End-stage renal disease and metalworking fluid exposure.

OBJECTIVE: Despite increasing prevalence of end-stage renal disease (ESRD), little attention has been directed to how occupational exposures may contribute to risk. Our objective was to investigate the relationship between metalworking fluids (MWF) and ESRD in a cohort of 36 703 male autoworkers. METHODS: We accounted for competing risk of death, using the subdistribution hazard approach to estimate subhazard ratios (sHRs) and 95% CIs in models with cubic splines for cumulative exposure to MWF (straight, soluble or synthetic). RESULTS: Based on 501 ESRD cases and 13 434 deaths, we did not observe an association between MWF and ESRD overall. We observed modest associations between MWF and ESRD classification of glomerulonephritis and diabetic nephropathy. For glomerulonephritis, the 60th percentile of straight MWF was associated with an 18% increased subhazard (sHR=1.18, 95% CI: 0.99 to 1.41). For diabetic nephropathy, the subhazard increased 28% at the 60th percentile of soluble MWF (sHR=1.28, 95% CI: 1.00 to 1.64). Differences by race suggest that black males may have higher disease rates following MWF exposure. CONCLUSIONS: Exposure to straight and soluble MWF may be related to ESRD classification, though this relationship should be further examined.

Effect of Heat Treatment on Residual Stress of Cold Sprayed Nickel-based Superalloys.

Residual stress formation during cold spraying process may result in deteriorative effects on the performance of coating materials. The objective of this investigation is to characterize residual stress built-up in two well-known nickel-based superalloys (Inconel 625 and Inconel 718) deposited using cold spraying technique. To this end, the residual stress was precisely measured using x-ray diffraction method. Here, residual stress in the subsurface regions was only studied because the surface properties may alter during sample preparation. The average residual stress was slightly higher in Inconel 625 compared to the Inconel 718 sample. Heat treatment at 800 °C helped in the reduction of porosities which exerted tensile stress in subsurface regions of both coatings. Stresses with opposite signs could cancel each other and result in reduction of residual stress after heat treatment. However, the recovery of residual stress was higher for Inconel 718 coating. In the next step as-sprayed and heat-treated coating samples were subjected to microindentation test to measure their hardness and study the crack formation in the samples. The as-sprayed Inconel 625 exhibited higher hardness than Inconel 718, but the hardness of Inconel 625 decreased more drastically after heat treatment. While the cracks were formed on both as-sprayed samples around indents, no cracks were found in the heat-treated samples. The results from this study will contribute to better understanding the performance of cold spray deposited superalloys under service conditions and the effect of stress relaxation heat treatment on elimination of residual stress.

Admixture mapping identifies African and Amerindigenous local ancestry loci associated with fetal growth.

Fetal growth is an important determinant of cardiometabolic disease risk during childhood and adulthood. The genetic architecture of fetal growth remains largely understudied in ancestrally diverse populations. We conducted genome-wide admixture mapping scan and analysis of genetic ancestry among Hispanic American, African American, European American, and Asian American pregnant women to identify genetic loci associated with fetal growth measures across 13-40 weeks gestation. Fetal growth measures were associated with genome-wide average African, European, Amerindigenous and East Asian ancestry proportions (P ranged from10-3 to 4.8 × 10-2). Admixture mapping analysis identified ten African ancestry loci and three Amerindigenous ancestry loci significantly associated with fetal growth measures at Bonferroni-corrected levels of significance (P ranged from 2.18 × 10-8 to 3.71 × 10-6). At the chr2q23.3-24.2 locus in which higher African ancestry was associated with long bone (femur and humerus) lengths, the T allele of rs13030825 (GALNT13) was associated with longer humerus length in African Americans (ß = 0.44, P = 6.25 × 10-6 at week 27; ß = 0.39, P = 7.72 × 10-5 at week 40). The rs13030825 SNP accounted for most of the admixture association at the chr2q23.3-24.2 locus and has substantial allele frequency difference between African and European reference samples (FST = 0.55, P = 0.03). Regulatory annotation shows that rs13030825 overlaps with the serum response factor (SRF) transcription factor previously implicated in postnatal bone development of mice. Overall, we identified ancestry-related maternal genetic loci that influence fetal growth, shedding light on molecular pathways that regulate fetal growth and potential effects on health across the lifespan.Clinical trials registration ClinicalTrials.gov, NCT00912132.

