Ana Navas-Acien

Publications (77)436.58 Total impact

• Article: Kidney Function and Tobacco Smoke Exposure in US Adolescents.

  Esther García-Esquinas, Lauren F Loeffler, Virginia M Weaver, Jeffrey J Fadrowski, Ana Navas-Acien
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  ABSTRACT: BACKGROUND AND OBJECTIVE:Active smoking and secondhand smoke (SHS) are known risk factors for kidney disease in adults. We evaluated the association between exposure to active smoking or SHS and kidney function in US adolescents.METHODS:This is a cross-sectional study in 7516 adolescents aged 12-17 who participated in NHANES 1999-2010 and had serum creatinine and cotinine measures. Active smoking was defined as self-reported smoking or serum cotinine concentrations >10 ng/mL. SHS was defined as nonactive smokers who self-reported living with ≥1 smokers or serum cotinine concentrations ≥ 0.05 ng/mL. Kidney function was determined by using the chronic kidney disease in children estimated glomerular filtration rate (eGFR) equation.RESULTS:Median (interquartile range) eGFR and serum cotinine concentrations were 96.8 (85.4-109.0) mL/minute per 1.73 m(2) and 0.07 (0.03-0.59) ng/mL, respectively. After multivariable adjustment, eGFR decreased 1.1 mL/minute per 1.73 m(2) (95% confidence interval [CI]: -1.8 to -0.3) per interquartile range increase in serum cotinine concentrations. The mean (95%CI) difference in eGFR for serum cotinine tertiles 1, 2, and 3 among children exposed to SHS compared to unexposed were -0.4 (-1.9 to 1.2), -0.9 (-2.7 to 0.9), and -2.2 (-4.0 to -0.4) mL/minute per 1.73 m(2), respectively (P = .03). The corresponding values among tertiles of active smokers compared to unexposed were 0.2 (-2.2 to 2.6), -1.9 (-3.8 to 0.0), and -2.6 (-4.6 to -0.6) mL/minute per 1.73 m(2) (P = .01).CONCLUSIONS:Tobacco smoke exposure was associated with decreased eGFR in US adolescents, supporting the possibility that tobacco smoke effects on kidney function begin in childhood.
  PEDIATRICS 04/2013; · 4.47 Impact Factor
• Article: Cadmium Exposure and Incident Cardiovascular Disease.

  Maria Tellez-Plaza, Eliseo Guallar, Barbara V Howard, Jason G Umans, Kevin A Francesconi, Walter Goessler, Ellen K Silbergeld, Richard B Devereux, Ana Navas-Acien
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  ABSTRACT: BACKGROUND:: Cadmium is a widespread toxic metal with potential cardiovascular effects, but no studies have evaluated cadmium and incident cardiovascular disease. We evaluated the association of urine cadmium concentration with cardiovascular disease incidence and mortality in a large population-based cohort. METHODS:: We conducted a prospective cohort study of 3348 American Indian adults 45-74 years of age from Arizona, Oklahoma, and North and South Dakota, who participated in the Strong Heart Study in 1989-1991. Urine cadmium was measured using inductively coupled plasma mass spectrometry. Follow-up extended through 31 December 2008. RESULTS:: The geometric mean cadmium level in the study population was 0.94 μg/g (95% confidence interval [CI] = 0.92-0.96). We identified 1084 cardiovascular events, including 400 deaths. After adjustment for sociodemographic and cardiovascular risk factors, the hazard ratios (HRs) (comparing the 80th to the 20th percentile of urine cadmium concentrations) was 1.43 for cardiovascular mortality (95% CI = 1.21-1.70) and 1.34 for coronary heart disease mortality (1.10-1.63). The corresponding HRs for incident cardiovascular disease, coronary heart disease, stroke, and heart failure were 1.24 (1.11-1.38), 1.22 (1.08-1.38), 1.75 (1.17-2.59), and 1.39 (1.01-1.94), respectively. The associations were similar in most study subgroups, including never-smokers. CONCLUSIONS:: Urine cadmium, a biomarker of long-term exposure, was associated with increased cardiovascular mortality and increased incidence of cardiovascular disease. These findings support that cadmium exposure is a cardiovascular risk factor.
  Epidemiology (Cambridge, Mass.) 03/2013; · 5.51 Impact Factor
• Article: Heritability and Preliminary Genome-Wide Linkage Analysis of Arsenic Metabolites in Urine.

