, blood lead levels, and bone lead levels among 98 recently postpartum women living in Mexico City. Lead levels in the patella (representing trabecular bone) and tibia (representing cortical bone) were measured by K X-ray fluorescence (KXRF). Multivariate linear regression models showed that significant predictors of higher blood lead included a history of preparing or storing food in lead-glazed ceramic ware, lower milk consumption, and higher levels of lead in patella bone. A 34 micrograms/g increase in patella lead (from the medians of the lowest to the highest quartiles) was associated with an increase in blood lead of 2.4 micrograms/dl. Given the measurement error associated with KXRF and the extrapolation of lead burden from a single bone site, this contribution probably represents an underestimate of the influence of trabecular bone on blood lead. Significant predictors of bone lead in multivariate models included years living in Mexico City, lower consumption of high calcium content foods, and nonuse of calcium supplements for the patella and years living in Mexico City, older age, and lower calcium intake for tibia bone. Low consumption of milk and cheese, as compared to the highest consumption category (every day), was associated with an increase in tibia bone lead of 9.7 micrograms Pb/g bone mineral. The findings of this cross-sectional study suggest that patella bone is a significant contributor to blood lead during lactation and that consumption of high calcium content foods may protect against the accumulation of lead in bone.     

Proton magnetic resonance spectroscopic evidence of glial effects of cumulative lead exposure in the adult human hippocampus

BACKGROUND: Exposure to lead is known to have adverse effects on cognition in several different populations. Little is known about the underlying structural and functional correlates of such exposure in humans. OBJECTIVES: We assessed the association between cumulative exposure to lead and levels of different brain metabolite ratios in vivo using magnetic resonance spectroscopy (MRS). METHODS: We performed MRS on 15 men selected from the lowest quintile of patella bone lead within the Department of Veterans Affairs' Normative Aging Study (NAS) and 16 from the highest to assess in the hippocampal levels of the metabolites N-acetylaspartate, myoinositol, and choline, each expressed as a ratio with creatine. Bone lead concentrations-indicators of cumulative lead exposure-were previously measured using K-X-ray fluorescence spectroscopy. MRS was performed on the men from 2002 to 2004. RESULTS: A 20-microg/g bone and 15-microg/g bone higher patella and tibia bone lead concentration--the respective interquartile ranges within the whole NAS--were associated with a 0.04 [95% confidence interval (CI), 0.00-0.08; p = 0.04] and 0.04 (95% CI, 0.00-0.08; p = 0.07) higher myoinositol-to-creatine ratio in the hippocampus. After accounting for patella bone lead declines over time, analyses adjusted for age showed that the effect of a 20-microg/g bone higher patella bone lead level doubled (0.09; 95% CI, 0.01-0.17; p = 0.03). CONCLUSIONS: Cumulative lead exposure is associated with an increase in the myinositol-to-creatine ratio. These data suggest that, as assessed with MRS, glial effects may be more sensitive than neuronal effects as an indicator of cumulative exposure to lead in adults.     

Cumulative Lead Exposure and Age at Menopause in the Nurses’ Health Study Cohort

Background: Early menopause has been associated with many adverse health outcomes, including increased risk of cardiovascular disease morbidity and mortality. Lead has been found to be adversely associated with female reproductive function, but whether exposures experienced by the general population are associated with altered age at menopause has not been explored.Objective: Our goal was to assess the association between cumulative lead exposure and age at natural menopause.Methods: Self-reported menopausal status and bone lead concentration measured with K-shell X-ray fluorescence—a biomarker of cumulative lead exposure—were obtained from 434 women participants in the Nurses’ Health Study.Results: The mean (± SD) age at natural menopause was 50.8 ± 3.6 years. Higher tibia lead level was associated with younger age at menopause. In adjusted analyses, the average age of menopause for women in the highest tertile of tibia lead was 1.21 years younger (95% CI: –2.08, –0.35) than for women in the lowest tertile (p-trend = 0.006). Although the number of cases was small (n = 23), the odds ratio for early menopause (< 45 years of age) was 5.30 (95% CI: 1.42, 19.78) for women in the highest tertile of tibia lead compared with those in the lowest tertile (p-trend = 0.006). There was no association between patella or blood lead and age at menopause.Conclusions: Our results support an association between low-level cumulative lead exposure and an earlier age at menopause. These data suggest that low-level lead exposure may contribute to menopause-related health outcomes in older women through effects on age at menopause.Citation: Eum KD, Weisskopf MG, Nie LH, Hu H, Korrick SA. 2014. Cumulative lead exposure and age at menopause in the Nurses’ Health Study Cohort. Environ Health Perspect 122:229–234; http://dx.doi.org/10.1289/ehp.1206399     

