Maternal bone lead contribution to blood lead during and after pregnancy

We examined bone lead contribution to blood lead in a group of 311 immigrant women, 99% from Latin America, during the third trimester of pregnancy and 1 to 2 months after delivery. We measured in vivo tibia and calcaneus (heel) bone lead concentration in the postdelivery period with K shell X-ray fluorescence. Prenatal and postnatal geometric mean (range) blood lead level was 2.2 microg/dL (0.4 to 38.7) and 2.8 microg/dL (0.4 to 25.4), reflecting low current exposure. Postnatal blood lead level was significantly higher than prenatal (P<0.0001). Mean (range) tibia and calcaneus lead concentration was 6.7 microg/g (-33.7 to 62.2) and 8.4 microg/g (- 30.1 to 66.4), reflecting varying but elevated past lead exposure. Mean calcaneus lead concentration was significantly higher than mean tibia lead concentration (P = 0.055). Variance-weighted multiple regression and structural equation models showed that both calcaneus and tibia lead were directly associated with prenatal blood lead but only calcaneus lead was associated with postnatal blood lead. Increasing natural log years in the United States independently predicted decreasing calcaneus and third-trimester blood lead. The data suggest that while some exogenous lead sources and modulators of blood lead level, such as use of lead-glazed pottery and calcium in the diet, control lead exposure during and after pregnancy, endogenous lead sources from past exposure before immigration continue to influence blood lead levels in this sample.     

Levels of lead in breast milk and their relation to maternal blood and bone lead levels at one month postpartum

Despite the many well-recognized benefits of breast-feeding for both mothers and infants, detectable levels of lead in breast milk have been documented in population studies of women with no current environmental or occupational exposures. Mobilization of maternal bone lead stores has been suggested as a potential endogenous source of lead in breast milk. We measured lead in breast milk to quantify the relation between maternal blood and bone lead levels and breast-feeding status (exclusive vs. partial) among 310 lactating women in Mexico City, Mexico, at 1 month postpartum. Umbilical cord and maternal blood samples were collected at delivery. Maternal breast milk, blood, and bone lead levels were obtained at 1 month postpartum. Levels of lead in breast milk ranged from 0.21 to 8.02 microg/L (ppb), with a geometric mean (GM) of 1.1 microg/L; blood lead ranged from 1.8 to 29.9 microg/dL (GM = 8.4 microg/dL); bone lead ranged from < 1 to 67.2 microg/g bone mineral (patella) and from < 1 to 76.6 microg/g bone mineral (tibia) at 1 month postpartum. Breast milk lead was significantly correlated with umbilical cord lead [Spearman correlation coefficient (rS) = 0.36, p < 0.0001] and maternal blood lead (rS= 0.38, p < 0.0001) at delivery and with maternal blood lead (rS = 0.42, p < 0.0001) and patella lead (rS= 0.15, p < 0.01) at 1 month postpartum. Mother's age, years living in Mexico City, and use of lead-glazed ceramics, all predictive of cumulative lead exposure, were not significant predictors of breast milk lead levels. Adjusting for parity, daily dietary calcium intake (milligrams), infant weight change (grams), and breast-feeding status (exclusive or partial lactation), the estimated effect of an interquartile range (IQR) increase in blood lead (5.0 microg/dL) was associated with a 33% increase in breast milk lead [95% confidence interval (CI), 24 to 43%], whereas an IQR increase in patella lead (20 microg/g) was associated with a 14% increase in breast milk lead (95% CI, 5 to 25%). An IQR increase in tibia lead (12.0 microg/g) was associated with a 5% increase in breast milk lead (95% CI, -3% to 14%). Our results indicate that even among a population of women with relatively high lifetime exposure to lead, levels of lead in breast milk are low, influenced both by current lead exposure and by redistribution of bone lead accumulated from past environmental exposures.     