Maternal cardiometabolic factors and genetic ancestry influence epigenetic aging of the placenta.

Disruption of physiological aging of the placenta can lead to pregnancy complications and increased risk for cardiometabolic diseases during childhood and adulthood. Maternal metabolic and genetic factors need to operate in concert with placental development for optimal pregnancy outcome. However, it is unknown whether maternal cardiometabolic status and genetic ancestry contribute to differences in placental epigenetic age acceleration (PAA). We investigated whether maternal prepregnancy obesity, gestational weight gain (GWG), blood pressure, and genetic ancestry influence PAA. Among 301 pregnant women from 4 race/ethnic groups who provided placenta samples at delivery as part of the National Institute of Child Health and Human Development Fetal Growth Studies, placental DNA methylation age was estimated using 62 CpGs known to predict placental aging. PAA was defined to be the difference between placental DNA methylation age and gestational age at birth. Percentage of genetic ancestries was estimated using genotype data. We found that a 1 kg/week increase in GWG was associated with up to 1.71 (95% CI: -3.11, -0.32) week lower PAA. Offspring Native American ancestry and African ancestry were associated, respectively, with higher and lower PAA among Hispanics, and maternal East Asian ancestry was associated with lower PAA among Asians (p < 0.05). Among mothers with a male offspring, blood pressure was associated with lower PAA across all three trimesters (p < 0.05), prepregnancy obesity compared to normal weight was associated with 1.24 (95% CI: -2.24, -0.25) week lower PAA. In summary, we observed that maternal cardiometabolic factors and genetic ancestry influence placental epigenetic aging and some of these influences may be male offspring-specific.

The role of dental insurance in mitigating mortality among working-age U.S. adults with periodontitis.

AIM: To assess the relationship of dental insurance with all-cause mortality and mortality due to cardiovascular diseases (CVD), diabetes mellitus (DM), and cerebrovascular diseases (CBD) among those with periodontitis. MATERIALS AND METHODS: NHANES III and its associated mortality data set were used in this study. The outcome variables were "all-cause mortality" and "combined mortality" due to CVD, DM, and CBD. The independent variable was dental insurance stratified over periodontitis status. Unweighted frequencies with weighted column percentages were used for descriptive statistics, and chi-square test was applied for significance. Cox proportional hazard models were used for stratified multivariable analyses. All analyses were performed in SAS v9.4 accounting for survey data complexities. Significance level was kept at 5%. RESULTS: The mortality was 14.58% for all-cause mortality and 4.06% for combined mortality among those with periodontitis in this study. Dental insurance significantly reduced the hazard of all-cause mortality among those with periodontitis (HR: 0.75; 95% CI: 0.61 - 0.93), adjusted for covariates. However, no association of dental insurance with combined mortality was observed among periodontitis group. CONCLUSIONS: Dental insurance reduces hazard of all-cause mortality among those with periodontitis. Dental insurance ensures access to dentists and improves oral and dental health. Longitudinal study is needed to establish causality.

Early pregnancy dyslipidemia is associated with placental DNA methylation at loci relevant for cardiometabolic diseases.