Associations of bone mineral density and lead levels in blood, tibia, and patella in urban-dwelling women

OBJECTIVE: The objective of this study was to evaluate the relations between bone mineral density (BMD) and lead in blood, tibia, and patella and to investigate how BMD modifies these lead biomarkers in older women. DESIGN: In this study, we used cross-sectional analysis. PARTICIPANTS: We studied 112 women, 50-70 years of age, including both whites and African Americans, residing in Baltimore, Maryland. MEASUREMENTS: We measured lumbar spine BMD, blood and bone lead by dual energy X-ray absorptiometry, anodic stripping voltammetry, and (109)Cd-induced K-shell X-ray fluorescence, respectively. We measured vitamin D receptor and apolipoprotein E (APOE) genotypes using standard methods. RESULTS: Mean (+/- SD) BMD and lead levels in blood, tibia, and patella were 1.02+/-0.16 g/cm(2), 3.3+/-2.2 microg/dL, 19.7+/-13.2 microg/g, and 5.7+/-15.3 microg/g, respectively. In adjusted analysis, higher BMD was associated with higher tibia lead levels (p=0.03). BMD was not associated with lead levels in blood or patella. There was evidence of significant effect modification by BMD on relations of physical activity with blood lead levels and by APOE genotype on relations of BMD with tibia lead levels. There was no evidence that BMD modified relations between tibia lead or patella lead and blood lead levels. CONCLUSIONS: We believe that BMD represents the capacity of bone that can store lead, by substitution for calcium, and thus the findings may have relevance for effect-size estimates in persons with higher BMD. RELEVANCE TO CLINICAL PRACTICE: The results have implications for changes in lead kinetics with aging, and thus the related risk of health effects associated with substantial early- and midlife lead exposure in older persons.     

Predictors of plasma lead among lithographic print shop workers in Mexico City

BACKGROUND: Plasma lead is considered a biological marker that reflects the fraction of lead in blood that is toxicologically available. We examined the relationship between plasma lead and other biomarkers of lead exposure in 69 lithographic print shop workers. METHODS: Lead was measured in plasma and whole blood (by inductively coupled plasma-magnetic sector mass spectrometry), in bone (by 109Cd X-ray fluorescence), and in hand wipes and occupational air samples. Personal hygiene habits at work were surveyed. RESULTS: Mean age was 47 years and 86% (n=59) were men. Mean lead levels were 0.3 microg/L in plasma, 11.9 microg/dL in blood, 46.7 microg/g in patella, and 27.6 microg/g in tibia. Taken together, two multivariate linear models explained 57% of variability in plasma lead levels. Predictors for the first model were lead in patella (beta = 0.006), blood (beta = 0.008), and hygiene index (beta = -0.11). Predictors for the second model were lead in tibia (beta = 0.008), blood (beta = 0.008), and hygiene index (beta = -0.13). CONCLUSIONS: This study demonstrates that accumulated bone stores and hygiene habits are both significant independent predictors of plasma lead levels in active workers at this print shop.     

Lead exposure and amyotrophic lateral sclerosis

BACKGROUND: Previous interview-based studies have suggested that exposure to neurotoxicants including metals might be related to ALS. METHODS: We evaluated the relation of lead exposure to ALS, using both biological measures and interviews, in a case-control study conducted in New England from 1993 to 1996. Cases (N = 109) were recruited at two hospitals in Boston, MA. Population controls (N = 256) identified by random-digit dialing were frequency-matched to cases by age, sex, and region of residence within New England. RESULTS: Risk of ALS was associated with self-reported occupational exposure to lead (odds ratio [OR] = 1.9; 95% confidence interval [CI] = 1.1-3.3), with a dose response for lifetime days of lead exposure. Blood and bone lead levels were measured in most cases (N = 107) and in a subset of controls (N = 41). Risk of ALS was associated with elevations in both blood and bone lead levels. ORs were 1.9 (95% CI = 1.4-2.6) for each microg/dl increase in blood lead, 3.6 (95% CI = 0.6-20.6) for each unit increase in log-transformed patella lead, and 2.3 (95% CI = 0.4-14.5) for each unit increase in log-transformed tibia lead. CONCLUSIONS: These results are consistent with previous reports and suggest a potential role for lead exposure in the etiology of ALS.     