  Maria Tellez-Plaza, Matthew O Gribble, V Saroja Voruganti, Kevin A Francesconi, Walter Goessler, Jason G Umans, Ellen K Silbergeld, Eliseo Guallar, Nora Franceschini, Kari E North, Wen H Kao, Jean W Maccluer, Shelley A Cole, Ana Navas-Acien
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  ABSTRACT: BACKGROUND: Arsenic (III) methyltransferase (AS3MT) has been related to urine arsenic metabolites in association studies. Other genes might play a role in arsenic metabolism and excretion. OBJECTIVE: To evaluate genetic determinants of urine arsenic metabolites in American Indian adults from the Strong Heart Study (SHS). METHODS: We evaluated heritability of urine arsenic metabolites [% inorganic arsenic (iAs), % monomethylarsonate (MMA), and % dimethylarsinate (DMA)] in 2,907 SHS participants with urine arsenic measurements and at least one relative within the cohort. We conducted a preliminary linkage analysis in a subset of 487 participants with available genotypes on ~400 short tandem repeat markers using a general pedigree variance component approach for localizing quantitative trait loci (QTL). RESULTS: The median (interquartile range) for %iAs, %MMA and %DMA were 7.7% (5.4, 10.7%), 13.6% (10.5, 17.1%) and 78.4% (72.5, 83.1%), respectively. The estimated heritability was 53% for %iAs, 50% for %MMA and 59% for %DMA. After adjustment for sex, age, smoking, body mass index, alcohol, region and total urine arsenic concentrations, LOD scores indicated suggestive evidence for genetic linkage with QTLs influencing urine arsenic metabolites on chromosomes 9 (LOD=2.05 for % iAs and 2.10 for % MMA), 5 (LOD=2.03 for % iAs) and 11 (LOD=1.94 for %iAs). A peak for % DMA on chromosome 10 within 2 megabases of AS3MT had an LOD=1.80. CONCLUSIONS: This population-based family study in American Indian communities supports a genetic contribution to variation in the distribution of arsenic metabolites in urine, and potentially the involvement of genes beyond AS3MT.
  Environmental Health Perspectives 01/2013; · 7.04 Impact Factor
• Article: Menthol Cigarettes, Race/Ethnicity and Biomarkers of Tobacco Use in US Adults: The 1999- 2010 National Health and Nutrition Examination Survey (NHANES).

  Miranda R Jones, Benjamin J Apelberg, Maria Tellez-Plaza, Jonathan M Samet, Ana Navas-Acien
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  ABSTRACT: BACKGROUND: In the US, cigarette flavorings are banned, with the exception of menthol. The cooling effects of menthol could facilitate the absorption of tobacco toxicants. We examined levels of biomarkers of tobacco exposure among US smokers of menthol and non-menthol cigarettes. METHODS: We studied 4,603 White, African-American, and Mexican-American current smokers ≥ 20 years of age who participated in the National Health and Nutrition Examination Survey from 1999 through 2010 and had data on cigarette type and serum cotinine, blood cadmium, and blood lead concentrations. Urinary total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol) (NNAL) was studied in 1,607 participants with available measures. RESULTS: A total of 3,210 (74.3%) participants smoked non-menthol cigarettes compared to 1,393 (25.7%) participants who smoked menthol cigarettes. The geometric mean concentrations comparing smokers of non-menthol to menthol cigarettes were 163.1 vs. 175.9 ng/mL for serum cotinine; 0.95 vs. 1.02 µg/L for blood cadmium; 1.87 vs. 1.75 µg/dL for blood lead; and 0.27 vs. 0.23 ng/mL for urine NNAL. After multivariable adjustment, the ratios (95% confidence interval [CI]) comparing smokers of menthol to non-menthol cigarettes were 1.03 (0.95, 1.11) for cotinine, 1.10 (1.04, 1.16) for cadmium, 0.95 (0.90, 1.01) for lead, and 0.81 (0.65, 1.01) for NNAL. CONCLUSIONS: In a representative sample of US adult smokers, current menthol cigarette use was associated with increased concentration of blood cadmium, an established carcinogen and highly toxic metal, but not with other biomarkers. Impact: These findings provide information regarding possible differences in exposure to toxic constituents among menthol cigarette smokers compared to non-menthol cigarette smokers.
  Cancer Epidemiology Biomarkers &amp Prevention 12/2012; · 4.12 Impact Factor
• Article: Smoking, Menthol Cigarettes, and Peripheral Artery Disease in U.S. Adults.

