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Hypertension is associated with body mass index (BMI) and cardiovascular and cerebrovascular diseases (CCDs). Whether hypertension modifies the relationship between BMI and CCDs is still unclear. We examined the association between BMI and CCDs and tested whether effect measure modification was present by hypertension. We identified a population-based sample of 3,942 participants in Shuncheng, Fushun, Liaoning, China. Hypertension was defined as any past use of antihypertensive medication or having a measured systolic/diastolic blood pressure ≥130/80 mm Hg. BMI was calculated from measured body weight and body height. Data on diagnosed CCDs were self-reported and validated in the medical records. We used logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations between BMI and CCDs. Higher BMI was associated with increased odds of having CCDs (OR = 1.19, 95% CI: 1.07–1.31). This association was significantly modified by hypertension (P for interaction 0.10). Although higher BMI was associated with increased odds of CCDs, the relationship was mainly limited to hypertensive patients.

Introduction: Epidemiological studies investigating the association between carnitine and breast cancer are scarce. Materials and Methods: This 1:1 age-matched retrospective case-control study identified 991 female breast cancer cases and 991 female controls without breast cancer using pathological testing. We used targeted metabolomics technology to measure 16 types of whole blood carnitine compounds, such as free carnitine (C0) and octadecanoylcarnitine (C18). Results: The average age for cases and controls was approximately 50 ± 8.7 years. After adjusting for covariates, each standard deviation (SD) increase in malonylcarnitine (C3DC; OR 0.91; 95% CI 0.83-1.00), decenoylcarnitine (C10:1; OR 0.87; 95% CI 0.79-0.96), and decadienoylcarnitine (C10:2; OR 0.90; 95% CI 0.82-0.99) level was associated with decreased odds of breast cancer. However, higher butyrylcarnitine (C4) levels were associated with increased odds of breast cancer (OR 1.12; 95% CI 1.02-1.23). No statistically significant relationship was noted between other carnitine compounds and breast cancer. The false discovery rates for C3DC, C4, C10:1 and C10:2 were 0.172, 0.120, 0.064 and 0.139, respectively. Conclusions: Higher levels of C3DC, C10:1, and C10:2 were protective factors for breast cancer, whereas increased C4 levels were a risk factor for the disease. [ABSTRACT FROM AUTHOR]

In vitro and vivo studies indicate that oxidative stress contributes to bone loss. Fluorescent oxidation products (FlOPs) are novel biomarkers of oxidative stress; they reflect global oxidative damage of lipids, proteins, carbohydrates, and DNA. However, whether FlOPs are associated with bone mineral density (BMD) is still unclear. In the present study, we examined the association between FlOPs and BMD among male veterans. This cross-sectional study was conducted among participants recruited from the Department of Medical Examination, The Second Hospital of Jilin University in Jilin, China. We identified male veterans who were at least 50 y old between June and October of 2019. Plasma FlOPs were measured with a fluorescent microplate reader (excitation/emission wavelength: 320/420 nm). BMD were measured by dual-energy X-ray absorptiometry (DXA). The association between FlOPs and BMD was tested by multivariable linear regression models. A total of 164 male veterans were enrolled in the study, the average age was 56.6 y. After adjusting for covariates, veterans who had FlOP levels in the highest tertile had a statistically significant lower femoral neck (β = -0.044; p = 0.007) and total hip BMD (β = -0.045; p = 0.020) as compared to those with FlOP levels in the lowest tertile. Similar results were found when FlOPs were treated as a continuous variable (per 1-SD increase, β = -0.014 and p = 0.033 for femoral neck BMD; β = -0.016 and p = 0.047 for total hip BMD). Higher FlOP levels were associated with lower BMD among male veterans. [ABSTRACT FROM AUTHOR]