Correlates of bone and blood lead levels among middle-aged and elderly women

In 1993-1995, the authors evaluated risk factors for elevated blood and bone lead levels in 264 Boston, Massachusetts, area women previously selected for a case-control study of lead and hypertension. Bone lead was measured at the tibia and patella with K x-ray fluorescence. Blood lead was analyzed by graphite furnace atomic absorption. Participants were aged 46-74 years and had mean lead levels of 3 (standard deviation, 2) micro g/dl (blood), 13 (standard deviation, 9) micro g/g (tibia), and 17 (standard deviation, 11) micro g/g (patella). In multivariate linear regression models, use of postmenopausal estrogen (inverse) and alcohol intake (positive) were significantly associated with blood lead levels. Both bone lead measures were significantly and positively associated with blood lead but only among postmenopausal women not using estrogen; for example, an increase from the first to the fifth quintile of tibia lead level (19 micro g/g) was associated with a 1.7- micro g/dl increase in blood lead (p = 0.0001) in this group. Older age and lower parity were associated with higher tibia lead; only age was associated with patella lead. The observed interaction of bone lead with estrogen status in determining blood lead supports the hypothesis that increased bone resorption, as occurs postmenopausally because of decreased estrogen production, results in heightened release of bone lead stores into blood.     

Association between prenatal lead exposure and blood pressure in children

Background: Lead exposure in adults is associated with hypertension. Altered prenatal nutrition is associated with subsequent risks of adult hypertension, but little is known about whether prenatal exposure to toxicants, such as lead, may also confer such risks.Objectives: We investigated the relationship of prenatal lead exposure and blood pressure (BP) in 7- to 15-year-old boys and girls.Methods: We evaluated 457 mother–child pairs, originally recruited for an environmental birth cohort study between 1994 and 2003 in Mexico City, at a follow-up visit in 2008–2010. Prenatal lead exposure was assessed by measurement of maternal tibia and patella lead using in vivo K-shell X-ray fluorescence and cord blood lead using atomic absorption spectrometry. BP was measured by mercury sphygmomanometer with appropriate-size cuffs.Results: Adjusting for relevant covariates, maternal tibia lead was significantly associated with increases in systolic BP (SBP) and diastolic BP (DBP) in girls but not in boys (p-interaction with sex = 0.025 and 0.007 for SBP and DBP, respectively). Among girls, an interquartile range increase in tibia lead (13 μg/g) was associated with 2.11-mmHg [95% confidence interval (CI): 0.69, 3.52] and 1.60-mmHg (95% CI: 0.28, 2.91) increases in SBP and DBP, respectively. Neither patella nor cord lead was associated with child BP.Conclusions: Maternal tibia lead, which reflects cumulative environmental lead exposure and a source of exposure to the fetus, is a predisposing factor to higher BP in girls but not boys. Sex-specific adaptive responses to lead toxicity during early-life development may explain these differences.     

Lead and hypertension in a sample of middle-aged women

OBJECTIVES: The role of lead exposure as a risk factor for hypertension is less well defined among women than among men. This case-control study assessed the relation of blood and bone lead concentrations to hypertension in women. METHODS: Cases and controls were a subsample of women from the Nurses' Health Study. Hypertension was defined as a physician diagnosis of hypertension between 1988 and 1994 or measured systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg. RESULTS: Mean (SD) blood lead concentration was 0.15 (0.11) mumol/L; mean tibia and patella lead concentrations by K-x-ray fluorescence were 13.3 (9.0) and 17.3 (11.1) micrograms/g, respectively. After adjustment for potentially confounding factors, an increase from the 10th to the 90th percentile of patella lead values (25 micrograms/g) was associated with approximately 2-fold (95% confidence interval = 1.1, 3.2) increased risk of hypertension. There was no association between hypertension and either blood or tibia lead concentrations. CONCLUSIONS: These findings support a potentially important role for low-level lead exposure as a risk factor for hypertension among non-occupationally exposed women.     

Blood lead level and blood pressure during pregnancy in South Central Los Angeles

In many studies in which the relationship between blood pressure and blood lead level has been examined, investigators have found significant--but small--associations. There was only one previous report of a significant association of blood lead with blood pressure in pregnant women. We measured blood lead level and sitting blood pressure of 1,627 women in their third trimester of pregnancy. We eliminated subjects with known causes of hypertension. Most women (98.4%) were normotensive. We controlled for body mass index, age, and stress--among other factors--and constructed multiple-regression models of lead association with diastolic and systolic blood pressures. Immigrants (73% of total) had significantly higher blood lead levels and different blood pressures than nonimmigrants, suggesting that analysis be stratified by "immigrant, nonimmigrant" status. Positive relationships between blood lead level and blood pressure were found only for immigrants (p < or = .001). From the 5th to 95th blood-lead percentiles (0.9-6.2 microg/dl) in immigrants, systolic blood pressure increased 2.8 mm Hg, and diastolic blood pressure increased 2.4 mm Hg. Higher prior lead exposure of immigrants (97.7% from Latin countries) than nonimmigrants might explain the differential effect of these low levels of blood lead on blood pressure in nonimmigrants. Perhaps some immigrants are at higher risk than nonimmigrants for lead-associated elevated blood pressure during pregnancy, despite blood lead levels within the currently considered acceptable range.     

