210 research outputs found
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Human exposure to nitro musks and the evaluation of their potential toxicity: an overview
Synthetic nitro musks are fragrant chemicals found in household and personal care products. The use of these products leads to direct exposures via dermal absorption, as well as inhalation of contaminated dust and volatilized fragrances. Evidence also suggests that humans are exposed to low doses of these chemicals through oral absorption of contaminated liquids and foods. As these compounds are lipophilic, they and their metabolites, have been found not only in blood, but also breast milk and adipose tissue. After personal use, these environmentally persistent pollutants then pass through sewage treatment plants through their effluent into the environment. Little is known about the biological effects in humans after such a prolonged low dose exposure to these chemicals. While epidemiologic studies evaluating the effects of nitro musk exposures are lacking, there is limited evidence that suggest blood levels of nitro musks are inversely related to luteal hormone levels. This is supported by animal models and laboratory studies that have shown that nitro musks are weakly estrogenic. Nitro musks exposure has been associated with an increased risk of tumor formation in mice. The evidence suggests that while nitro musks by themselves are not genotoxic, they may increase the genotoxicity of other chemicals. However, animal models for nitro musk exposure have proven to be problematic since certain outcomes are species specific. This may explain why evidence for developmental effects in animals is conflicting and inconclusive. Given that animal models and cell-line experiments are suggestive of adverse outcomes, further epidemiologic studies are warranted
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Association between Blood Lead and Walking Speed in the National Health and Nutrition Examination Survey (NHANES 1999–2002)
Background: Walking speed is a simple and reliable measure of motor function that is negatively associated with adverse health events in older people, including falls, disability, hospital admissions, and mortality. Lead has adverse affects on human health, particularly on the vascular and neurological systems. Objective: We explored the hypothesis that lead is associated with slower walking speed. Methods: We used U.S. National Health and Nutrition Examination Survey (NHANES) cross-sectional data from 1999–2002. The time to walk 20 ft (walking speed) was measured among 1,795 men and 1,798 women ≥ 50 years of age. The association between walking speed and quintiles of blood lead concentration was estimated separately in men and women using linear regression models adjusted for age, education, ethnicity, alcohol use, smoking status, height, and waist circumference. Results: Mean blood lead concentrations and walking speeds were 2.17 μg/dL and 3.31 ft/sec in women, and 3.18 μg/dL and 3.47 ft/sec in men, respectively. Among women, walking speed decreased with increasing quintiles of blood lead, resulting in an estimated mean value that was 0.11 ft/sec slower (95% CI: –0.19, –0.04; p-trend = 0.005) for women with blood lead concentrations in the highest versus lowest quintile. In contrast, lead was not associated with walking speed in men. Conclusion: Blood lead concentration was associated with decreased walking speed in women, but not in men. Our results contribute to the growing evidence that lead exposure, even at low levels, is detrimental to public health
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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-μg/g bone and 15-μg/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-μg/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
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Exposure to Polyfluoroalkyl Chemicals and Attention Deficit/Hyperactivity Disorder in U.S. Children 12–15 Years of Age
Background: Polyfluoroalkyl chemicals (PFCs) have been widely used in consumer products. Exposures in the United States and in world populations are widespread. PFC exposures have been linked to various health impacts, and data in animals suggest that PFCs may be potential developmental neurotoxicants. Objectives: We evaluated the associations between exposures to four PFCs and parental report of diagnosis of attention deficit/hyperactivity disorder (ADHD). Methods: Data were obtained from the National Health and Nutrition Examination Survey (NHANES) 1999–2000 and 2003–2004 for children 12–15 years of age. Parental report of a previous diagnosis by a doctor or health care professional of ADHD in the child was the primary outcome measure. Perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorohexane sulfonic acid (PFHxS) levels were measured in serum samples from each child. Results: Parents reported that 48 of 571 children included in the analysis had been diagnosed with ADHD. The adjusted odds ratio (OR) for parentally reported ADHD in association with a 1-μg/L increase in serum PFOS (modeled as a continuous predictor) was 1.03 [95% confidence interval (CI), 1.01–1.05]. Adjusted ORs for 1-μg/L increases in PFOA and PFHxS were also statistically significant (PFOA: OR = 1.12; 95% CI, 1.01–1.23; PFHxS: OR = 1.06; 95% CI, 1.02–1.11), and we observed a nonsignificant positive association with PFNA (OR = 1.32; 95% CI, 0.86–2.02). Conclusions: Our results, using cross-sectional data, are consistent with increased odds of ADHD in children with higher serum PFC levels. Given the extremely prevalent exposure to PFCs, follow-up of these data with cohort studies is needed
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Decreased sex ratio following maternal exposure to polychlorinated biphenyls from contaminated Great Lakes sport-caught fish: a retrospective cohort study.