BACKGROUND: Prenatal exposure to endocrine disruptors has been associated with increased risk of childhood obesity. However, epidemiologic studies on polybrominated diphenyl ethers (PBDEs) are limited despite animal studies indicating PBDEs' potential role as an obesogen. OBJECTIVES: We investigated whether maternal concentrations of BDEs 28, 47, 99, 100, 153, and ΣPBDEs during pregnancy were associated with anthropometric measures in children aged 1-8 years. METHODS: We examined 318 mother--child pairs in the Health Outcomes and Measures of the Environment (HOME) Study, a birth cohort enrolled from 2003 through 2006 (Cincinnati, OH). Serum PBDEs were measured at 16 ± 3 weeks gestation. We measured child height (1-8 years), weight (1-8 years), body mass index (BMI) (2-8 years), waist circumference (4-8 years), and body fat (8 years). To account for repeated measures, we used linear mixed models and generalized estimating equations to estimate associations between maternal PBDEs and child anthropometric measures. RESULTS: We found no statistically significant associations between prenatal PBDEs and height or weight z-score. A 10-fold increase in maternal serum BDE-153 was associated with lower BMI 2-score (β = -0.36; 95% CI: -0.60, -0.13) at 2-8 years, smaller waist circumference (β = -1.81 cm; 95% CI: -3.13, -0.50) at 4-8 years, and lower percent body fat (β = -2.37%; 95% CI: -4.21, -0.53) at 8 years. A decrease in waist circumference at 4-8 years was observed with a 10-fold increase in BDE-100 (β = -1.50 cm; 95% CI: -2.93, -0.08) and ΣPBDEs (β = -1.57 cm; 95% CI: -3.11, -0.02). CONCLUSIONS: Reverse causality may have resulted in prenatal PBDEs, particularly BDE-153, and decreased BMI, waist circumference, and body fat. Environ Health Perspect 124:1891-1897; http://dx.doi.org/10.1289/EHP139, Introduction Childhood obesity is associated with adverse health effects, including diabetes, dyslipidemia, fatty liver disease, and hypertension (Daniels 2009). Between 1980 and 2013, the global prevalence of childhood obesity increased [...]

Summary : Higher intake of β-carotene and β-cryptoxanthin were associated with lower risk of osteoporosis. A very high intake of lutein + zeaxanthin was also associated with lower risk of osteoporosis. These results support the beneficial role of carotenoids on bone health. Purpose: To examine the associations of α-carotene, β-carotene, β-cryptoxanthin, lycopene, and lutein + zeaxanthin intake with the risk of osteoporosis based on the cross-sectional data from the National Health and Nutrition Examination Survey (NHANES), 2005–2018. Methods: This study identified individuals ≥ 50 years old with valid and complete data on carotenoid intake and bone mineral density (BMD). Intake of α-carotene, β-carotene, β-cryptoxanthin, lycopene, and lutein + zeaxanthin was averaged from two 24-h recall interviews. BMD was measured by dual-energy X-ray absorptiometry (DXA) and converted to T-scores; osteoporosis was defined as a T-score ≤ − 2.5. We used logistic regression models to test the associations between carotenoids and osteoporosis, adjusting for factors such as age, sex, race, and education. Results: Participants were on average 61.9 years of age, with 57.5% identifying as females. Higher quintiles of β-carotene (odds ratio [OR] for quintile 5 vs. 1:0.33; 95% CI: 0.19–0.59; P for trend = 0.010) and β-cryptoxanthin intake (OR for quintile 5 vs. 1:0.61; 95% CI: 0.39–0.97; P for trend = 0.037) were associated with reduced risk of osteoporosis. Similar and marginally significant results for lutein + zeaxanthin intake was found (OR for quintile 5 vs. 1:0.53; 95% CI: 0.30–0.94; P for trend = 0.076). There was no association of α-carotene and lycopene intake with osteoporosis. These associations did not differ by sex (all P_interaction > 0.05). Conclusions: Higher β-carotene and β-cryptoxanthin intake was associated with decreased osteoporosis risk. A very high intake of lutein + zeaxanthin was also associated with lower risk of osteoporosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Polybrominated diphenyl ethers (PBDEs) reduce blood concentrations of thyroid hormones in laboratory animals, but it is unclear whether PBDEs disrupt thyroid hormones in pregnant women or newborn infants. OBJECTIVES: We investigated the relationship between maternal PBDE levels and thyroid hormone concentrations in maternal and cord sera. Methods: we used data from the Health Outcomes and Measures of the Environment (HOME) Study, a prospective birth cohort of 389 pregnant women in Cincinnati, Ohio, who were enrolled from 2003 through 2006 and delivered singleton infants. Maternal serum PBDE concentrations were measured at enrollment (16 ± 3 weeks of gestation). Thyroid hormone concentrations were measured in maternal serum at enrollment (n = 187) and in cord serum samples (n = 256). RESULTS: Median maternal serum concentrations of BDEs 28 and 47 were 1.0 and 19.1 ng/g lipid, respectively. A 10-fold increase in BDEs 28 and 47 concentrations was associated with a 0.85-µg/dL [95% confidence interval (CI): 0.05, 1.64] and 0.82-µg/dL (95% CI: 0.12, 1.51) increase in maternal total thyroxine concentrations ([TT.sub.4]), respectively. Both congeners were also positively associated with maternal free thyroxine ([FT.sub.4]). We also observed positive associations between BDE-47 and maternal total and free triiodothyronine ([TT.sub.4] and [FT.sub.3]). A 10-fold increase in BDE-28 was associated with elevated [FT.sub.3] concentrations (β = 0.14 µg/mL; 95% CI: 0.02, 0.26). In contrast, maternal PBDE levels were not associated with thyroid hormone concentrations in cord serum. CONCLUSIONS: These findings suggest that maternal PBDE exposure, particularly BDEs 28 and 47, are associated with maternal concentrations of [T.sub.4] and [T.sub.3] during pregnancy. http://dx.doi.org/10.1289/ehp.1408996, Introduction Polybrominated diphenyl ethers (PBDEs), synthetic flame retardants, have been used in the manufacture of consumer products, including furniture foam, carpet padding, and electronics. Because they are semivolatile and are [...]