Very low maternal lead level in pregnancy and birth outcomes in an eastern Massachusetts population

PurposeMaternal lead exposure is associated with poor birth outcomes in populations with moderate to high blood levels. However, no studies have looked at exposure levels commonly experienced by US women.MethodsWe evaluated the relationship between maternal red blood cell (RBC) lead levels in midpregnancy and birth outcomes in 949 mother–child pairs in a prebirth cohort. We used multiple linear regression and logistic regression, adjusted for potential confounders including maternal age, race, prepregnancy body mass index, and smoking to relate maternal lead to infant birth size and risk for preterm birth (<37 weeks).ResultsMean RBC lead level was 1.2 μg/dL (range, 0.0–5.0). Mean (standard deviation) birthweight was 3505 (520) g, birthweight for gestational age z-score 0.22 (0.93), and length of gestation 39.5 (1.7) weeks. Mothers in the highest versus lowest lead quartile did not have higher odds (OR, 1.85; 95% confidence interval [CI], 0.79–4.34) of preterm delivery; after stratifying by child sex, there was an association among males (OR, 5.51; 95% CI, 1.21–25.15) but not females (OR, 0.82; 95% CI, 0.24–2.85). Maternal RBC lead was not associated with any continuous outcomes in combined or sex-stratified analyses.ConclusionsMaternal lead exposure, even at very low levels, may adversely affect some childbirth outcomes, particularly preterm birth among males.     

Chronic air pollution exposure during pregnancy and maternal and fetal C-reactive protein levels: the Generation R Study

Background: Exposure to air pollution has been associated with higher C-reactive protein (CRP) levels, suggesting an inflammatory response. Not much is known about this association in pregnancy.Objectives: We investigated the associations of air pollution exposure during pregnancy with maternal and fetal CRP levels in a population-based cohort study in the Netherlands.Methods: Particulate matter (PM) with an aerodynamic diameter ≤ 10 μm (PM₁₀) and nitrogen dioxide (NO₂) levels were estimated at the home address using dispersion modeling for different averaging periods preceding the blood sampling (1 week, 2 weeks, 4 weeks, and total pregnancy). High-sensitivity CRP levels were measured in maternal blood samples in early pregnancy (n = 5,067) and in fetal cord blood samples at birth (n = 4,450).Results: Compared with the lowest quartile, higher PM₁₀ exposure levels for the prior 1 and 2 weeks were associated with elevated maternal CRP levels (> 8 mg/L) in the first trimester [fourth PM₁₀ quartile for the prior week: odds ratio (OR), 1.32; 95% confidence interval (CI): 1.08, 1.61; third PM₁₀ quartile for the prior 2 weeks: OR, 1.28; 95% CI: 1.06, 1.56]; however, no clear dose–response relationships were observed. PM₁₀ and NO₂ exposure levels for 1, 2, and 4 weeks preceding delivery were not consistently associated with fetal CRP levels at delivery. Higher long-term PM₁₀ and NO₂ exposure levels (total pregnancy) were associated with elevated fetal CRP levels (> 1 mg/L) at delivery (fourth quartile PM₁₀: OR, 2.18; 95% CI: 1.08, 4.38; fourth quartile NO₂: OR, 3.42; 95% CI: 1.36, 8.58; p-values for trend < 0.05).Conclusions: Our results suggest that exposure to air pollution during pregnancy may lead to maternal and fetal inflammatory responses.     

Association of Osteoarthritis with Perfluorooctanoate and Perfluorooctane Sulfonate in NHANES 2003–2008

Background: Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are persistent, synthetic industrial chemicals. Perfluorinated compounds are linked to health impacts that may be relevant to osteoarthritis, cartilage repair, and inflammatory responses.Objectives: We investigated whether PFOA and PFOS exposures are associated with prevalence of osteoarthritis, and whether associations differ between men and women.Methods: We used multiple logistic regression to estimate associations between serum PFOA and PFOS concentrations and self-reported diagnosis of osteoarthritis in persons 20–84 years of age who participated in NHANES during 2003–2008. We adjusted for potential confounders including age, income, and race/ethnicity. Effects by sex were estimated using stratified models and interaction terms.Results: Those in the highest exposure quartile had higher odds of osteoarthritis compared with those in the lowest quartile [odds ratio (OR) for PFOA = 1.55; 95% CI: 0.99, 2.43; OR for PFOS = 1.77; 95% CI: 1.05, 2.96]. When stratifying by sex, we found positive associations for women, but not men. Women in the highest quartiles of PFOA and PFOS exposure had higher odds of osteoarthritis compared with those in the lowest quartiles (OR for PFOA = 1.98; 95% CI: 1.24, 3.19 and OR for PFOS = 1.73; 95% CI: 0.97, 3.10).Conclusions: Higher concentrations of serum PFOA were associated with osteoarthritis in women, but not men. PFOS was also associated with osteoarthritis in women only, though effect estimates for women were not significant. More research is needed to clarify potential differences in susceptibility between women and men with regard to possible effects of these and other endocrine-disrupting chemicals.     