The longitudinal association of lead with blood pressure

BACKGROUND: Several investigators have reported an association of blood lead or bone lead with increased blood pressure and hypertension, but questions remain concerning whether these effects are acute or chronic in nature. METHODS: In this longitudinal study, we evaluated the relation of lead, measured in blood and tibia, to changes in blood pressure between 1994 and 1998. We studied 496 current and former employees of a chemical-manufacturing facility in the eastern United States who had previous occupational exposure to inorganic and organic lead. Cohort members who provided three or four blood pressure measurements during the study were included. RESULTS: Mean age at baseline was 55.8 years with a mean of 18 years since last occupational exposure to lead. Blood lead at baseline averaged 4.6 microg/dL (standard deviation [SD] = 2.6) or 0.22 micromole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-microg/gm (SD = 9.4) bone mineral. Change in systolic blood pressure during the study was associated with lead dose, with an average annual increase of 0.64 mmHg (standard error [SE] = 0.25), 0.73 mmHg (SE = 0.26), and 0.61 mmHg (SE = 0.27) for every standard deviation increase in blood lead at baseline, tibia lead at year three, or peak past tibia lead, respectively. CONCLUSIONS: The results support an etiologic role for lead in the elevation of systolic blood pressure among adult males and are consistent with both acute and chronic modes of action.     

Exposure to famine during gestation, size at birth, and blood pressure at age 59 y: evidence from the dutch famine

We compared blood pressure of individuals (mean age 59 y) born in western Holland between January 1945 and March 1946 (mothers exposed to the Dutch Famine before or during gestation; n = 359) to blood pressure of unexposed individuals born before or conceived after the famine (n = 299) or same-sex siblings of subjects in series 1 or 2 (n = 313). Mean (SD) systolic and diastolic blood pressure were 140.3 (20.3) and 85.8 (11.0) mmHg, respectively; prevalence of hypertension (prior diagnosis of hypertension or with measured systolic/diastolic blood pressure above 140/90 mmHg) was 61.8%. Birth weight was inversely related to systolic (−4.14 mmHg per kg; 95% confidence interval (CI) −7.24, −1.03; p < 0.01) and diastolic (−2.09 mmHg per kg; 95% CI −3.77, −0.41; p < 0.05) blood pressure and to the prevalence of hypertension (odds ratio 0.67 per kg, 95% CI: 0.49, 0.93) (all age- and sex-adjusted). Any famine exposure of at least 10 weeks duration was associated with elevated systolic (2.77 mmHg; 95% CI 0.25, 5.30; p < 0.05) and diastolic (1.27 mmHg; 95% CI −0.13, 2.66; p = 0.08) blood pressure and with hypertension prevalence (odds ratio 1.44; 95% CI 1.04, 2.00; p < 0.05) in age- and sex-adjusted models. Exposure to famine during gestation may predispose to the development of hypertension in middle age.     

Low-level lead exposure and elevations in blood pressure during pregnancy

Background

Lead exposure is associated with elevated blood pressure during pregnancy; however, the magnitude of this relationship at low exposure levels is unclear.

Objectives

Our goal was to determine the association between low-level lead exposure and blood pressure during late pregnancy.

Methods

We collected admission and maximum (based on systolic) blood pressures during labor and delivery among 285 women in Baltimore, Maryland. We measured umbilical cord blood lead using inductively coupled plasma mass spectrometry. Multivariable models were adjusted for age, race, median household income, parity, smoking during pregnancy, prepregnancy body mass index, and anemia. These models were used to calculate benchmark dose values.

Results

Geometric mean cord blood lead was 0.66 μg/dL (95% confidence interval, 0.61–0.70). Comparing blood pressure measurements between those in the highest and those in the lowest quartile of lead exposure, we observed a 6.87-mmHg (1.51–12.21 mmHg) increase in admission systolic blood pressure and a 4.40-mmHg (0.21–8.59 mmHg) increase in admission diastolic blood pressure after adjustment for confounders. Corresponding values for maximum blood pressure increase were 7.72 (1.83–13.60) and 8.33 (1.14–15.53) mmHg. Benchmark dose lower limit values for a 1-SD increase in blood pressure were < 2 μg/dL blood lead for all blood pressure end points.

