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Effect of Residential Lead-Hazard Interventions on Childhood Blood Lead Concentrations and Neurobehavioral Outcomes: A Randomized Clinical Trial.
Braun, JM, Hornung, R, Chen, A, Dietrich, KN, Jacobs, DE, Jones, R, Khoury, JC, Liddy-Hicks, S, Morgan, S, Vanderbeek, SB, et al
JAMA pediatrics. 2018;(10):934-942
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IMPORTANCE Childhood lead exposure is associated with neurobehavioral deficits. The effect of a residential lead hazard intervention on blood lead concentrations and neurobehavioral development remains unknown. OBJECTIVE To determine whether a comprehensive residential lead-exposure reduction intervention completed during pregnancy could decrease residential dust lead loadings, prevent elevated blood lead concentrations, and improve childhood neurobehavioral outcomes. DESIGN, SETTING, AND PARTICIPANTS This longitudinal, community-based randomized clinical trial of pregnant women and their children, the Health Outcomes and Measures of the Environment (HOME) Study, was conducted between March 1, 2003, and January 31, 2006. Pregnant women attending 1 of 9 prenatal care clinics affiliated with 3 hospitals in the Cincinnati, Ohio, metropolitan area were recruited. Of the 1263 eligible women, 468 (37.0%) agreed to participate and 355 women (75.8%) were randomized in this intention-to-treat analysis. Participants were randomly assigned to receive 1 of 2 interventions designed to reduce residential lead or injury hazards. Follow-up on children took place at 1, 2, 3, 4, 5, and 8 years of age. Data analysis was performed from September 2, 2017, to May 6, 2018. MAIN OUTCOMES AND MEASURES Residential dust lead loadings were measured at baseline and when children were 1 and 2 years of age. At 1, 2, 3, 4, 5, and 8 years of age, the children's blood lead concentrations as well as behavior, cognition, and executive functions were assessed. RESULTS Of the 355 women randomized, 174 (49.0%) were assigned to the intervention group (mean [SD] age at delivery, 30.1 (5.5) years; 119 [68.3%] self-identified as non-Hispanic white) and 181 (50.9%) to the control group (mean [SD] age at delivery, 29.2 [5.7] years; 123 [67.9%] self-identified as non-Hispanic white). The intervention reduced the dust lead loadings for the floor (24%; 95% CI, -43% to 1%), windowsill (40%; 95% CI, -60% to -11%), and window trough (47%; 95% CI, -68% to -10%) surfaces. The intervention did not statistically significantly reduce childhood blood lead concentrations (-6%; 95% CI, -17% to 6%; P = .29). Neurobehavioral test scores were not statistically different between children in the intervention group than those in the control group except for a reduction in anxiety scores in the intervention group (β = -1.6; 95% CI, -3.2 to -0.1; P = .04). CONCLUSIONS AND RELEVANCE Residential lead exposures, as well as blood lead concentrations in non-Hispanic black children, were reduced through a comprehensive lead-hazard intervention without elevating the lead body burden. However, this decrease did not result in substantive neurobehavioral improvements in children. TRIAL REGISTRATION ClinicalTrials.gov identifier: NCT00129324.
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Sex-Specific Associations between One-Carbon Metabolism Indices and Posttranslational Histone Modifications in Arsenic-Exposed Bangladeshi Adults.
Howe, CG, Liu, X, Hall, MN, Ilievski, V, Caudill, MA, Malysheva, O, Lomax-Luu, AM, Parvez, F, Siddique, AB, Shahriar, H, et al
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2017;(2):261-269
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BACKGROUND Posttranslational histone modifications (PTHMs) are altered by arsenic, an environmental carcinogen. PTHMs are also influenced by nutritional methyl donors involved in one-carbon metabolism (OCM), which may protect against epigenetic dysregulation. METHODS We measured global levels of three PTHMs, which are dysregulated in cancers (H3K36me2, H3K36me3, H3K79me2), in peripheral blood mononuclear cells (PBMC) from 324 participants enrolled in the Folic Acid and Creatine Trial, a randomized trial in arsenic-exposed Bangladeshi adults. Sex-specific associations between several blood OCM indices (folate, vitamin B12, choline, betaine, homocysteine) and PTHMs were examined at baseline using regression models, adjusted for multiple tests by controlling for the false discovery rate (PFDR). We also evaluated the effects of folic acid supplementation (400 μg/d for 12 weeks), compared with placebo, on PTHMs. RESULTS Associations between choline and H3K36me2 and between vitamin B12 and H3K79me2 differed significantly by sex (Pdiff < 0.01 and <0.05, respectively). Among men, plasma choline was positively associated with H3K36me2 (PFDR < 0.05), and among women, plasma vitamin B12 was positively associated with H3K79me2 (PFDR < 0.01). Folic acid supplementation did not alter any of the PTHMs examined (PFDR = 0.80). CONCLUSIONS OCM indices may influence PTHMs in a sex-dependent manner, and folic acid supplementation, at this dose and duration, does not alter PTHMs in PBMCs. IMPACT This is the first study to examine the influences of OCM indices on PTHMs in a population that may have increased susceptibility to cancer development due to widespread exposure to arsenic-contaminated drinking water and a high prevalence of hyperhomocysteinemia. Cancer Epidemiol Biomarkers Prev; 26(2); 261-9. ©2016 AACR.