  Miranda R Jones, Benjamin J Apelberg, Jonathan M Samet, Ana Navas-Acien
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  ABSTRACT: INTRODUCTION: Cigarette flavorings, with the exception of menthol, have been banned in the United States under the Family Smoking Prevention and Tobacco Control Act. Given the large number of menthol cigarette smokers in the United States, we investigated whether cigarette type (nonmenthol or menthol) is associated with peripheral artery disease (PAD). METHODS: The authors studied 5,973 adults, 40 years of age and older, who participated in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2004. Smoking status and cigarette type were derived from self-reported questionnaires. PAD was defined as an ankle-brachial blood pressure index <0.9 in at least 1 leg. RESULTS: Fifty percent of participants were never-smokers compared to 31%, 14%, and 5% of former, current nonmenthol, and current menthol cigarette smokers, respectively. The weighted prevalence of PAD in the study population was 5%. After multivariable adjustment, the odds ratios for PAD were 1.44 (95% CI: 0.97, 2.15), 3.65 (95% CI: 1.57, 8.50), and 2.51 (95% CI: 1.09, 5.80) comparing former, current nonmenthol cigarette smokers, and current menthol cigarette smokers to never-smokers. The associations between smoking and PAD were similar for smokers of nonmenthol and menthol cigarettes (p value for heterogeneity = .59). CONCLUSIONS: In a representative sample of the U.S. population, current use of both menthol and nonmenthol cigarettes was associated with increased prevalence of PAD, with no difference in risk between cigarette types.
  Nicotine & Tobacco Research 12/2012; · 2.58 Impact Factor
• Article: Urine Arsenic and Prevalent Albuminuria: Evidence From a Population-Based Study.

  Laura Y Zheng, Jason G Umans, Maria Tellez-Plaza, Fawn Yeh, Kevin A Francesconi, Walter Goessler, Ellen K Silbergeld, Eliseo Guallar, Barbara V Howard, Virginia M Weaver, Ana Navas-Acien
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  ABSTRACT: BACKGROUND: Long-term arsenic exposure is a major global health problem. However, few epidemiologic studies have evaluated the association of arsenic with kidney measures. Our objective was to evaluate the cross-sectional association between inorganic arsenic exposure and albuminuria in American Indian adults from rural areas of Arizona, Oklahoma, and North and South Dakota. STUDY DESIGN: Cross-sectional. SETTING & PARTIPANTS: Strong Heart Study locations in Arizona, Oklahoma, and North and South Dakota. 3,821 American Indian men and women aged 45-74 years with urine arsenic and albumin measurements. PREDICTOR: Urine arsenic. OUTCOMES: Urine albumin-creatinine ratio and albuminuria status. MEASUREMENTS: Arsenic exposure was estimated by measuring total urine arsenic and urine arsenic species using inductively coupled plasma mass spectrometry (ICPMS) and high-performance liquid chromatography-ICPMS, respectively. Urine albumin was measured by automated nephelometric immunochemistry. RESULTS: The prevalence of albuminuria (albumin-creatinine ratio ≥30 mg/g) was 30%. Median value for the sum of inorganic and methylated arsenic species was 9.7 (IQR, 5.8-15.6) μg per gram of creatinine. Multivariable-adjusted prevalence ratios of albuminuria (albumin-creatinine ratio ≥30 mg/g) comparing the 3 highest to lowest quartiles of the sum of inorganic and methylated arsenic species were 1.16 (95% CI, 1.00-1.34), 1.24 (95% CI, 1.07-1.43), and 1.55 (95% CI, 1.35-1.78), respectively (P for trend <0.001). The association between urine arsenic and albuminuria was observed across all participant subgroups evaluated and was evident for both micro- and macroalbuminuria. LIMITATIONS: The cross-sectional design cannot rule out reverse causation. CONCLUSIONS: Increasing urine arsenic concentrations were cross-sectionally associated with increased albuminuria in a rural US population with a high burden of diabetes and obesity. Prospective epidemiologic and mechanistic evidence is needed to understand the role of arsenic as a kidney disease risk factor.
  American Journal of Kidney Diseases 11/2012; · 5.43 Impact Factor
• Article: Arsenic Exposure, Diabetes Prevalence, and Diabetes Control in the Strong Heart Study.

  Matthew O Gribble, Barbara V Howard, Jason G Umans, Nawar M Shara, Kevin A Francesconi, Walter Goessler, Ciprian M Crainiceanu, Ellen K Silbergeld, Eliseo Guallar, Ana Navas-Acien
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  ABSTRACT: This study evaluated the association of arsenic exposure, as measured in urine, with diabetes prevalence, glycated hemoglobin, and insulin resistance in American Indian adults from Arizona, Oklahoma, and North and South Dakota (1989-1991). We studied 3,925 men and women 45-74 years of age with available urine arsenic measures. Diabetes was defined as a fasting glucose level of 126 mg/dL or higher, a 2-hour glucose level of 200 mg/dL or higher, a hemoglobin A1c (HbA1c) of 6.5% or higher, or diabetes treatment. Median urine arsenic concentration was 14.1 µg/L (interquartile range, 7.9-24.2). Diabetes prevalence was 49.4%. After adjustment for sociodemographic factors, diabetes risk factors, and urine creatinine, the prevalence ratio of diabetes comparing the 75th versus 25th percentiles of total arsenic concentrations was 1.14 (95% confidence interval: 1.08, 1.21). The association between arsenic and diabetes was restricted to participants with poor diabetes control (HbA1c ≥8%). Arsenic was positively associated with HbA1c levels in participants with diabetes. Arsenic was not associated with HbA1c or with insulin resistance (assessed by homeostatic model assessment to quantify insulin resistance) in participants without diabetes. Urine arsenic was associated with diabetes control in a population from rural communities in the United States with a high burden of diabetes. Prospective studies that evaluate the direction of the relation between poor diabetes control and arsenic exposure are needed.
  American journal of epidemiology 10/2012; · 5.59 Impact Factor
• Article: Protecting the World From Secondhand Tobacco Smoke Exposure: Where Do We Stand and Where Do We Go From Here?