Conclusions

A significant association between low-level lead exposures and elevations in maternal blood pressure during labor and delivery can be observed at umbilical blood lead levels < 2 μg/dL.     

Bone lead levels and blood pressure endpoints: a meta-analysis

BACKGROUND: Previous reviews have shown increases in blood pressure and hypertension associated with increases in lead levels in blood. We performed a meta-analysis of the association of bone lead levels with systolic blood pressure, diastolic blood pressure, and hypertension using published data. METHODS: We searched Medline, Embase, and Toxline for epidemiologic studies on bone lead levels and blood pressure endpoints. We used inverse-variance weighted random-effects models to summarize the association of tibia or patella lead levels with blood pressure endpoints. RESULTS: We summarized data from 3 prospective studies and 5 cross-sectional studies. All studies measured lead levels in tibia bone and 3 studies measured lead levels in patella. For a 10 microg/g increase in tibia lead, the cross-sectional summary increases in blood pressure were 0.26 mm Hg for systolic (95% confidence interval = 0.02 to 0.50) and 0.02 mm Hg for diastolic (-0.15 to 0.19). The summary odds ratio for hypertension was 1.04 (1.01 to 1.07). For a 10 microg/g increase in patella lead, the summary odds ratio for hypertension was 1.04 (0.96 to 1.12). CONCLUSION: Systolic blood pressure and hypertension risk were associated with lead levels in tibia bone, but the magnitude of the summary estimates was small. These summary estimates, however, were based on published data and we could not evaluate nonlinear dose-response relationships, the relative contribution of bone and blood lead levels, or the influence of differences in study populations. A more detailed characterization of the association of bone lead levels and blood pressure endpoints would require a pooled analysis of individual participant data from existing studies.     

Season Modifies the Relationship between Bone and Blood Lead Levels: The Normative Aging Study

Bone serves as a repository for 75% and 90–95% of lead in children and adults, respectively. Bone lead mobilization heightens during times of increased bone turnover, such as pregnancy, lactation, hyperthyroidism, and the rapid growth of childhood. Blood lead levels show seasonal periodicity. Children demonstrate peak blood lead levels in midsummer and a secondary peak in late winter. Pregnant women demonstrate the highest mean blood lead levels in winter (January-March) and the lowest in summer (July-September). This fluctuation in blood lead levels may be related to seasonal patterns of environmental exposures, but it may also be partially related to the increased mobilization of bone lead stores during the winter months. We performed bone lead measurements using a K-x-ray fluorescent instrument to determine micrograms of lead per gram of bone mineral (parts per million) in middle-aged and elderly men who participated in the Normative Aging Study. We obtained measurements of blood and bone lead during the high sun exposure months of May-August (summer; n = 290); the intermediate sun exposure months of March, April, September, and October (spring/fall; n = 283); and the low sun exposure months of November-February (winter; n = 191). Mean blood lead concentrations were 5.8 μg/dl, 6.1 μg/dl, and 6.6 μg/dl for the summer, spring/fall, and winter, respectively. Mean patella (trabecular bone) lead concentrations were 34.3 μg/gm, 29.7 μ/gm, and 29.0 μg/gm for the summer, spring/fall, and winter time periods, respectively. In multivariate regression models, adjusted for age, smoking, alcohol ingestion, and dietary intake of iron and vitamin C, the authors found a strong interaction between season and bone lead level—with bone lead levels exerting an almost 2-fold greater influence on blood levels during the winter months than the summer months. The authors concluded that elevated blood lead levels in winter may be related to increased mobilization of endogenous bone lead stores, potentially from decreased exposure to sunlight, lower levels of activated vitamin D, and enhanced bone resorption.     