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Widespread sucralose exposure in a randomized clinical trial in healthy young adults.
Sylvetsky, AC, Walter, PJ, Garraffo, HM, Robien, K, Rother, KI
The American journal of clinical nutrition. 2017;(4):820-823
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Background: Low-calorie sweeteners (LCSs) are found in many foods and beverages, but consumers may not realize their presence, and their role in appetite, weight, and health is controversial. Although consumption limits based on toxicologic safety are well established, the threshold required to exert clinically relevant metabolic effects is unknown.Objectives: This study aimed to determine whether individuals who do not report consumption of LCSs can be correctly characterized as "unexposed" and to investigate whether instructions to avoid LCSs are effective in minimizing exposure.Design: Eighteen healthy 18- to 35-y-old "nonconsumers" (<1 food or beverage with LCSs/mo) enrolled in a 2-wk trial designed to evaluate the effects of LCSs on the gut microbiota. The trial consisted of 3 visits. At baseline, participants were counseled extensively about avoiding LCSs. After the run-in, participants were randomly assigned to consume diet soda containing sucralose or carbonated water (control) 3 times/d for 1 wk. Food diaries were maintained throughout the study, and a spot urine sample was collected at each visit.Results: At baseline, 8 participants had sucralose in their urine (29.9-239.0 ng/mL; mean ± SD: 111.4 ± 91.5 ng/mL). After the run-in, sucralose was found in 8 individuals (2 of whom did not have detectable sucralose at baseline) and ranged from 25.0 to 1062.0 ng/mL (mean ± SD: 191.7 ± 354.2 ng/mL). Only 1 participant reported consumption of an LCS-containing food before her visit. After the intervention, sucralose was detected in 3 individuals randomly assigned to receive carbonated water (26-121 ng/mL; mean ± SD: 60.7 ± 52.4 ng/mL).Conclusions: Despite the selection of healthy volunteers with minimal reported LCS consumption, more than one-third were exposed to sucralose at baseline and/or before randomization, and nearly half were exposed after assignment to the control. This shows that instructions to avoid LCSs are not effective and that nondietary sources (e.g., personal care products) may be important contributors to overall exposure. This trial was registered at clinicaltrials.gov as NCT02877186.
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Kernel Density Estimation as a Measure of Environmental Exposure Related to Insulin Resistance in Breast Cancer Survivors.
Jankowska, MM, Natarajan, L, Godbole, S, Meseck, K, Sears, DD, Patterson, RE, Kerr, J
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2017;(7):1078-1084
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Background: Environmental factors may influence breast cancer; however, most studies have measured environmental exposure in neighborhoods around home residences (static exposure). We hypothesize that tracking environmental exposures over time and space (dynamic exposure) is key to assessing total exposure. This study compares breast cancer survivors' exposure to walkable and recreation-promoting environments using dynamic Global Positioning System (GPS) and static home-based measures of exposure in relation to insulin resistance.Methods: GPS data from 249 breast cancer survivors living in San Diego County were collected for one week along with fasting blood draw. Exposure to recreation spaces and walkability was measured for each woman's home address within an 800 m buffer (static), and using a kernel density weight of GPS tracks (dynamic). Participants' exposure estimates were related to insulin resistance (using the homeostatic model assessment of insulin resistance, HOMA-IR) controlled by age and body mass index (BMI) in linear regression models.Results: The dynamic measurement method resulted in greater variability in built environment exposure values than did the static method. Regression results showed no association between HOMA-IR and home-based, static measures of walkability and recreation area exposure. GPS-based dynamic measures of both walkability and recreation area were significantly associated with lower HOMA-IR (P < 0.05).Conclusions: Dynamic exposure measurements may provide important evidence for community- and individual-level interventions that can address cancer risk inequities arising from environments wherein breast cancer survivors live and engage.Impact: This is the first study to compare associations of dynamic versus static built environment exposure measures with insulin outcomes in breast cancer survivors. Cancer Epidemiol Biomarkers Prev; 26(7); 1078-84. ©2017 AACR.