Production of organophosphate esters (OPEs), which represent a major flame-retardant class present in consumer goods, has increased over the past 2 decades. Experimental studies suggest that OPEs may be associated with thyroid hormone disruption, but few human studies have examined this association. We quantified OPE metabolites in the urine of 298 pregnant women from Cincinnati, Ohio, in the Health Outcomes and Measures of the Environment Study (enrolled 2003–2006) at 3 time points (16 and 26 weeks' gestation, and at delivery), and thyroid hormones in 16-week maternal and newborn cord sera. Urinary bis(1,3-dichloro-2-propyl)-phosphate concentrations were generally associated with decreased triiodothyronine and thyroxine levels and increased thyroid-stimulating hormone levels in maternal and newborn thyroid hormones in quartile dose–response analyses and multiple informant models. There was weaker evidence for thyroid hormone alterations in association with diphenyl-phosphate and di- n -butyl-phosphate. Bis-2-chloroethyl-phosphate was not associated with alterations in thyroid hormones in any analyses. We did not observe any evidence of effect modification by infant sex. These results suggest that gestational exposure to some OPEs may influence maternal and neonatal thyroid function, although replication in other cohorts is needed. [ABSTRACT FROM AUTHOR]

Background Epidemiological studies have historically focused on single toxicants, or toxic chemicals, and neurodevelopment, even though the interactions of chemicals and nutrients may result in additive, synergistic, antagonistic, or potentiating effects on neurological endpoints. Investigating the impact of environmentally-relevant chemical mixtures, including heavy metals and endocrine disrupting chemicals (EDCs), is more reflective of human exposures and may result in more refined environmental policies to protect the public. Objective In this review, we provide a summary of epidemiological studies that have analyzed chemical mixtures of heavy metals and EDCs and neurobehavior utilizing multi-chemical models, including frequentist and Bayesian methods. Content Studies investigating chemicals and neurobehavior have the opportunity to not only examine the impact of chemical mixtures, but they can also identify chemicals from a mixture that may play a key role in neurotoxicity, investigate interactive effects, estimate non-linear dose response, and identify potential windows of susceptibility. The examination of neurobehavioral domains is particularly challenging given that traits emerge and change over time and subclinical nuances of neurobehavior are often unrecognized. To date, only a handful of epidemiological studies examining neurodevelopment have utilized multi-pollutant models in the investigation of heavy metals and EDCs. However, these studies were successful in identifying contaminants of importance from the exposure mixtures. Summary and Outlook Investigators are encouraged to broaden their focus to include more environmentally relevant mixtures of chemicals using advanced statistical approaches, particularly to aid in identifying potential mechanisms underlying associations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies of prenatal exposure to drinking-water nitrate and birth defects in offspring have not accounted for water consumption patterns or potential interaction with nitrosatable drugs. OBJECTIVES: We examined the relation between prenatal exposure to drinking-water nitrate and selected birth defects, accounting for maternal water consumption patterns and nitrosatable drug exposure. METHODS: With data from the National Birth Defects Prevention Study, we linked addresses of 3,300 case mothers and 1,121 control mothers from the Iowa and Texas sites to public water supplies and respective nitrate measurements. We assigned nitrate levels for bottled water from collection of representative samples and standard laboratory testing. Daily nitrate consumption was estimated from self-reported water consumption at home and work. RESULTS: With the lowest tertile of nitrate intake around conception as the referent group, mothers of babies with spina bifida were 2.0 times more likely (95% CI: 1.3, 3.2) to ingest [greater than or equal to] 5 mg nitrate daily from drinking water (vs. < 0.91 mg) than control mothers. During 1 month preconception through the first trimester, mothers of limb deficiency, cleft palate, and cleft lip cases were, respectively, 1.8 (95% CI: 1.1, 3.1), 1.9 (95% CI: 1.2, 3.1), and 1.8 (95% CI: 1.1, 3.1) times more likely than control mothers to ingest [greater than or equal to] 5.42 mg of nitrate daily (vs. < 1.0 mg). Higher water nitrate intake did not increase associations between prenatal nitrosatable drug use and birth defects. CONCLUSIONS: Higher water nitrate intake was associated with several birth defects in offspring, but did not strengthen associations between nitrosatable drugs and birth defects. http://dx.doi.org/10.1289/ehp.1206249, Introduction Nitrate is one of the most widespread chemical contaminants in aquifers around the world (Spalding and Exner 1993). Results from several epidemiologic studies have suggested an association between prenatal [...]