Screening housing to prevent lead toxicity in children

OBJECTIVE: Screening children to identify those with blood lead levels > or = 10 microg/dl fails to protect children from lead-associated cognitive deficits and behavioral problems. To broaden our efforts at primary prevention, screening criteria are needed to identify lead-contaminated housing before children are unduly exposed. The purpose of this study was to identify and validate housing characteristics associated with children having elevated blood lead levels (> or = 10 microg/dl). METHODS: Two existing studies were used to examine housing characteristics linked with undue lead exposure: a cross-sectional study of 205 children aged 12 to 31 months, and a random sample from a longitudinal study of 276 children followed from 6 to 24 months of age. Logistic regression analysis was conducted to examine the association of children's blood lead levels > or = 10 microg/dl. RESULTS: The mean age of the 481 children was 17.8 months; 99 (20.6%) had a blood lead concentration of 10 microg/dl or higher. The following characteristics were associated with blood lead concentration > or = 10 microg/dl: floor lead loading > 15 microg/ft2 (odds ratio [OR]=2.2; 95% confidence interval [CI] 1.3, 3.8); rental housing (OR=3.2; 95% CI 1.3, 7.6); poor housing condition (OR=2.1; CI 1.2, 3.6); African American race (OR=3.3; CI 1.9, 6.1); paint chip ingestion (OR=5.8; CI 1.3, 26.5); and soil ingestion (OR=2.2; CI 1.1, 4.2). Housing characteristics including rental status, lead-contaminated floor dust, and housing condition had a range of sensitivity from 47% to 92%; specificity from 28% to 76%; a positive predictive value from 25% to 34%; and a negative predictive value of 85% to 93%. CONCLUSIONS: Housing characteristics and floor dust lead levels can be used to screen housing to identify lead hazards prior to occupancy, before purchasing a home, or after renovation to prevent children's exposure to lead hazards.     

Lead concentrations in relation to multiple biomarkers of cardiovascular disease: the Normative Aging Study

Background: Lead exposure has been associated with cardiovascular disease (CVD) in animal and human studies. However, the mechanisms of action have not been fully elucidated. We therefore examined the relationship between lead and multiple biomarkers of CVD.Methods: Participants were older men from the Normative Aging Study without preexisting coronary heart disease, diabetes, or active infection at baseline (n = 426). Serum biomarkers included lipid profile [total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides] and inflammatory markers [C-reactive protein, intercellular adhesion molecule-1, interleukin-6, and tumor necrosis factor receptor-2 (TNF-R2)]. We measured lead in blood and in bone by K-shell X-ray fluorescence. In this sample, 194 men (44.3%) had two or more repeated measures, resulting in 636 observations for analysis. We conducted analyses using mixed effects models with random subject intercepts.Results: Lead levels were associated with several CVD biomarkers, including levels of TNF-R2 and lipid markers. Specifically, in multivariable models, a 50% increase in blood lead level was associated with 26% increased odds of high TNF-R2 levels (> 5.52 ng/mL; odds ratio = 1.26; 95% confidence interval: 1.09, 1.45). There were positive associations of blood lead level with total cholesterol and HDL levels, and these associations were more evident when modeled as continuous outcomes than when categorized using clinically relevant cut points. In addition, longitudinal analyses indicated a significant increase in TNF-R2 levels over time to be associated with high blood lead level at the preceding visit.Conclusions: Blood lead level may be related with CVD in healthy older men through its association with TNF-R2 levels. In addition, the magnitude of the association of blood lead level with TNF-R2 level increased with age in the study population.     

Cumulative Exposure to Lead in Relation to Cognitive Function in Older Women

Background

Recent data indicate that chronic low-level exposure to lead is associated with accelerated declines in cognition in older age, but this has not been examined in women.

Objective

We examined biomarkers of lead exposure in relation to performance on a battery of cognitive tests among older women.

Methods

Patella and tibia bone lead—measures of cumulative exposure over many years—and blood lead, a measure of recent exposure, were assessed in 587 women 47–74 years of age. We assessed their cognitive function 5 years later using validated telephone interviews.