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Biomonitoring Human Exposure to Household Air Pollution and Association with Self-reported Health Symptoms - A Stove Intervention Study in Peru.
Li, Z, Commodore, A, Hartinger, S, Lewin, M, Sjödin, A, Pittman, E, Trinidad, D, Hubbard, K, Lanata, CF, Gil, AI, et al
Environment international. 2016;:195-203
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BACKGROUND Household air pollution (HAP) from indoor biomass stoves contains harmful pollutants, such as polycyclic aromatic hydrocarbons (PAHs), and is a leading risk factor for global disease burden. We used biomonitoring to assess HAP exposure and association with self-reported symptoms in 334 non-smoking Peruvian women to evaluate the efficacy of a stove intervention program. METHODS We conducted a cross-sectional study within the framework of a community randomized control trial. Using urinary PAH metabolites (OH-PAHs) as the exposure biomarkers, we investigated whether the intervention group (n=155, with new chimney-equipped stoves) were less exposed to HAP compared to the control group (n=179, with mostly open-fire stoves). We also estimated associations between the exposure biomarkers, risk factors, and self-reported health symptoms, such as recent eye conditions, respiratory conditions, and headache. RESULTS We observed reduced headache and ocular symptoms in the intervention group than the control group. Urinary 2-naphthol, a suggested biomarker for inhalation PAH exposure, was significantly lower in the intervention group (GM with 95% CI: 13.4 [12.3, 14.6] μg/g creatinine) compared to control group (16.5 [15.0, 18.0] μg/g creatinine). Stove type and/or 2-naphthol was associated with a number of self-reported symptoms, such as red eye (adjusted OR with 95% CI: 3.80 [1.32, 10.9]) in the past 48h. CONCLUSIONS Even with the improved stoves, the biomarker concentrations in this study far exceeded those of the general populations and were higher than a no-observed-genotoxic-effect-level, indicating high exposure and a potential for increased cancer risk in the population.
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Development of a prognostic model based on demographic, environmental and lifestyle information for predicting incidences of symptomatic respiratory or gastrointestinal infection in adult office workers.
Hovi, T, Ollgren, J, Haapakoski, J, Savolainen-Kopra, C
Trials. 2016;(1):545
Abstract
BACKGROUND Occurrence of respiratory tract infection (RTI) or gastrointestinal tract infection (GTI) is known to vary between individuals and may be a confounding factor in the analysis of the results of intervention trials. We aimed at developing a prognostic model for predicting individual incidences of RTI and GTI on the basis of data collected in a hand-hygiene intervention trial among adult office workers, and comprising a prior-to-onset questionnaire on potential infection-risk factors and weekly electronic follow-up reports on occurrence of symptoms of, and on exposures to RTI or GTI. METHODS A mixed-effect negative binomial regression model was used to calculate a predictor-specific incidence rate ratio for each questionnaire variable and for each of the four endpoints, and predicted individual incidences for symptoms of and exposures to RTI and GTI. In the fitting test these were then compared with the observed incidences. RESULTS Out of 1270 eligible employees of six enterprises, 683 volunteered to participate in the trial. Ninety-two additional participants were recruited during the follow-up. Out of the 775 registered participants, 717 returned the questionnaire with data on potential predictor variables and follow-up reports for determination of outcomes. Age and gender were the strongest predictors of both exposure to, and symptoms of RTI or GTI, although no gender difference was seen in the RTI incidence. In addition, regular use of public transport, and history of seasonal influenza vaccination increased the risk of RTI. The individual incidence values predicted by the model showed moderate correlation with those observed in each of the four categories. According to the Cox-Snell multivariate formula the model explained 11.2% of RTI and 3.3% of GTI incidences. Resampling revealed mean and 90% confidence interval values of 10.9 (CI 6.9-14.5)% for RTI and 2.4 (0.6-4.4)% for GTI. CONCLUSION The model created explained a relatively small proportion of the occurrence of RTI or GTI. Unpredictable exposure to disease agents, and individual susceptibility factors are likely to be key determinants of disease emergence. Yet, the model might be useful in prerandomization stratification of study population in RTI intervention trials where the expected difference between trial arms is relatively small. TRIAL REGISTRATION Registered at ClinicalTrials.gov with Identifier NCT00821509 on 12 March 2009.
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[Long-term effect of environmental cadmium exposure on human body's mineral metabolic balance].