Determinants of bone and blood lead concentrations in the early postpartum period

OBJECTIVE—This study investigated determinants of bone and blood lead concentrations in 430 lactating Mexican women during the early postpartum period and the contribution of bone lead to blood lead.
METHODS—Maternal venous lead was measured at delivery and postpartum, and bone lead concentrations, measured with in vivo K-x ray fluorescence, were measured post partum. Data on environmental exposure, demographic characteristics, and maternal factors related to exposure to lead were collected by questionnaire. Linear regression was used to examine the relations between bone and blood lead, demographics, and environmental exposure variables.
RESULTS—Mean (SD) blood, tibial, and patellar lead concentrations were 9.5 (4.5) µg/dl, 10.2 (10.1) µg Pb/g bone mineral, and 15.2 (15.1) µg Pb/g bone mineral respectively. These values are considerably higher than values for women in the United States. Older age, the cumulative use of lead glazed pottery, and higher proportion of life spent in Mexico City were powerful predictors of higher bone lead concentrations. Use of lead glazed ceramics to cook food in the past week and increased patellar lead concentrations were significant predictors of increased blood lead. Patellar lead concentrations explained one third of the variance accounted for by the final blood lead model. Women in the 90th percentile for patella lead had an untransformed predicted mean blood lead concentration 3.6 µg/dl higher than those in the 10th percentile.
CONCLUSIONS—This study identified the use of lead glazed ceramics as a major source of cumulative exposure to lead, as reflected by bone lead concentrations, as well as current exposure, reflected by blood lead, in Mexico. A higher proportion of life spent in Mexico City, a proxy for exposure to leaded gasoline emissions, was identified as the other major source of cumulative lead exposure. The influence of bone lead on blood lead coupled with the long half life of lead in bone has implications for other populations and suggests that bone stores may pose a threat to women of reproductive age long after exposure has declined.


Keywords: postpartum; blood lead; bone lead     

Environmental carbon monoxide related to pregnancy hypertension

Carbon monoxide pollution frequently occurs due to auto exhaust, industrial emissions, and/or cigarette smoke. Exogenous and endogenous carbon monoxide affects blood pressure; however, the relation of carbon monoxide exposure to pregnancy hypertension has not been systematically examined. For the present study the authors recruited a total of 2,707 apparently healthy, non-obese, non-smoking mothers, aged between 15 and 40 years, who had singleton births, and who lived within two miles of the selected air monitoring stations in Tehran, Iran, to study the relation of ambient carbon monoxide to pregnancy hypertension (>140 mmHg systolic and/or >90 mmHg diastolic after the 20th week of gestation). A relatively small but statistically significant elevation in mean postpartum diastolic blood pressure (mean ± SD, 69.5 ± 9.8 mmHg) was observed in the mothers' who were exposed to relatively high ambient carbon monoxide (mean = 14.1 ppm) compared to mothers exposed to lower carbon monoxide (mean = 1.8 ppm) concentrations (mean ± SD, 68.0 ± 8.3 mmHg, p < 0.01). The authors found twice the rate of pregnancy hypertension in the relatively higher carbon monoxide exposed mothers than the mothers with lower exposure (adjusted odds ratio = 2.02, 95% CI 1.35-3.03). Findings of the present study suggest that high level ambient carbon monoxide exposure is associated with pregnancy hypertension.     

Stress as a potential modifier of the impact of lead levels on blood pressure: the normative aging study

BACKGROUND: Lead exposure and psychological stress have been independently associated with hypertension in various populations, and animal studies suggest that when they co-occur, their effects may be exacerbated. OBJECTIVES: We examined whether psychological stress modifies the impact of cumulative lead exposure (measured as bone lead levels) on hypertension and blood pressure in Boston-area community-exposed men participating in the Normative Aging Study. METHODS: We evaluated the modifying effect of stress on lead exposure on baseline hypertension status (513 participants) and on blood pressure in those without hypertension (237 participants), cross-sectionally. In baseline nonhypertensives, we examined the same risk factors in relation to prospective risk of developing hypertension. RESULTS: Cross-sectional analysis revealed a positive interaction between stress and tibia lead on systolic blood pressure, after adjusting for age, body mass index, family history of high blood pressure, education, smoking, alcohol consumption, physical activity, and nutritional factors. In prospective multivariate analyses, high stress also modified the effect of tibia lead and patella lead on the risk of developing hypertension. Those reporting high stress had 2.66 [95% confidence interval (CI), 1.43-4.95] times the risk of developing hypertension per standard deviation increase in tibia lead and had 2.64 (95% CI, 1.42-4.92) times the risk per standard deviation increase in patella lead. CONCLUSION: To our knowledge, these are the first analyses to look at interactive effects of stress and lead on hypertension in humans. These results suggest that the effect of lead on hypertension is most pronounced among highly stressed individuals, independent of demographic and behavioral risk factors.     