Toxicological studies indicate that poly- and perfluoroalkyl substances (PFAS) may be neurotoxic, but human studies have yet to provide compelling evidence for PFAS' impact on cognitive abilities. To test whether prenatal and childhood PFAS are associated with cognitive abilities at 8 years and whether sex modifies these associations. We included 221 mother-child pairs from the Health Outcomes and Measures of the Environment (HOME) Study, a birth cohort in Cincinnati, OH (USA). We quantified PFAS in maternal serum at 16 ± 3 weeks gestation and in child serum at 3 and 8 years. We used the Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) at age 8 years, assessing Full Scale IQ (FSIQ), verbal comprehension, perceptual reasoning, working memory, and processing speed. We used multiple informant models to estimate covariate-adjusted differences in WISC-IV scores by repeated ln-transformed PFAS. Prenatal and childhood perfluorooctane sulfonate (PFOS) and perfluorohexane sulfonate (PFHxS) were not associated with WISC-IV measures. We observed an increase of 4.1-points (95% CI 0.3, 8.0) and 5.7-points (95% CI 1.2, 10.2) in working memory with 1-ln unit increase in prenatal perfluorooctanoate (PFOA) and perfluorononanoate (PFNA), respectively. In addition, PFNA at 3 years was associated with better FSIQ and perceptual reasoning. Child sex modified the relationship between prenatal PFOA and FSIQ; the association was positive in females only. Sex also modified the association between concurrent PFOS and FSIQ, with males having higher scores. We did not observe adverse associations between prenatal and childhood PFAS and cognitive function at age 8 years. • PFOS and PFHxS were not associated with Full Scale IQ (FSIQ) at 8 years. • Prenatal PFOA and PFNA were positively associated with working memory at 8 years. • Child sex modified prenatal PFOA associations, with higher FSIQ scores in females. • We observed higher scores on several WISC scales in males, but not in females. • Findings do not support that PFAS are adversely associated with cognitive function. [ABSTRACT FROM AUTHOR]

Abstract Background Animal studies suggest polybrominated diphenyl ethers (PBDEs) may be obesogens. However, epidemiologic studies investigating childhood exposure to PBDEs and adiposity are limited, with several reporting an inverse association. Objectives To investigate associations between repeated childhood PBDE concentrations and adiposity measures at age 8 years. Methods We examined 206 children from the Health Outcomes and Measures of the Environment Study, a birth cohort in Cincinnati, OH (2003–2006). Serum PBDEs were measured at ages 1, 2, 3, 5, and 8 years. We used multiple imputation to estimate missing PBDE concentrations. At 8 years, we measured weight, height, waist circumference, and body fat percentage. We used multiple informant models to estimate age-specific associations between PBDEs and adiposity measures. Results We observed significant inverse associations between BDE-153 with all adiposity measures that became increasingly stronger with later childhood measurements. A 10-fold increase in BDE-153 at ages 1 and 8 years was associated with 2% (95% CI −3.9, −0.1) and 7% (95% CI −9.1, −4.7) lower body fat, respectively. No statistically significant associations were found with BDE-28, -47, -99, or -100. Child sex modified some associations; inverse associations between BDE-153 and body fat were stronger among boys, while positive and null associations were noted among girls. Conclusions Childhood BDE-153 concentrations were inversely associated with adiposity measures and these associations became stronger as BDE-153 measurements were more proximal to adiposity measures. Inverse associations could be attributed to reverse causality arising from greater storage of PBDEs in adipose tissue of children with higher adiposity. Highlights • Findings do not support postnatal PBDEs are associated with increased adiposity. • BDE-28, -47, -99, -100, and ∑PBDEs were not associated with adiposity at 8 years. • There was a pattern of inverse associations between BDE-153 and adiposity measures. • Child sex modified BDE-153 associations, with decreases in body fat % in males, but not in females. • Reverse causality may have resulted in inverse associations. [ABSTRACT FROM AUTHOR]