  Joaquin Barnoya, Ana Navas-Acien
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  ABSTRACT: INTRODUCTION: Article 8 of the Framework Convention on Tobacco Control mandates all signatory countries to "protect citizens from exposure to tobacco smoke in workplaces, public transport and indoor public places." Even though there has been great progress in the implementation of Article 8, still most of the world population remains exposed to secondhand smoke (SHS). In this article, we sought to summarize the research that supports Article 8, where do we stand, and current research gaps and future directions.Discussion: Secondhand smoke is an established cause of heart disease and several types of cancer. Additional research is needed to reach final conclusions for diseases where evidence is only suggestive of causality. The only solution to SHS exposure in public places is banning smoking indoors. Research on the gaming industry and nightclubs, particularly in developing countries, needs to be disseminated to support their inclusion in smoke-free laws. Aside from indoor bans, additional research is needed for outdoor and multiunit housing bans and in support of measures that protect children and other vulnerable populations. The impact of smoke-free laws on other health outcomes, besides heart disease and respiratory outcomes, is another area where further research is needed. Thirdhand smoke assessment and health effects are also likely to be a topic of further research. As new tobacco products emerge, evaluating SHS exposure and effects will be vital.Conclusions: Furthering research in support of Article 8 can contribute to reach the final goal of protecting everyone from SHS exposure.
  Nicotine & Tobacco Research 10/2012; · 2.58 Impact Factor
• Article: Association of markers of chronic viral hepatitis and blood mercury levels in US reproductive-age women from NHANES 2001-2008: a cross-sectional study.

  Mary C Sheehan, Thomas A Burke, Patrick N Breysse, Ana Navas-Acien, John McGready, Mary A Fox
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  ABSTRACT: BACKGROUND: Methylmercury (MeHg) is a neurotoxin primarily found in seafood; exposures in reproductive-age women are of concern due to vulnerability of the developing fetus. MeHg is mainly eliminated via an enterohepatic cycle involving the liver and gallbladder. Dysfunction in these organs has been associated with slower MeHg elimination in laboratory animals. We hypothesized that women testing positive for chronic hepatitis B (HBV) or C (HCV), both associated with risk of longer-term liver and gallbladder impairment, would have higher total blood mercury (TBHg) concentrations than those negative for the viruses, reflecting slower MeHg elimination. METHODS: Geometric mean (GM) TBHg levels from a representative sample of over 5,000 seafood-consuming, reproductive-age women from eight years (2001-2008) of the US NHANES survey were compared by viral hepatitis status (as determined by serological assay) using multiple linear regression. Adjustment was made for estimated MeHg intake from seafood consumption, social and demographic variables and other predictors. RESULTS: Women with chronic HBV had 1.52 (95% CI 1.13, 2.05, p < 0.01) times the GM TBHg of women who had not come into contact with the virus. The positive association was strongest in those with most severe disease. A modest negative association was found with HCV markers. CONCLUSIONS: While study design prevents inferences on causality, the finding that MeHg biomarkers differ by hepatitis status in this population suggests viral hepatitis may alter the pace of MeHg elimination. Offspring of HBV-infected seafood-consuming women may be at higher risk of MeHg-induced developmental delays than offspring of those uninfected. Possible reasons for the unanticipated negative association with HCV are explored.
  Environmental Health 09/2012; 11(1):62. · 2.65 Impact Factor
• Article: Arsenic Exposure and Cardiovascular Disease:An Updated Systematic Review.

  Katherine Moon, Eliseo Guallar, Ana Navas-Acien
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  ABSTRACT: In epidemiologic studies, high-chronic arsenic exposure has been associated with cardiovascular disease, despite methodological limitations. At low-moderate arsenic levels, the evidence was inconclusive. Here, we update a previous systematic review (Am J Epidemiol 2005;162:1037-49) examining the association between arsenic exposure and cardiovascular disease. Eighteen studies published since 2005 were combined with 13 studies from the previous review. We calculated pooled relative risks by comparing the highest versus the lowest exposure category across studies. For high exposure (arsenic in drinking water > 50 μg/L), the pooled relative risks (95 % confidence interval) for cardiovascular disease, coronary heart disease, stroke, and peripheral arterial disease were 1.32 (95 % CI:1.05-1.67), 1.89 (95 % CI:1.33-2.69), 1.08 (95 % CI:0.98-1.19), and 2.17 (95 % CI:1.47-3.20), respectively. At low-moderate arsenic levels, the evidence was inconclusive. Our review strengthens the evidence for a causal association between high-chronic arsenic exposure and clinical cardiovascular endpoints. Additional high quality studies are needed at low-moderate arsenic levels.
  Current Atherosclerosis Reports 09/2012; · 2.66 Impact Factor
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  Available from: James Repace

  Article: Environmental monitoring of secondhand smoke exposure.