Association of low-level blood lead and blood pressure in NHANES 1999-2006

This study investigated whether low blood-lead levels (≤10 μg/dL) were associated with blood pressure (BP) outcomes. The authors analyzed data from National Health and Nutrition Examination Survey 1999-2006 and participants aged 20 years or older. Outcome variables were systolic and diastolic BP measurements, pulse pressure, and hypertension status. Multivariable linear and logistic regressions stratified by race/ethnicity and gender were performed. Blood lead levels (BLL) were significantly correlated with higher systolic BP among black men and women, but not white or Mexican-American participants. BLLs were significantly associated with higher diastolic BPs among white men and women and black men, whereas, a negative association was observed in Mexican-American men that had, also, a wider pulse pressure. Black men in the 90th percentile of blood lead distribution (BLL≥3.50 μg/dL) compared to black men in the 10th percentile of blood lead distribution (BLL≤0.7 μg/dL) had a significant increase of risk of having hypertension (adjusted POR=2.69; 95% CI: 1.08-6.72). In addition, blood cadmium was significantly associated with hypertension and systolic and diastolic blood. This study found that, despite the continuous decline in blood lead in the U.S. population, lead exposure disparities among race and gender still exist.     

Occupational determinants of bone and blood lead levels in middle aged and elderly men from the general community: the Normative Aging Study

BACKGROUND: Few studies of the general population have investigated risk factors for elevated levels of lead in bone in relation to occupation. METHODS: Six hundred and fifty six community-exposed men had their bone and blood lead levels measured (by K-X-ray fluorescence). Based on their occupational histories, participants were categorized into those who worked in white-collar (WC) occupations (59%) or blue-collar (BC) occupations (41%). No subjects had worked in a primary lead industry (e.g., smelting). RESULTS: In multivariate regression models that adjusted for age, race, education, smoking, alcohol ingestion and retirement status, BC subjects had tibia and patella lead concentrations that were 5.5 (95% CI: 3.2-7.8) and 6.5 (95% CI: 3.1-9.8) microg/g higher than WC subjects, respectively. Interaction terms pairing race with occupational status indicated that in non-white BC subjects, tibia and patella lead levels were higher still by 11.3 (95% CI: -2 to 24.5) and 20.5 (95% CI: 1.2-39.8) microg/g, respectively. Blood lead levels were low for these mostly retired men (mean [SD]: 6.1 [3.9] microg/g) and in multivariate regression models, occupational status was not a significant predictor of blood lead levels; however, an interaction between race and occupational status was also suggested, with non-white BC subjects having blood lead levels that were predicted to be higher by 4.5 (95% CI: 0.3-8.7) microg/dl. CONCLUSIONS: Bone lead levels are higher in the men who worked in BC occupations even if they have not worked in primary lead-exposed occupations. This effect is markedly stronger in non-white BC workers and suggests an interaction between occupational exposures and race/ethnicity with respect to cumulative exposure to lead. A similar interaction was suggested by models of blood lead levels.     

Cumulative community-level lead exposure and pulse pressure: the normative aging study

BACKGROUND: Pulse pressure increases with age in industrialized societies as a manifestation of arterial stiffening. Lead accumulates in the vasculature and is associated with vascular oxidative stress, which can promote functional and structural vascular disease. OBJECTIVES: We tested the hypothesis that cumulative community-level lead exposure, measured with K-X-ray fluorescence, is associated with pulse pressure in a cohort of adult men. METHODS AND RESULTS: In a cross-sectional analysis of 593 men not treated with antihypertensive medication, tibia lead was positively associated with pulse pressure (p < 0.001). Adjusting for age, race, diabetes, family history of hypertension, education, waist circumference, alcohol intake, smoking history, height, heart rate, fasting glucose, and total cholesterol-to-HDL ratio, increasing quintiles of tibia lead remained associated with increased pulse pressure (ptrend = 0.02). Men with tibia lead above the median (19.0 microg/g) had, on average, a 4.2-mmHg (95% confidence interval, 1.9-6.5) higher pulse pressure than men with tibia lead level below the median. In contrast, blood lead level was not associated with pulse pressure. CONCLUSIONS: These data indicate that lead exposure may contribute to the observed increase in pulse pressure that occurs with aging in industrialized societies. Lead accumulation may contribute to arterial aging, perhaps providing mechanistic insight into the observed association of low-level lead exposure with cardiovascular mortality.     

Hormone replacement therapy may reduce the return of endogenous lead from bone to the circulation.