Aim: To identify placental DNA methylation changes that are associated with early pregnancy maternal dyslipidemia. Materials & methods: We analyzed placental genome-wide DNA methylation (n = 262). Genes annotating differentially methylated CpGs were evaluated for gene expression in placenta (n = 64). Results: We found 11 novel significant differentially methylated CpGs associated with high total cholesterol, low-density lipoprotein cholesterol and triglycerides, and low high-density lipoprotein cholesterol. High triglycerides were associated with decreased methylation of cg02785814 (ALX4) and decreased expression of ALX4 in placenta. Genes annotating the differentially methylated CpGs play key roles in lipid metabolism and were enriched in dyslipidemia pathways. Functional annotation found cis-methylation quantitative trait loci for genetic loci in ALX4 and EXT2. Conclusion: Our findings lend novel insights into potential placental epigenetic mechanisms linked with maternal dyslipidemia. Trial Registration: ClinicalTrials.gov, NCT00912132.

Trans-ethnic meta-analysis of genome-wide association studies identifies maternal ITPR1 as a novel locus influencing fetal growth during sensitive periods in pregnancy.

Abnormal fetal growth is a risk factor for infant morbidity and mortality and is associated with cardiometabolic diseases in adults. Genetic influences on fetal growth can vary at different gestation times, but genome-wide association studies have been limited to birthweight. We performed trans-ethnic genome-wide meta-analyses and fine mapping to identify maternal genetic loci associated with fetal weight estimates obtained from ultrasound measures taken during pregnancy. Data included 1,849 pregnant women from four race/ethnic groups recruited through the NICHD Fetal Growth Studies. We identified a novel genome-wide significant association of rs746039 [G] (ITPR1) with reduced fetal weight from 24 to 33 weeks gestation (P<5x10-8; log10BF>6). Additional tests revealed that the SNP was associated with head circumference (P = 4.85x10-8), but not with abdominal circumference or humerus/femur lengths. Conditional analysis in an independent sample of mother-offspring pairs replicated the findings and showed that the effect was more likely maternal but not fetal. Trans-ethnic approaches successfully narrowed down the haplotype block that contained the 99% credible set of SNPs associated with head circumference. We further demonstrated that decreased placental expression of ITPR1 was correlated with increased placental epigenetic age acceleration, a risk factor for reduced fetal growth, among male fetuses (r = -0.4, P = 0.01). Finally, genetic risk score composed of known maternal SNPs implicated in birthweight among Europeans was associated with fetal weight from mid-gestation onwards among Whites only. The present study sheds new light on the role of common maternal genetic variants in the inositol receptor signaling pathway on fetal growth from late second trimester to early third trimester. Clinical Trial Registration: ClinicalTrials.gov, NCT00912132.

Placental DNA methylation changes associated with maternal prepregnancy BMI and gestational weight gain.

BACKGROUND: Maternal obesity prior to or during pregnancy influences fetal growth, predisposing the offspring to increased risk for obesity across the life course. Placental epigenetic mechanisms may underlie these associations. We conducted an epigenome-wide association study to identify placental DNA methylation changes associated with maternal prepregnancy body mass index (BMI) and rate of gestational weight gain at first (GWG1), second (GWG2), and third trimester (GWG3). METHOD: Participants of the NICHD Fetal Growth Studies with genome-wide placental DNA methylation (n = 301) and gene expression (n = 75) data were included. Multivariable-adjusted regression models were used to test the associations of 1 kg/m2 increase in prepregnancy BMI or 1 kg/week increase in GWG with DNA methylation levels. Genes harboring top differentially methylated CpGs (FDR P < 0.05) were evaluated for placental gene expression. We assessed whether DNA methylation sites known to be associated with BMI in child or adult tissues, were also associated with maternal prepregnancy BMI in placenta. RESULTS: Prepregnancy BMI was associated with DNA methylation at cg14568196[EGFL7], cg15339142[VETZ], and cg02301019[AC092377.1] (FDR P < 0.05, P ranging from 1.4 × 10-10 to 1.7 × 10-9). GWG1 or GWG2 was associated with DNA methylation at cg17918270[MYT1L], cg20735365[DLX5], and cg17451688[SLC35F3] (FDR P < 0.05, P ranging from 6.4 × 10-10 to 1.2 × 10-8). Both prepregnancy BMI and DNA methylation at cg1456819 [EGFL7] were negatively correlated with EGFL7 expression in placenta (P < 0.05). Several CpGs previously implicated in obesity traits in children and adults were associated with prepregnancy BMI in placenta. Functional annotations revealed that EGFL7 is highly expressed in placenta and the differentially methylated CpG sites near EGFL7 and VEZT were cis-meQTL targets in blood. CONCLUSIONS: We identified placental DNA methylation changes at novel loci associated with prepregnancy BMI and GWG. The overlap between CpGs associated with obesity traits in placenta and other tissues in children and adults suggests that epigenetic mechanisms in placenta may give insights to early origins of obesity.