Abstract Background Despite evidence from toxicological studies describing the potential neurotoxicity of perfluoroalkyl substances (PFAS), their role in neurodevelopment remains uncertain amid inconsistent findings from epidemiological studies. Methods Using data from 218 mother-child dyads from the Health Outcomes and Measures of the Environment Study, we examined prenatal and childhood (3 and 8 years) serum concentrations of four PFAS and inattention, impulsivity, and visual spatial abilities. At 8 years, we used the Conners' Continuous Performance Test-II to assess attention and impulse control and the Virtual Morris Water Maze (VMWM) to measure visual spatial abilities. Results In multiple informant models, there was no evidence to indicate that prenatal or childhood PFAS are associated with attention. However, there was an inverse association between prenatal ln-perfluorooctanoate (PFOA) and errors of commission (β = −2.0, 95% Confidence Interval [CI] −3.8, −0.3). Ln-perfluorononanoate (PFNA) at 3 years was associated with longer (poorer) VMWM completion times of 3.6 seconds (CI 1.6, 5.6). However, higher concurrent concentrations of ln-perfluorohexane sulfonate (PFHxS) (β = −2.4 s, 95% CI −4.4, −0.3) were associated with shorter (better) times. Higher prenatal PFHxS was positively associated with percentage of traveling distance in the correct quadrant (β = 4.2%, 95% CI 0.8, 7.7), indicating better performance. Conclusion Findings were mixed for prenatal and childhood PFAS concentrations and visual spatial abilities. There is not enough evidence to support that PFAS are associated with visual spatial abilities as assessed by the VMWM or CPT-II measures of inattention or impulsivity in children at age 8 years. Highlights • Prenatal and childhood PFAS are not associated with CPT-II measures of inattention at 8 years. • Inconsistent associations were noted between PFNA and PFHxS with VMWM performance at 8 years. • Findings do not support associations between PFAS and VMWM measures of visual spatial abilities. [ABSTRACT FROM AUTHOR]

Abstract Background Toxicological studies highlight the potential neurotoxicity of perfluoroalkyl substances (PFAS) during fetal development. However, few epidemiological studies have examined the impact of childhood PFAS on neurodevelopment. Methods We employed data from 208 children in the Health Outcomes and Measures of the Environment Study, a birth cohort (Cincinnati, OH), to examine associations of six serum PFAS concentrations measured at 3 and 8 years with executive function assessed at 8 years using the validated parent-completed Behavior Rating Inventory of Executive Function survey. We used multiple informant models to identify susceptible windows of neurotoxicity to PFAS and executive function. We investigated trajectories of PFAS concentrations and whether sex modified these associations. Results Each ln-increase in perfluorononanoate (PFNA) at 8 years was associated with a 3.4-point increase (95% CI 0.4, 6.3) in metacognition score, indicating poorer function. Children with PFNA above the median at 8 years had poorer global executive functioning compared to children with concentrations consistently below median levels (β = 6.5, 95% CI 0.2, 12.9). Higher concurrent PFNA was associated with poorer behavior regulation among males, while associations among females were null (p PFNA × sex = 0.018). Children with higher concurrent perfluorooctanoate (PFOA) had increased odds of being at risk of having clinical impairments in metacognition (OR = 3.18, 95% CI 1.17, 8.60). There were no associations between perfluorooctane sulfonate and perfluorohexane sulfonate and executive function. Conclusions PFNA and PFOA at 8 years, but not 3 years, may be related to poorer executive function at 8 years. Results need to be confirmed in cohort studies with larger sample sizes. Highlights • PFAS concentrations at age 3 years were not associated with executive function at age 8 years. • Concurrent PFNA was associated with impairments in metacognition and global executive function at 8 years. • A sexually dimorphic relationship may be present, with males more sensitive to PFNA neurotoxicity. • Childhood PFNA and PFOA, to a lesser extent, may be neurotoxic with regard to executive function. [ABSTRACT FROM AUTHOR]