Results

Mean ± SD lead levels in tibia, patella, and blood were 10.5 ± 9.7 μg/g bone, 12.6 ± 11.6 μg/g bone, and 2.9 ± 1.9 μg/dL, respectively, consistent with community-level exposures. In multivariable-adjusted analyses of all cognitive tests combined, levels of all three lead biomarkers were associated with worse cognitive performance. The association between bone lead and letter fluency score differed dramatically from the other bone lead-cognitive score associations, and exclusion of this particular score from the combined analyses strengthened the associations between bone lead and cognitive performance. Results were statistically significant only for tibia lead: one SD increase in tibia lead corresponded to a 0.051-unit lower standardized summary cognitive score (95% confidence interval: −0.099 to −0.003; p = 0.04), similar to the difference in cognitive scores we observed between women who were 3 years apart in age.

Conclusions

These findings suggest that cumulative exposure to lead, even at low levels experienced in community settings, may have adverse consequences for women’s cognition in older age.     

Maternal dietary intake of polyunsaturated fatty acids modifies the relationship between lead levels in bone and breast milk

Whereas dietary fats are known to influence bone mineral density, little is known about their effect on the skeletal stores of lead that are a pervasive source of fetal and infant lead exposure from heightened mobilization during pregnancy and lactation. This cross-sectional study examined the potential influence of maternal dietary intake of saturated and unsaturated fats on the relationship of lead levels in bone and breast milk during lactation. Lead was measured in blood, breast milk, and bone (patella and tibia) at 1 mo postpartum in 310 women in Mexico City. Dietary nutrient intake was assessed using a validated FFQ. Multivariate linear regression analyses were used to study the influence of dietary saturated and unsaturated fats on the association between bone and breast milk lead. In multivariate models that included both the dietary intake of SFA and PUFA, an interquartile range increase in patella lead [approximately 20 microg/g (0.097 micromol/g)] was associated with a 24% (95% CI = 5-43) higher increase in breast milk lead in women in the lowest tertile of PUFA intake compared with those in the highest tertile of PUFA intake. Monounsaturated fatty acids did not modify the relationship between lead levels in patella and breast milk. In conclusion, higher maternal dietary intake of PUFA may limit the transfer of lead from bone to breast milk.     

65岁及以上社区老年人高血压病收缩压控制情况与认知功能关联性

  目的  探究老年高血压病人SBP控制情况和认知功能的关系。  方法  采用多阶段整群抽样,对年龄≥65岁的社区老年人进行现场调查, 使用标准水银血压计连续两次测量右臂血压值,采用简明精神状态量表(mini-mental state examination, MMSE)评估认知功能,并采用多因素Logistic回归分析模型分析SBP控制情况和认知功能的关系。  结果  强化控制(SBP＜120 mm Hg)(OR=1.519,95% CI:1.187~1.945)增高认知障碍患病风险。年龄分层发现,强化控制增加70岁及以上老人的认知障碍患病风险(均有P < 0.05)。对高血压病史分层发现,10年以上高血压病程老人,强化控制和控制不良(SBP≥140 mm Hg)均与认知障碍患病率增加正相关(均有P < 0.05)。进一步对10年以上高血压病程老人年龄分层,发现65~69岁老人中,控制不良与认知障碍患病风险增加相关(P=0.023)。  结论  高血压病程较长的老人中,65~69岁老人应严格控制SBP,70岁及以上老人应谨慎控制SBP。     

Lead concentrations in elderly urban people related to blood pressure and mental performance: results from a population-based study

BACKGROUND: The Kungsholmen project is a longitudinal study of ageing and dementia conducted in Stockholm in 1987. In a 1994-96 follow-up, 804 subjects had their blood samples analyzed for lead. METHODS: Lead concentration in blood in an elderly population aged 75+ (mean age of 88.4 years) was studied in relation to age, blood pressure (BP), body mass index (BMI), cognitive function measured with Mini-Mental State Examination (MMSE), gender, and smoking. RESULTS: The mean blood lead level (n = 762) was 3.7 microg/dL (0.18 micromol/L) whole blood with a standard deviation of 2.3, (0.11). There was a contribution of gender with men having higher blood lead levels than women (beta = -0.20; P = 0.000001) but not of smoking habits (beta = 0.07; P = 0.08) when these variables were entered into a multiple regression model with lead as the dependent variable (R = 0.22; P < 0.000001). Different multiple regression models were tested with lead as the dependent variable. No relation was found between lead concentrations and age, BMI, systolic BP, diastolic BP, or MMSE. Systolic and diastolic BP were correlated to BMI (R = 0.10; P = 0.01 and R = 0.22; P = 0.000 001, respectively). CONCLUSIONS: In this elderly population from a specified area of Stockholm it is unlikely that lead exposure affects BP or cognition. However, high lead levels in blood may reflect earlier occupational exposure or life style factors.