Differential DNA Methylation in Placenta Associated With Maternal Blood Pressure During Pregnancy.

Abnormal blood pressure during pregnancy is associated with impaired fetal growth, predisposing the offspring to cardiometabolic abnormalities over the life-course. Placental DNA methylation may be the regulatory pathway through which maternal blood pressure influences fetal and adult health outcomes. Epigenome-wide association study of 301 participants with placenta sample examined associations between DNA methylation and millimetre of mercury increases in systolic and diastolic blood pressure in each trimester. Findings were further examined using gene expression, gene pathway, and functional annotation analyses. Cytosine-(phosphate)-guanine (CpGs) known to be associated with cardiometabolic traits were evaluated. Increased maternal systolic and diastolic blood pressure were associated with methylation of 3 CpGs in the first, 6 CpGs in the second, and 15 CpGs in the third trimester at 5% false discovery rate (P values ranging from 6.6×10-15 to 2.3×10-7). Several CpGs were enriched in pathways including cardiovascular-metabolic development (P=1.0×10-45). Increased systolic and diastolic blood pressure were associated with increased CpG methylation and gene expression at COL12A1, a collagen family gene known for regulatory functions in the heart. Out of 304 previously reported CpGs known to be associated with cardiometabolic traits, 36 placental CpGs were associated with systolic and diastolic blood pressure in our data. The present study provides the first evidence for associations between placental DNA methylation and increased maternal blood pressure during pregnancy at genes implicated in cardiometabolic diseases. Identification of blood pressure-associated methylated sites in the placenta may provide clues to early origins of cardiometabolic dysfunction and inform guidelines for early prevention. Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00912132.

Sex differences in the associations of placental epigenetic aging with fetal growth.

Identifying factors that influence fetal growth in a sex-specific manner can help unravel mechanisms that explain sex differences in adverse neonatal outcomes and in-utero origins of cardiovascular disease disparities. Premature aging of the placenta, a tissue that supports fetal growth and exhibits sex-specific epigenetic changes, is associated with pregnancy complications. Using DNA methylation-based age estimator, we investigated the sex-specific relationship of placental epigenetic aging with fetal growth across 13-40 weeks gestation, neonatal size, and risk of low birth weight. Placental epigenetic age acceleration (PAA), the difference between DNA methylation age and gestational age, was associated with reduced fetal weight among males but with increased fetal weight among females. PAA was inversely associated with fetal weight, abdominal circumference, and biparietal diameter at 32-40 weeks among males but was positively associated with all growth measures among females across 13-40 weeks. A 1-week increase in PAA was associated with 2-fold (95% CI 1.2, 3.2) increased odds for low birth weight and 1.5-fold (95% CI 1.1, 2.0) increased odds for small-for-gestational age among males. In all, fetal growth was significantly reduced in males but not females exposed to a rapidly aging placenta. Epigenetic aging of the placenta may underlie sex differences in neonatal outcomes.

Maternal BMI-Increasing Genetic Risk Score and Fetal Weights among Diverse US Ethnic Groups.