Background Polybrominated diphenyl ethers (PBDEs) reduce serum thyroid hormone concentrations in animal studies, but few studies have examined the impact of early-life PBDE exposures on thyroid hormone disruption in childhood. Methods We used data from 162 mother-child pairs from the Health Outcomes and Measures of the Environment Study (2003–2006, Cincinnati, OH). We measured PBDEs in maternal serum at 16 ± 3 weeks gestation and in child serum at 1–3 years. Thyroid hormones were measured in serum at 3 years. We used multiple informant models to investigate associations between prenatal and early-life PBDE exposures and thyroid hormone levels at age 3 years. Results Prenatal PBDEs were associated with decreased thyroid stimulating hormone (TSH) levels at age 3 years. A 10-fold increase in prenatal ∑PBDEs (BDE-28, -47, -99, -100, and -153) was associated with a 27.6% decrease (95% CI −40.8%, −11.3%) in TSH. A ten-fold increase in prenatal ∑PBDEs was associated with a 0.25 pg/mL (0.07, 0.43) increase in free triiodothyronine (FT 3 ). Child sex modified associations between prenatal PBDEs and thyroid hormones, with significant decrements in TSH among females and decreased free T 4 (FT 4 ) in males. Prenatal ∑PBDEs were not associated with TT 4 , FT 4 , or total T 3 . Conclusions These findings suggest an inverse relationship between prenatal ∑PBDEs and TSH at 3 years. Associations may be sexually dimorphic, with an inverse relationship between prenatal BDE-47 and -99 and TSH in females and null associations among males. [ABSTRACT FROM AUTHOR]

Prenatal exposure to polybrominated diphenyl ethers (PBDEs) have been reported to impair executive function in children, but little is known whether childhood PBDE exposures play a role. Using the Health Outcomes and Measures of the Environment (HOME) Study, a prospective birth cohort in the greater Cincinnati area, we investigated the association between repeated measures of PBDEs during childhood and executive function at 8 years in 208 children and whether effect modification by child sex was present. We used child serum collected at 1, 2, 3, 5, and 8 years to measure PBDEs. The Behavior Rating Inventory of Executive Function was completed by parents to assess executive function at 8 years. We used multiple informant models to examine childhood PBDEs during several exposure windows. Null associations were observed between early childhood PBDEs and executive function. However, we observed significant adverse associations between a 10-fold increase in concurrent concentrations of BDE-28 (β=4.6, 95% CI 0.5, 8.7) and BDE-153 (β=4.8, 95% CI 0.8, 8.8) with behavioral regulation. In addition, PBDEs at 8 years were significantly associated with poorer emotional and impulse control. No associations were noted between childhood PBDEs and metacognition or global executive function. However, child sex significantly modified the associations, with significantly poorer executive function among males with higher concurrent BDE-153, and null associations in females. Our study findings suggest that concurrent PBDE exposures during childhood may be associated with poorer executive function, specifically behavior regulation. Males may also be more sensitive to adverse associations of concurrent PBDEs on executive function. [ABSTRACT FROM AUTHOR]

Exposure to polybrominated diphenyl ethers (PBDEs) during fetal development may be associated with deficits in attention and impulse control. However, studies examining postnatal PBDE exposures and inattention and impulsivity have been inconsistent. Using data from 214 children in the Health Outcomes and Measures of the Environment (HOME) Study, a prospective pregnancy and birth cohort with enrollment from 2003 to 2006 in the Greater Cincinnati Area, we investigated the relationship of both prenatal and postnatal PBDE exposures with attention and impulse control. Serum PBDEs were measured at 16 ± 3 weeks of gestation and during childhood at 1, 2, 3, 5, and 8 years. We assessed children's attention and impulse control using the Conners' Continuous Performance Test-Second Edition (CPT-II) at 8 years. We used multiple informant models to estimate associations of repeated PBDE measures with inattention and impulsivity. There was a pattern of associations between PBDEs and poorer performance on CPT-II measures of attention. For BDE-153, adverse associations extended to exposures at preschool and kindergarten ages; ten-fold increases in exposure were associated with higher omission errors (BDE-153 at 3 years: β = 4.0 [95% CI: − 2.4, 10.5]; at 5 years: β = 4.6 [95% CI: − 2.8, 12.0]; at 8 years: β = 4.1 [95% CI: − 3.4, 11.5]). Longer hit reaction times, indicated by the exponential part of the hit reaction curve, were also observed with 10-fold increases in BDE-153 during the prenatal period and throughout childhood (Prenatal: β = 15.0 milliseconds (ms) [95% CI: − 15.8, 45.8]; 5 years: β = 20.6 ms [95% CI: − 20.8, 61.9]; 8 years: β = 28.6 ms [95% CI: − 12.1, 69.4]). Significant impairment in discriminability, as indicated by detectability (d′), between targets and non-targets was also noted with 5 and 8-year PBDE concentrations. Associations between PBDEs and inattention significantly differed by child sex, with males performing more poorly than females with regard to omission errors and measures of reaction times. Collectively, these results do not strongly support that PBDEs are associated with poorer impulse and attention control among 8 year old children. However, there may be a possible relationship between prenatal and concurrent PBDEs and inattention, which requires additional research. [ABSTRACT FROM AUTHOR]