Ling, HT, Huang, R, Liang, XX, Li, ZX, Wang, J, Tan, JB, Wu, SX, Wang, P, Chen, ZH, Huang, Q, et al
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]. 2016;(4):316-21
Abstract
OBJECTIVE To investigate the effect of long-term exposure to environmental cadmium on eight mineral element's metabolic balance of human body. METHODS To choose a high cadmium area polluted by smelting and mining north of Guangdong province and a cadmium-free area with a similar economic level, and living and eating habit of residents as a contrast from April 2011 to August 2012. Stratified random sampling and clustered sampling method were adopted to choose the non-occupationally cadmium-exposed respondents who have lived in local area for more than 15 years, older than 40 years, having local rice and vegetable as the main dietary source, with simple and relatively stable diet, and without diabetes, kidney disease, thyroid disease, liver disease or other history of chronic disease. This study included 298 respondents, of whom 155 were in cadmium exposure group and 143 in control group. Questionnaires was used to acquire their health status and their morning urine samples were collected. Electrolytically coupled plasma mass spectrometry (ICP-MS) was used to test the concentrations of sodium(Na), magnesium (Mg), phosphorus (P), potassium (K), calcium (Ca), copper (Cu), zinc (Zn) and iodine (I). The Mann-Whitney U test method was used to compare the differences of concentrations of urinary cadmium, Na, Mg, P, K, Ca, Cu, Zn, I, and the ratio of Na to K (Na/K), Ca to P (Ca/P) between exposed group and control group.χ(2) test was used to compare the abnormal rate of urinary cadmium between exposed group and control group. Pearson correlation and multiple regression method were used to investigate the relationship between urinary cadmium levels, gender, age, smoking, passive smoking, and minerals. RESULTS The urinary cadmium level P50 (P25-P75) in exposed group was 5.45 (2.62-10.68) μg/g·cr, which was higher than that of the control group, which was 1.69 (1.22-2.36) μg/g·cr (Z=-10.49,P<0.001). The abnormal rate of urinary cadmium was 51.6% (80/155), which was higher than that of the control group (2.8 %(4/143)) (χ(2)= 87.56, P<0.001). The urinary Ca, Cu, Zn, and I level P50 (P25-P75) of exposed group were 173.80 (114.40-251.70), 20.55 (14.95-28.44), 520.23 (390.25-647.15), and 246.94 (203.65-342.97) μg/g·cr, which were higher than those in control group (142.42 (96.87-179.11), 15.44 (12.26-20.98), 430.09 (309.85-568.78) and 213.85 (156.70-281.63) μg/g·cr, respectively) (Z values were-4.33,-5.04,-3.47 and-4.24, all P values <0.001). The urinary P, K level P50 (P25-P75) of exposed group were 582.50 (463.20-742.8), 890.10(666.00-1 305.40) μg/g·cr, which were lower than control group (694.50 (546.20-851.17), 1 098.58(904.53-1 479.18) μg/g·cr) (Z values were-3.36,-4.02, all P values <0.001). on Based the results of Pearson correlation analysis, urinary cadmium was positively correlated with urinary Ca, Cu, Zn, and I, and the correlation coefficients were 0.31, 0.61, 0.38, and 0.25, respectively (all P values <0.05). Based on the results of multiple regression analysis, urinary cadmium levels contributed most to the metabolic balance of urinary Ca, Cu, Zn and I. The standardized regression coefficients were 0.31, 0.59, 0.39, and 0.24, respectively (all P values<0.001). CONCLUSION Long-term environmental exposure to cadmium affected the metabolic balance of Ca, Cu, Zn and I in human body.
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Mitigating aflatoxin exposure to improve child growth in Eastern Kenya: study protocol for a randomized controlled trial.
Hoffmann, V, Jones, K, Leroy, J
Trials. 2015;:552
Abstract
BACKGROUND While the few studies that have looked at the association between stunting and aflatoxin exposure have found surprisingly large effects, the results remain inconclusive due to a lack of randomized controlled studies. This protocol describes a non-blinded, cluster-randomized controlled trial with the specific objective of testing the impact of reduced aflatoxin exposure on (individual) child linear growth. METHODS/DESIGN Participants were recruited from among households containing women in the last 5 months of pregnancy in 28 maize-growing villages within Meru and Tharaka-Nithi Counties in Kenya. Households in villages assigned to the intervention group are offered rapid testing of their stored maize for the presence of aflatoxin each month; any maize found to contain more than 10 ppb aflatoxin is replaced with an equal amount of maize that contains less than this concentration of the toxin. They are also offered the opportunity to buy maize that has been tested and found to contain less than 10 ppb aflatoxin at local shops. Clusters (villages) were allocated to the intervention group (28 villages containing 687 participating households) or control group (28 villages containing 536 participating households) using a random number generator. The trial, which is funded by United Kingdom (UK) aid from the UK government, the Global Food Security Portal, and the Ministry for Foreign Affairs of Finland, is currently ongoing. DISCUSSION This study is the first randomized controlled trial (RCT) to test for a causal impact of aflatoxin exposure on child growth. Whether or not this relationship is found, its results will have implications for the prioritization of aflatoxin control efforts by governments in affected regions, as well as international donors. TRIAL REGISTRATION American Economic Association RCT Registry # 0000105 . Initial registration date: 6 November 2013, last updated 30 December 2014.