  Benjamin J Apelberg, Lisa M Hepp, Erika Avila-Tang, Lara Gundel, S Katharine Hammond, Melbourne F Hovell, Andrew Hyland, Neil E Klepeis, Camille C Madsen, Ana Navas-Acien, James Repace, Jonathan M Samet, Patrick N Breysse
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  ABSTRACT: The complex composition of secondhand smoke (SHS) provides a range of constituents that can be measured in environmental samples (air, dust and on surfaces) and therefore used to assess non-smokers' exposure to tobacco smoke. Monitoring SHS exposure (SHSe) in indoor environments provides useful information on the extent and consequences of SHSe, implementing and evaluating tobacco control programmes and behavioural interventions, and estimating overall burden of disease caused by SHSe. The most widely used markers have been vapour-phase nicotine and respirable particulate matter (PM). Numerous other environmental analytes of SHS have been measured in the air including carbon monoxide, 3-ethenylpyridine, polycyclic aromatic hydrocarbons, tobacco-specific nitrosamines, nitrogen oxides, aldehydes and volatile organic compounds, as well as nicotine in dust and on surfaces. The measurement of nicotine in the air has the advantage of reflecting the presence of tobacco smoke. While PM measurements are not as specific, they can be taken continuously, allowing for assessment of exposure and its variation over time. In general, when nicotine and PM are measured in the same setting using a common sampling period, an increase in nicotine concentration of 1 μg/m(3) corresponds to an average increase of 10 μg/m(3) of PM. This topic assessment presents a comprehensive summary of SHSe monitoring approaches using environmental markers and discusses the strengths and weaknesses of these methods and approaches.
  Tobacco control 09/2012; · 3.85 Impact Factor
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  Available from: PubMed Central

  Article: Cadmium exposure and all-cause and cardiovascular mortality in the U.S. general population.

  Maria Tellez-Plaza, Ana Navas-Acien, Andy Menke, Ciprian M Crainiceanu, Roberto Pastor-Barriuso, Eliseo Guallar
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  ABSTRACT: Urine cadmium concentrations were associated with all-cause and cardiovascular mortality in men in the 1988-1994 U.S. National Health and Nutrition Examination Survey (NHANES) population. Since 1988, cadmium exposure has decreased substantially in the United States. The associations between blood and urine cadmium and cardiovascular disease (CVD) mortality at more recent levels of exposure are unknown. We evaluated the prospective association of blood and urine cadmium concentrations with all-cause and CVD mortality in the 1999-2004 U.S. population. We followed 8,989 participants who were ≥ 20 years of age for an average of 4.8 years. Hazard ratios for mortality end points comparing the 80th to the 20th percentiles of cadmium distributions were estimated using Cox regression. The multivariable adjusted hazard ratios [95% confidence intervals (CIs)] for blood and urine cadmium were 1.50 (95% CI: 1.07, 2.10) and 1.52 (95% CI: 1.00, 2.29), respectively, for all-cause mortality, 1.69 (95% CI: 1.03, 2.77) and 1.74 (95% CI: 1.07, 2.83) for CVD mortality, 1.98 (95% CI: 1.11, 3.54) and 2.53 (95% CI: 1.54, 4.16) for heart disease mortality, and 1.73 (95% CI: 0.88, 3.40) and 2.09 (95% CI: 1.06, 4.13) for coronary heart disease mortality. The population attributable risks associated with the 80th percentile of the blood (0.80 μg/L) and urine (0.57 μg/g) cadmium distributions were 7.0 and 8.8%, respectively, for all-cause mortality and 7.5 and 9.2%, respectively, for CVD mortality. We found strongly suggestive evidence that cadmium, at substantially low levels of exposure, remains an important determinant of all-cause and CVD mortality in a representative sample of U.S. adults. Efforts to further reduce cadmium exposure in the population could contribute to a substantial decrease in CVD disease burden.
  Environmental Health Perspectives 04/2012; 120(7):1017-22. · 7.04 Impact Factor
• Article: Uric acid level and elevated blood pressure in US adolescents: National Health and Nutrition Examination Survey, 1999-2006.