Organophosphate esters (OPEs) are developmental toxicants in experimental studies of animals, but limited evidence is available in humans. We included 340 mother-infant pairs in the Health Outcomes and Measures of the Environment (HOME) Study (Cincinnati, Ohio, USA) for the analysis. We evaluated gestational exposure to OPEs with gestation age at birth and newborn anthropometric measures. We quantified four OPE urinary metabolites at 16 weeks and 26 weeks of gestation. We extracted gestational age at birth, newborn weight, length, and head circumference from the chart review. We calculated z-scores for these anthropometric measures and the ponderal index. We used multiple informant models to examine the associations between repeated OPE measurements and the outcomes. We used modified Poisson regression to estimate the association of gestational exposure to OPEs with preterm birth. We also explored effect modification by infant sex and the potential mediation effect by the highest maternal blood pressure and glucose levels. We found that bis(2-chloroethyl) phosphate (BCEP) at 16 weeks and diphenyl phosphate at 26 weeks of pregnancy were positively associated with gestational age and inversely associated with preterm birth. In female newborns, BCEP at 16 weeks was inversely related to birth weight and length z-scores. In male newborns, we observed negative associations of 26-week di-n-butyl phosphate with the ponderal index at birth. No mediation by the highest maternal blood pressure or glucose levels during pregnancy was identified. In this cohort, gestational exposure to some OPEs was associated with gestational age, preterm birth, and neonatal anthropometric measures. Certain associations tended to be window- and infant sex-specific. [Display omitted] • BCEP was positively associated with gestation age and inversely with preterm birth. • DPHP was positively associated with gestation age and inversely with preterm birth. • BCEP was inversely associated with birth weight and length z-scores in females. • DNBP was inversely associated with the ponderal index at birth in males. • Associations of OPEs and pregnancy outcomes might be window- and infant sex-specific. [ABSTRACT FROM AUTHOR]

The authors examined the responses of 63 primary care physicians to diabetes clinical protocols (DCPs) for the management of type II diabetes (T2DM). We measured physician demographics, current diabetes patient loads, and responses to DCPs (physician attitudes, physician familiarity, and physician recommendation of DCPs) using a 20-question electronic survey. Results of the survey indicate that primary care physicians may be unfamiliar with the benefits of diabetes clinical protocols for the self-management of T2DM. Given the importance of diabetes self-management education in controlling T2DM, those interested in implementing DCPs should address the beliefs and attitudes of primary care physicians. [ABSTRACT FROM AUTHOR]

Previous epidemiologic studies of maternal exposure to drinking water nitrate did not account for bottled water consumption. The objective of this National Birth Defects Prevention Study (NBDPS) (USA) analysis was to assess the impact of bottled water use on the relation between maternal exposure to drinking water nitrate and selected birth defects in infants born during 1997-2005. Prenatal residences of 1,410 mothers reporting exclusive bottled water use were geocoded and mapped; 326 bottled water samples were collected and analyzed using Environmental Protection Agency Method 300.0. Median bottled water nitrate concentrations were assigned by community; mothers' overall intake of nitrate in mg/day from drinking water was calculated. Odds ratios for neural tube defects, limb deficiencies, oral cleft defects, and heart defects were estimated using mixed-effects models for logistic regression. Odds ratios (95% CIs) for the highest exposure group in offspring of mothers reporting exclusive use of bottled water were: neural tube defects [1.42 (0.51, 3.99)], limb deficiencies [1.86 (0.51,6.80)], oral clefts [1.43 (0.61,3.31)], and heart defects [2.13, (0.87, 5.17)]. Bottled water nitrate had no appreciable impact on risk for birth defects in the NBDPS. [ABSTRACT FROM AUTHOR]