OBJECTIVE: Associations between maternal genetic risk for obesity and fetal weight were examined at the end of the first (13 weeks 6 days), second (27 weeks 6 days), and third (40 weeks 0 days) trimesters of pregnancy among four race/ethnic groups in the US. METHODS: For 603 white, 591 black, 535 Hispanic, and 216 Asian women, maternal genetic risk score (GRS) was calculated as the sum of 189 BMI-increasing alleles and was categorized into high or low GRS. Associations between GRS (continuous and categorical) and estimated fetal weight were tested overall and stratified by prepregnancy BMI, gestational weight gain (GWG), and fetal sex. RESULTS: High GRS compared with low GRS was associated with increased fetal weight at the end of the second (ß: 22.7 g; 95% CI: 2.4-43.1; P = 0.03) and third trimesters (ß: 88.3 g; 95% CI: 9.0-167.6; P = 0.03) among Hispanic women. The effect of GRS was stronger among Hispanic women with normal prepregnancy weight, adequate first trimester GWG, or inadequate second trimester GWG (P < 0.05). Among Asian women, high GRS was associated with increased weight among male fetuses but decreased weight among female fetuses (P < 0.05). CONCLUSIONS: Maternal obesity genetic risk was associated with fetal weight with potential effect modifications by maternal prepregnancy BMI, GWG, and fetal sex.

Maternal dyslipidemia during early pregnancy and epigenetic ageing of the placenta.

Disruption of physiological ageing of the placenta is associated with obstetric complications. Altered lipid metabolism is a known trigger of tissue ageing, but the effect of maternal dyslipidemia on placental ageing is not clearly understood. We examined the relationship between maternal dyslipidemia and placental age acceleration (PAA), an epigenetic ageing measure derived from the difference between DNA methylation age and chronological gestational age. We also assessed whether the association varies by maternal pre-pregnancy obesity status and fetal sex. Placental data were obtained as part of the NICHD Fetal Growth Studies that involved participants from four race/ethnic groups. Placental DNA methylation age was estimated using 62 CpGs that have previously been found to have high placental age prediction accuracy. We used multivariable linear regression to test associations between maternal dyslipidemia during early gestation (i.e., high-density lipoprotein cholesterol (HDLc), low-density lipoprotein cholesterol (LDLc), total cholesterol (TChol), and triglycerides) and PAA adjusting for fetal sex and socio-demographic factors. Among normal-weight women, low HDLc, compared to high HDLc, was associated with 0.82 (95% CI: 0.00, 1.64) weeks higher PAA. Among women with female neonates, low HDLc, compared to high HDLc, was associated with 1.20 (95% CI: 0.17, 2.24) weeks higher PAA. High TChol was associated with 1.28 (95% CI: 0.12, 2.45) weeks higher PAA among Whites. In all, the study found that maternal dyslipidemia due to low HDLc was associated with accelerated epigenetic ageing of the placenta among mothers with normal pre-pregnancy weight and a female fetus.

Maternal and Offspring Genetic Risk of Type 2 Diabetes and Offspring Birthweight Among African Ancestry Populations.