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Environmental risk factors for women with polycystic ovary syndrome in china: a population-based case-control study.
Zhang, J, Liu, XF, Liu, Y, Xu, LZ, Zhou, LL, Tang, LL, Zhuang, J, Li, TT, Guo, WQ, Hu, R, et al
Journal of biological regulators and homeostatic agents. 2014;(2):203-11
Abstract
Polycystic ovary syndrome (PCOS) is a common reproductive endocrinology disease with heterogeneous phenotype. Environmental factors are thought to be involved in the development of PCOS. The present study aimed to explore the potential environmental risk factors of PCOS. A cross-sectional study and stratified population-based case-control study were carried out. Pre-designed questionnaires were prepared, including questions about medication history, contact history of endocrine disruptors (EDs), environment and habituation. Fasting blood was collected for measurement of sex hormone, glucose and insulin. Matched logistic regression analysis was used to find the potential independent risk factor of PCOS. One thousand eight hundred fifty-four participants (aged 12-44 years) were analyzed in the cross-sectional investigation. One hundred sixty-nine PCOS patients and 338 matched controls were compared. PCOS patients were more frequent than controls in eating plastic-packaged food (p=0.001), contacting pesticide (p=0.021), eating fruit with pericarp (p=0.001), living beside a garbage heap (p=0.001), working at an acid plant (p=0.028), taking Chinese patent drugs (p=0.001), smoking (p=0.028) and drinking alcohol (p=0.001). However, PCOS patients were less likely to use kitchen ventilators (p=0.002), eat canned food (p=0.049), contact decorated materials, use skin care products (p=0.01) and cosmetics (p=0.027). No difference was found in taking antiepileptic drugs (p=0.93). Eating plastic-packaged food (p=0.001, OR=44.449), eating fruit with pericarp (p=0.03, OR=5.7) and drinking alcohol (p=0.001, OR=29.632) were found to be the independent risk factors for PCOS. The existence of an association between EDs and PCOS was proved. Plastic-packaged food, fruit with pericarp and drinking alcohol should be avoided as possible as we can. However, the causal relationships among these factors and PCOS should be proved by further research.
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Ozone exposure, vitamin C intake, and genetic susceptibility of asthmatic children in Mexico City: a cohort study.
Moreno-Macías, H, Dockery, DW, Schwartz, J, Gold, DR, Laird, NM, Sienra-Monge, JJ, Del Río-Navarro, BE, Ramírez-Aguilar, M, Barraza-Villarreal, A, Li, H, et al
Respiratory research. 2013;(1):14
Abstract
BACKGROUND We previously reported that asthmatic children with GSTM1 null genotype may be more susceptible to the acute effect of ozone on the small airways and might benefit from antioxidant supplementation. This study aims to assess the acute effect of ozone on lung function (FEF(25-75)) in asthmatic children according to dietary intake of vitamin C and the number of putative risk alleles in three antioxidant genes: GSTM1, GSTP1 (rs1695), and NQO1 (rs1800566). METHODS 257 asthmatic children from two cohort studies conducted in Mexico City were included. Stratified linear mixed models with random intercepts and random slopes on ozone were used. Potential confounding by ethnicity was assessed. Analyses were conducted under single gene and genotype score approaches. RESULTS The change in FEF(25-75) per interquartile range (60 ppb) of ozone in persistent asthmatic children with low vitamin C intake and GSTM1 null was -91.2 ml/s (p = 0.06). Persistent asthmatic children with 4 to 6 risk alleles and low vitamin C intake showed an average decrement in FEF(25-75) of 97.2 ml/s per 60 ppb of ozone (p = 0.03). In contrast in children with 1 to 3 risk alleles, acute effects of ozone on FEF25-75 did not differ by vitamin C intake. CONCLUSIONS Our results provide further evidence that asthmatic children predicted to have compromised antioxidant defense by virtue of genetic susceptibility combined with deficient antioxidant intake may be at increased risk of adverse effects of ozone on pulmonary function.