Background Diabetes self-care by patients has been shown to assist in the reduction of disease severity and associated medical costs. We compared the effectiveness of two different diabetes selfcare interventions on glycemic control in a racially/ethnically diverse population. We also explored whether reductions in glycated hemoglobin (HbA1c) will be more marked in minority persons. Methods We conducted an open-label randomized controlled trial of 376 patients with type 2 diabetes aged =18 years and whose last measured HbA1c was =7.5% (=58 mmol/mol). Participants were randomized to: 1) a Chronic Disease Self-Management Program (CDSMP; n = 101); 2) a diabetes self-care software on a personal digital assistant (PDA; n = 81); 3) a combination of interventions (CDSMP + PDA; n = 99); or 4) usual care (control; n = 95). Enrollment occurred January 2009-June 2011 at seven regional clinics of a university-affiliated multispecialty group practice. The primary outcome was change in HbA1c from randomization to 12 months. Data were analyzed using a multilevel statistical model. Results Average baseline HbA1c in the CDSMP, PDA, CDSMP + PDA, and control arms were 9.4%, 9.3%, 9.2%, and 9.2%, respectively. HbA1c reductions at 12 months for the groups averaged 1.1%, 0.7%, 1.1%, and 0.7%, respectively and did not differ significantly from baseline based on the model (P = .771). Besides the participants in the PDA group reporting eating more high-fat foods compared to their counterparts (P < .004), no other significant differences were observed in participants' diabetes self-care activities. Exploratory subanalysis did not reveal any marked reductions in HbA1c for minority persons but rather modest reductions for all racial/ethnic groups. Conclusions Although behavioral and technological interventions can result in some modest improvements in glycemic control, these interventions did not fare significantly better than usual care in achieving glycemic control. More research is needed to understand how these interventions can be most effective in clinical practice. The reduction in HbA1c levels found in our control group that received usual care also suggests that good routine care in an integrated healthcare system can lead to better glycemic control. [ABSTRACT FROM AUTHOR]

BACKGROUND Nitrosatable drugs, such as secondary or tertiary amines and amides react with nitrite in an acidic environment to form N-nitroso compounds, teratogens in animal models. Vitamin C is a known nitrosation inhibitor. METHODS Using data from the National Birth Defects Prevention Study, we assessed nitrosatable drug exposure and vitamin C intake during the first trimester among 11,606 case-mothers of infants with oral clefts, limb deficiencies (LDs), or congenital heart defects and 6807 control-mothers of infants without major birth defects during 1997-2005. Daily intake of vitamin C was estimated from maternal interviews that elicited information about supplement use and dietary intake. RESULTS With no reported use of nitrosatable drugs as the referent group, a lower odds ratio (OR) was observed for transverse LDs among births to mothers exposed to secondary amine drugs and daily vitamin C supplementation (adjusted odds ratio [aOR] 1.2, 95% confidence interval [CI] 0.83-1.8) compared with women taking these drugs and no supplementation (aOR 2.7, 95% CI 1.5-4.6). The OR for longitudinal LDs associated with secondary amine exposure was lower with daily dietary vitamin C intake ≥85 mg (aOR 1.2, 95% CI 0.68-2.0) compared with <85 mg (aOR 1.9, 95% CI 1.2-3.1). Daily vitamin C supplementation in combination with higher dietary vitamin C intake reduced associations between nitrosatable drug exposures and limb deficiencies and atrial septal defects not otherwise specified. CONCLUSION Prenatal dietary and vitamin C supplement intake may diminish the association between nitrosatable drug exposure during pregnancy and selected birth defects. Birth Defects Research (Part A) 97:515-531, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background: Dietary intake of nitrates, nitrites, and nitrosamines can increase the endogenous formation of N-nitroso compounds in the stomach. Results from animal studies suggest that these compounds might be teratogenic. We examined the relationship between maternal dietary intake of nitrates, nitrites (including plant and animal sources as separate groups), and nitrosamines and several types of birth defects in offspring. Methods: For this population-based case-control study, data from a 58-question food frequency questionnaire, adapted from the short Willett Food Frequency Questionnaire and administered as part of the National Birth Defects Prevention Study (NBDPS), were used to estimate daily intake of dietary nitrates, nitrites, and nitrosamines in a sample of 6544 mothers of infants with neural tube defects (NTD)s, oral clefts (OC)s, or limb deficiencies (LD)s and 6807 mothers of unaffected control infants. Total daily intake of these compounds was divided into quartiles based on the control mother distributions. Odds ratios (OR)s and 95% confidence intervals (CI)s were estimated using logistic regression; estimates were adjusted for maternal daily caloric intake, maternal race-ethnicity, education, dietary folate intake, high fat diet (> 30% of calories from fat), and state of residence. Results: While some unadjusted ORs for NTDS had 95% (CI)s that excluded the null value, none remained significant after adjustment for covariates, and the effect sizes were small (adjusted odds ratios [aOR] <1.12). Similar results were found for OCs and LDs with the exception of animal nitrites and cleft lip with/without cleft palate (aORs and CIs for quartile 4 compared to quartile 1 =1.24; CI=1.05-1.48), animal nitrites and cleft lip (4th quartile aOR=1.32; CI=1.01-1.72), and total nitrite and intercalary LD (4th quartile aOR=4.70; CI=1.23-17.93). Conclusions: Overall, odds of NTDs, OCs or LDs did not appear to be significantly associated with estimated dietary intake of nitrate, nitrite, and nitrosamines. [ABSTRACT FROM AUTHOR]