BACKGROUND: Fish from the Great Lakes are contaminated with polychlorinated biphenyls, which have been found to have several adverse reproductive effects. Several environmental contaminants have been found to alter the sex ratio of offspring at birth, but the evidence of such an effect of polychlorinated biphenyls has been inconsistent. METHODS: We examined parental serum polychlorinated biphenyl concentration in relation to the sex ratio of 173 children of mothers and 208 children of fathers from the Great Lakes region of the United States between 1970 and 1995. We calculated odds ratios for a male child using logistic regression and generalized estimating equations with adjustment for the year of birth of the child, maternal and paternal age, the mother's parity at the child's birth, and whether the child had an older brother. RESULTS: The adjusted odds ratio for having a male child among mothers in the highest quintile of serum polychlorinated biphenyl concentration was 0.18 (95% CI: 0.06–0.59) compared to mothers in the lowest quintile. Treating exposure as a continuous variable, the adjusted odds ratio for having a male child was 0.54 per unit increase in the natural log of maternal serum polychlorinated biphenyl concentration (95% CI: 0.33–0.89). There was little evidence of an association with paternal exposure. We found no association between either maternal or paternal serum dichlorodiphenyl-dichloroethene concentration and the sex ratio. CONCLUSIONS: These findings suggest that maternal exposure to polychlorinated biphenyls may decrease the sex ratio of offspring. These data add to the growing body of evidence that exposure to particular chemicals can alter the sex ratio at birth
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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.120639
Association of Cumulative Lead Exposure with Parkinson's Disease
BACKGROUND. Research using reconstructed exposure histories has suggested an association between heavy metal exposures, including lead, and Parkinson's disease (PD), but the only study that used bone lead, a biomarker of cumulative lead exposure, found a nonsignificant increase in risk of PD with increasing bone lead. OBJECTIVES. We sought to assess the association between bone lead and PD. METHODS. Bone lead concentrations were measured using 109Cd excited K-shell X-ray fluorescence from 330 PD patients (216 men, 114 women) and 308 controls (172 men, 136 women) recruited from four clinics for movement disorders and general-community cohorts. Adjusted odds ratios (ORs) for PD were calculated using logistic regression. RESULTS. The average age of cases and controls at bone lead measurement was 67 (SD = 10) and 69 (SD = 9) years of age, respectively. In primary analyses of cases and controls recruited from the same groups, compared with the lowest quartile of tibia lead, the OR for PD in the highest quartile was 3.21 [95% confidence interval (CI), 1.17-8.83]. Results were similar but slightly weaker in analyses restricted to cases and controls recruited from the movement disorders clinics only (fourth-quartile OR = 2.57; 95% CI, 1.11-5.93) or when we included controls recruited from sites that did not also contribute cases (fourth-quartile OR = 1.91; 95% CI, 1.01-3.60). We found no association with patella bone lead. CONCLUSIONS. These findings, using an objective biological marker of cumulative lead exposure among typical PD patients seen in our movement disorders clinics, strengthen the evidence that cumulative exposure to lead increases the risk of PD.National Institutes of Health (R01-ES010798, K01-ES01265
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Portable XRF Technology to Quantify Pb in Bone In Vivo
Lead is a ubiquitous toxicant. Bone lead has been established as an important biomarker for cumulative lead exposures and has been correlated with adverse health effects on many systems in the body. K-shell X-ray fluorescence (KXRF) is the standard method for measuring bone lead, but this approach has many difficulties that have limited the widespread use of this exposure assessment method. With recent advancements in X-ray fluorescence (XRF) technology, we have developed a portable system that can quantify lead in bone in vivo within 3 minutes. Our study investigated improvements to the system, four calibration methods, and system validation for in vivo measurements. Our main results show that the detection limit of the system is 2.9 ppm with 2 mm soft tissue thickness, the best calibration method for in vivo measurement is background subtraction, and there is strong correlation between KXRF and portable LXRF bone lead results. Our results indicate that the technology is ready to be used in large human population studies to investigate adverse health effects of lead exposure. The portability of the system and fast measurement time should allow for this technology to greatly advance the research on lead exposure and public/environmental health
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