  Lauren F Loeffler, Ana Navas-Acien, Tammy M Brady, Edgar R Miller, Jeffrey J Fadrowski
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  ABSTRACT: Uric acid is associated with cardiovascular disease and cardiovascular disease risk factors in adults, including chronic kidney disease, coronary artery disease, stroke, diabetes mellitus, preeclampsia, and hypertension. We examined the association between uric acid and elevated blood pressure in a large, nationally representative cohort of US adolescents, a population with a relatively low prevalence of cardiovascular disease and cardiovascular disease risk factors. Among 6036 adolescents 12 to 17 years of age examined in the 1999-2006 National Health and Nutrition Examination Survey, the mean age was 14.5 years, 17% were obese (body mass index: ≥95th percentile), and 3.3% had elevated blood pressure. Mean serum uric acid level was 5.0 mg/dL, and 34% had a uric acid level ≥5.5 mg/dL. In analyses adjusted for age, sex, race/ethnicity, and body mass index percentile, the odds ratio of elevated blood pressure, defined as a systolic or diastolic blood pressure ≥95th percentile for age, sex, and height, for each 0.1-mg/dL increase in uric acid level was 1.38 (95% CI: 1.16-1.65). Compared with <5.5 mg/dL, participants with a uric acid level ≥5.5 mg/dL had a 2.03 times higher odds of having elevated blood pressure (95% CI: 1.38-3.00). In conclusion, increasing levels of serum uric acid are associated with elevated blood pressure in healthy US adolescents. Additional prospective studies and clinical trials are needed to determine whether uric acid is merely a marker in a complex metabolic pathway or causal of hypertension and, thus, a potential screening and therapeutic target.
  Hypertension 02/2012; 59(4):811-7. · 6.21 Impact Factor
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  Available from: Patrick N Breysse

  Article: Secondhand tobacco smoke: an occupational hazard for smoking and non-smoking bar and nightclub employees.

  Miranda R Jones, Heather Wipfli, Shahida Shahrir, Erika Avila-Tang, Jonathan M Samet, Patrick N Breysse, Ana Navas-Acien
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  ABSTRACT: BACKGROUND: In the absence of comprehensive smoking bans in public places, bars and nightclubs have the highest concentrations of secondhand tobacco smoke, posing a serious health risk for workers in these venues. OBJECTIVE: To assess exposure of bar and nightclub employees to secondhand smoke, including non-smoking and smoking employees. METHODS: Between 2007 and 2009, the authors recruited approximately 10 venues per city and up to five employees per venue in 24 cities in the Americas, Eastern Europe, Asia and Africa. Air nicotine concentrations were measured for 7 days in 238 venues. To evaluate personal exposure to secondhand smoke, hair nicotine concentrations were also measured for 625 non-smoking and 311 smoking employees (N=936). RESULTS: Median (IQR) air nicotine concentrations were 3.5 (1.5-8.5) μg/m(3) and 0.2 (0.1-0.7) μg/m(3) in smoking and smoke-free venues, respectively. Median (IQR) hair nicotine concentrations were 6.0 (1.6-16.0) ng/mg and 1.7 (0.5-5.5) ng/mg in smoking and non-smoking employees, respectively. After adjustment for age, sex, education, living with a smoker, hair treatment and region, a twofold increase in air nicotine concentrations was associated with a 30% (95% CI 23% to 38%) increase in hair nicotine concentrations in non-smoking employees and with a 10% (2% to 19%) increase in smoking employees. CONCLUSIONS: Occupational exposure to secondhand smoke, assessed by air nicotine, resulted in elevated concentrations of hair nicotine among non-smoking and smoking bar and nightclub employees. The high levels of airborne nicotine found in bars and nightclubs and the contribution of this exposure to employee hair nicotine concentrations support the need for legislation measures that ensure complete protection from secondhand smoke in these venues.
  Tobacco control 01/2012; · 3.85 Impact Factor
• Article: Allergic rhinitis, chronic rhinosinusitis, and symptom severity: a population-based study.

  Sandra Y Lin, Douglas D Reh, Ana Navas-Acien
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  ABSTRACT: Approximately 20% of the U.S. population suffers from allergic rhinitis (AR), and chronic rhinosinusitis (CRS) is estimated to affect 12.5% of the population. Frequently, many patients suffer from both disorders. In this study, we evaluated the relationship between AR and chronic rhinosinusitis as far as impact on nasal symptoms in a community-based case-control study of adult nonsmokers. In Washington County, MD, 200 subjects were recruited and interviewed from the same community. Subjects were divided into 4 study groups: AR without CRS, CRS without AR, AR with CRS, and a control group without AR or CRS. A validated questionnaire was used to assess upper respiratory symptoms, and disease-specific quality of life. Upper respiratory symptoms were significantly more severe for the affected subjects when compared to controls. Symptom severity was greatest for the CRS groups with or without AR, followed by AR without CRS, and controls least symptomatic. Subjects with AR plus CRS were most likely to have had previous nasal surgery, and use nasal decongestants when compared to the other groups. While both AR and CRS are common in the United States, it appears that patients who suffer from both disorders have more severe symptoms and are more likely to have undergone nasal surgery than if they have only 1 of these disease states.
  International forum of allergy & rhinology. 01/2012; 2(1):51-6.
• Article: Arsenic species and selected metals in human urine: validation of HPLC/ICPMS and ICPMS procedures for a long-term population-based epidemiological study.