Hormone replacement therapy (HRT) in postmenopausal women suppresses the increase in bone resorption expected as circulating levels of endogenous estrogen decline. We tested the hypothesis that bone lead content might remain elevated in women on HRT. Fifty six women who at recruitment were on average 35 years postmenopausal were placed on calcium supplementation. Six months later 33 of these women were prescribed either low dose or moderate dose hormone replacement in addition to the calcium supplementation. After approximately 4 years of hormone replacement, lead content was measured at the tibia and calcaneus by in vivo fluorescence excitation, and lead concentrations were measured in serum, whole blood, and urine. Women not taking hormones had significantly lower lead concentrations in cortical bone compared to all women on HRT (p = 0.007). Tibia lead content (mean +/- SD) for women on calcium only was 11.13 +/- 6.22 microgram/g bone mineral. For women on HRT, tibia bone lead was 19.37 +/- 8.62 micrograms/g bone mineral on low-dose HRT and 16.87 +/- 11.68 micrograms/g bone mineral on moderate-dose HRT. There were no differences between groups for lead concentrations measured in trabecular bone, whole blood, serum or urine. Hormone replacement maintains cortical bone lead content. In women not on HRT, there will be a perimenopausal release of lead from bone.     

Environmental Carbon Monoxide Related to Pregnancy Hypertension

Carbon monoxide pollution frequently occurs due to auto exhaust, industrial emissions, and/or cigarette smoke. Exogenous and endogenous carbon monoxide affects blood pressure; however, the relation of carbon monoxide exposure to pregnancy hypertension has not been systematically examined. For the present study the authors recruited a total of 2,707 apparently healthy, non-obese, non-smoking mothers, aged between 15 and 40 years, who had singleton births, and who lived within two miles of the selected air monitoring stations in Tehran, Iran, to study the relation of ambient carbon monoxide to pregnancy hypertension (>140 mmHg systolic and/or >90 mmHg diastolic after the 20th week of gestation). A relatively small but statistically significant elevation in mean postpartum diastolic blood pressure (mean ± SD, 69.5 ± 9.8 mmHg) was observed in the mothers' who were exposed to relatively high ambient carbon monoxide (mean = 14.1 ppm) compared to mothers exposed to lower carbon monoxide (mean = 1.8 ppm) concentrations (mean ± SD, 68.0 ± 8.3 mmHg, p < 0.01). The authors found twice the rate of pregnancy hypertension in the relatively higher carbon monoxide exposed mothers than the mothers with lower exposure (adjusted odds ratio = 2.02, 95% CI 1.35–3.03). Findings of the present study suggest that high level ambient carbon monoxide exposure is associated with pregnancy hypertension.     

Risk factors for the incidence of hyperuricaemia: a 6-year longitudinal study of middle-aged Japanese men

BACKGROUND: Few longitudinal studies on the determinants of increase in serum uric acid (SUA) have been completed. METHODS: In all, 1445 hyperuricaemia-free (<7.5 mg/dl SUA, no medication for and no past history of hyperuricaemia) male office workers aged 30-54 years of T Corporation in Osaka, Japan were re-examined for six successive years. Subjects who were found to be hyperuricaemic or had started medication for hyperuricaemia during repeat surveys were defined as incident cases. RESULTS: Among the subjects (n = 1365) not receiving medication for hypertension, diabetes mellitus or renal disease, multivariate analysis using the Cox proportional hazards model indicated that the incidence of hyperuricaemia had significant relationships with body mass index (adjusted hazard ratio [HR] = 1.13 for a 2 kg/m2 increase; 95% CI: 1.02-1.26), mean blood pressure (HR = 1.07 for a 5 mmHg increase; 95% CI: 1.00-1.13), log triglyceride level (HR = 2.21 for a 10 mg/dl increase; 95% CI: 1.12-4.37), alcohol intake (HR = 2.33 for drinking 46.0 g of ethanol per day or more relative to non-drinking; 95% CI: 1.55-3.50) and smoking (HR = 0.65 for current-smoking relative to non-smoking; 95% CI: 0.46-0.92). Age (HR = 0.89 for a 5-year increase; 95% CI: 0.78-1.00) and haemoglobin A1c (HbA1c) (HR = 0.89 for a 0.5% increase; 95% CI: 0.78-1.00) achieved marginal significance. CONCLUSIONS: Obesity, high blood pressure, high triglyceride level, and alcohol intake are contributory factors for the development of hyperuricaemia among middle-aged Japanese men. High HbA1c level and smoking may be negative factors for the incidence of hyperuricaemia.