  Jürgen Scheer, Silvia Findenig, Walter Goessler, Kevin A Francesconi, Barbara Howard, Jason G Umans, Jonathan Pollak, Maria Tellez-Plaza, Ellen K Silbergeld, Eliseo Guallar, Ana Navas-Acien
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  ABSTRACT: Exposure to high inorganic arsenic concentrations in drinking water has been related to detrimental health effects, including cancers and possibly cardiovascular disease, in many epidemiological studies. Recent studies suggest that arsenic might elicit some of its toxic effects also at lower concentrations. The Strong Heart Study, a large epidemiological study of cardiovascular disease in American Indian communities, collected urine samples and performed medical examinations on 4,549 participants over a 10-year period beginning in 1989. We used anion-exchange HPLC/ICPMS to determine concentrations of arsenic species (methylarsonate, dimethylarsinate and arsenate) in 5,095 urine samples from the Strong Heart Study. We repeated the chromatography on a portion of the urine sample that had been oxidised, by addition of H(2)O(2), to provide additional information on the presence of As(III) species and thio-arsenicals, and by difference, of arsenobetaine and other non-retained cations. Total concentrations for As, Cd, Mo, Pb, Sb, Se, U, W, and Zn were also determined in the urine samples by ICPMS. The dataset will be used to evaluate the relationships between the concentrations of urinary arsenic species and selected metals with various cardiometabolic health endpoints. We present and discuss the analytical protocol put in place to produce this large and valuable dataset.
  Analytical methods 01/2012; 4(2):406-413. · 1.55 Impact Factor
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  Available from: PubMed Central

  Article: Arsenic exposure and hypertension: a systematic review.

  Lalita N Abhyankar, Miranda R Jones, Eliseo Guallar, Ana Navas-Acien
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  ABSTRACT: Environmental exposure to arsenic has been linked to hypertension in persons living in arsenic-endemic areas. We summarized published epidemiologic studies concerning arsenic exposure and hypertension or blood pressure (BP) measurements to evaluate the potential relationship. We searched PubMed, Embase, and TOXLINE and applied predetermined exclusion criteria. We identified 11 cross-sectional studies from which we abstracted or derived measures of association and calculated pooled odds ratios (ORs) using inverse-variance weighted random-effects models. The pooled OR for hypertension comparing the highest and lowest arsenic exposure categories was 1.27 [95% confidence interval (CI): 1.09, 1.47; p-value for heterogeneity = 0.001; I(2) = 70.2%]. In populations with moderate to high arsenic concentrations in drinking water, the pooled OR was 1.15 (95% CI: 0.96, 1.37; p-value for heterogeneity = 0.002; I(2) = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I(2) = 46.6%) before and after excluding an influential study, respectively. The corresponding pooled OR in populations with low arsenic concentrations in drinking water was 1.56 (95% CI: 1.21, 2.01; p-value for heterogeneity = 0.27; I(2) = 24.6%). A dose-response assessment including six studies with available data showed an increasing trend in the odds of hypertension with increasing arsenic exposure. Few studies have evaluated changes in systolic and diastolic BP (SBP and DBP, respectively) measurements by arsenic exposure levels, and those studies reported inconclusive findings. In this systematic review we identified an association between arsenic and the prevalence of hypertension. Interpreting a causal effect of environmental arsenic on hypertension is limited by the small number of studies, the presence of influential studies, and the absence of prospective evidence. Additional evidence is needed to evaluate the dose-response relationship between environmental arsenic exposure and hypertension.
  Environmental Health Perspectives 12/2011; 120(4):494-500. · 7.04 Impact Factor
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  Available from: Kathleen L Caldwell

  Article: Reduction in cadmium exposure in the United States population, 1988-2008: the contribution of declining smoking rates.

  Maria Tellez-Plaza, Ana Navas-Acien, Kathleen L Caldwell, Andy Menke, Paul Muntner, Eliseo Guallar
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  ABSTRACT: Public health policies such as tobacco control, air pollution reduction, and hazardous waste remediation may have reduced cadmium exposure among U.S. adults. However, trends in urine cadmium, a marker of cumulative cadmium exposure, have not been evaluated. We estimated the trends in urine cadmium concentrations in U.S. adults using data from the National Health and Nutrition Examination Surveys (NHANES) from 1988 to 2008. We also evaluated the impact of changes in the distribution of available cadmium determinants (age, sex, race, education, body mass index, smoking, and occupation) at the population level to explain cadmium trends. The study population included 19,759 adults ≥ 20 years of age with measures of urine cadmium and cadmium determinants. Age-adjusted geometric means of urine cadmium concentrations were 0.36, 0.35, 0.27, 0.27, 0.28, 0.25, and 0.26 µg/g creatinine in 1988-1991, 1991-1994, 1999-2000, 2001-2002, 2003-2004, 2005-2006, and 2007-2008, respectively. The age, sex, and race/ethnicity-adjusted percent reduction in urine cadmium geometric means comparing 1999-2002 and 2003-2008 with 1988-1994 were 27.8% (95% confidence interval: 22.3%, 32.9%) and 34.3% (29.9%, 38.4%), respectively (p-trend < 0.001), with reductions in all participant subgroups investigated. In never smokers, reductions in serum cotinine accounted for 15.6% of the observed reduction. In ever smokers, changes in smoking cessation, and cumulative and recent dose accounted for 17.1% of the observed reduction. Urine cadmium concentrations decreased markedly between 1988 and 2008. Declining smoking rates and changes in exposure to tobacco smoke may have played an important role in the decline of urine cadmium concentrations, benefiting both smokers and nonsmokers. Cadmium has been associated to several health outcomes in NHANES 1999-2008. Consequently, despite the observed decline, further reduction in cadmium exposure is needed.
  Environmental Health Perspectives 11/2011; 120(2):204-9. · 7.04 Impact Factor
• Article: Secondhand tobacco smoke: a source of lead exposure in US children and adolescents.

  Andria Apostolou, Esther Garcia-Esquinas, Jeffrey J Fadrowski, Pat McLain, Virginia M Weaver, Ana Navas-Acien
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  ABSTRACT: We evaluated the relationship between secondhand tobacco smoke (SHS) exposure and blood lead levels in US children and adolescents. We analyzed data from 6830 participants aged 3-19 years in the National Health and Nutrition Examination Survey (1999-2004) who were not active smokers and for whom SHS exposure information and blood lead measurements were available. After multivariable adjustment, participants in the highest quartile of serum cotinine (≥ 0.44 μg/L) had 28% (95% confidence interval = 21%, 36%) higher blood lead levels than had those in the lowest quartile (< 0.03 μg/L). Similarly, blood lead levels were 14% and 24% higher in children who lived with 1 or with 2 or more smokers, respectively, than they were in children living with no smokers. Among participants for whom lead dust information was available, the associations between SHS and blood lead levels were similar before and after adjustment for lead dust concentrations. SHS may contribute to increased blood lead levels in US children. Lead dust does not appear to mediate this association, suggesting inhalation as a major pathway of exposure. Eliminating SHS exposure could reduce lead exposure in children.
  American Journal of Public Health 08/2011; 102(4):714-22. · 3.93 Impact Factor
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  Available from: PubMed Central

  Article: Blood cadmium and estimated glomerular filtration rate in Korean adults.

  Young Hwangbo, Virginia M Weaver, Maria Tellez-Plaza, Eliseo Guallar, Byung-Kook Lee, Ana Navas-Acien
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  ABSTRACT: Cadmium is a nephrotoxicant at high exposure levels. Few studies have evaluated the role of cadmium in kidney function at low-exposure levels. We evaluated the association of blood cadmium with estimated glomerular filtration rate (eGFR) in the Korean adult population. We evaluated 1,909 adults ≥ 20 years of age who participated in the 2005 Korean National Health and Nutrition Examination Survey and had blood cadmium determinations. eGFR was calculated using the Modification of Diet in Renal Disease equation. Blood cadmium geometric means were 1.57 μg/L for men and 1.49 μg/L for women. The difference in eGFR levels that compared participants in the highest versus lowest cadmium tertiles, after multivariable adjustment, was -1.85 [95% confidence interval (CI): -3.55, -0.16] mL/min per 1.73 m2 in women and 0.67 (-1.16, 2.50) mL/min per 1.73 m2 in men. Among men, the association between blood cadmium and eGFR was modified by blood lead levels (p-value for interaction = 0.048). The fully adjusted differences in eGFR levels for a 2-fold increase in blood cadmium levels were -1.14 (-3.35, 1.07) and 1.84 (0.54, 3.14) mL/min per 1.73 m2 in men with blood lead levels below and above the median (2.75 μg/dL), respectively. Elevated blood cadmium levels were associated with lower eGFR in women, which supports the role of cadmium as a risk factor for chronic kidney disease. In men, there was no overall association, although elevated blood cadmium levels were associated with higher eGFR levels in men with high blood lead levels and nonstatistically associated with lower eGFR levels in men with low blood lead levels.
  Environmental Health Perspectives 08/2011; 119(12):1800-5. · 7.04 Impact Factor