OBJECTIVES: Maternal genetic risk of type 2 diabetes (T2D) can influence offspring birthweight through shared offspring genetic risk and by altering intrauterine glycemic status. The aim of this study was to estimate the independent effects of maternal and offspring genetic risk scores (GRSs) of T2D on offspring birthweight and the extent to which intrauterine glycemic traits mediate the effect of maternal GRSs on offspring birthweight. DESIGN: The study involved 949 mother-offspring pairs of African ancestry from the Hyperglycemia Adverse Pregnancy Outcome study. GRSs of T2D were calculated separately for mothers and offspring as the weighted sum of 91 T2D risk alleles identified in a genome-wide association study meta-analysis in African Americans. Linear regression models were fit to estimate changes in birthweight by quartiles of GRSs. Mediation analysis was implemented to estimate the direct and indirect effects of maternal GRS on offspring birthweight through cord blood C-peptide and maternal fasting and postchallenge glucose levels. RESULTS: Maternal and offspring GRSs were independently and differentially associated with offspring birthweight. Changes (95% CI) in birthweight across increasing quartiles of maternal GRSs were 0 g (reference), 83.1 g (6.5, 159.6), 103.1 g (26.0, 180.2), and 92.7 g (12.6, 172.8) (P trend = 0.041) and those of offspring GRSs were 0 (reference), -92.0 g (-169.2, -14.9), -64.9 g (-142.4, 12.6), and 2.0 g (-77.8, 81.7) (P trend = 0.032). Cord blood C-peptide mediated the effect of maternal GRS on offspring birthweight, whereas maternal postchallenge glucose levels showed additive effects with maternal GRS on birthweight. CONCLUSIONS: Maternal and offspring GRSs of T2D were independently and differentially associated with offspring birthweight.

Genetic overlap between birthweight and adult cardiometabolic diseases has implications for genomic medicine.

Before implementing therapeutic genomic interventions for optimizing health in early life, comprehensive understanding of their effect on several traits across the life course is warranted. Abnorml  birthweight is associated with cardiometabolic disease risk in adulthood; however, the extent of genetic pleiotropy in the association has not been comprehensively investigated. We tested for pleiotropy and enrichment of functional loci between birthweight and 15 cardiometabolic disease traits (CMD). We found significantly abundant genetic pleiotropy (P < 3.3 × 10-3) and enrichment of functional annotations (P < 3.3 × 10-3) in loci influencing both birthweight and CMD. We did not observe consistent effect directions of pleiotropic loci on the traits. A total of 67 genetic loci, of which 65 loci have been reported in previous genome-wide association studies, were associated with both birthweight and CMD at a false discovery rate of 5%. Two novel loci were associated with birthweight and adult coronary artery disease (rs2870463 in CTRB1) and with birthweight and adult waist circumference (rs12704673 in CALCR). Both loci are known to have regulatory effects on expression of nearby genes. In all, our findings revealed pervasive genetic pleiotropy in early growth and adulthood cardiometabolic diseases, implying the need for caution when considering genetic loci as therapeutic targets.

Influence of Fetal and Maternal Genetic Susceptibility to Obesity on Birthweight in African Ancestry Populations.

Fetal and maternal genetic propensity to obesity can influence birthweight. We investigated the effects of fetal and maternal genetic risk of obesity on birthweight and evaluated whether these genetic influences modify the well-known association between maternal pre-pregnancy body mass index (BMI) and birthweight. In 950 mother-baby pairs of African ancestry, a genetic risk score for adulthood obesity was generated for mothers (mGRS) and their babies (bGRS) as the weighted sum of BMI-increasing alleles of 97 single nucleotide polymorphisms known to be associated with BMI. The median GRS value was used as a cut-off to define high or low bGRS and mGRS. High bGRS was significantly associated with 70 g lower birthweight (95% Confidence Interval [CI] = -127.4 to -12.4) compared to low bGRS. mGRS was positively correlated with birthweight but the association was not significant. mGRS modified the significant birthweight-increasing effect of maternal pre-pregnancy BMI (P-for-interaction = 0.03); among mothers with low mGRS, those who were overweight or obese had 127.7 g heavier babies (95% CI = 27.1 to 228.2) compared to those who had normal weight. In summary, fetal obesity genetic risk loci exert direct influence on birthweight, and maternal loci modify the effect of pre-pregnancy BMI on birthweight.

Cross-sectional association of physical activity and periodontal antibodies.

BACKGROUND: The objective of this study was to evaluate the cross-sectional association between physical activity and serum IgG antibodies against selected periodontal microorganisms. METHODS: The study population consisted of 5,611 randomly selected US adults who participated in the National Health and Nutrition Examination Survey (NHANES) III (1988 to 1994), who were 40 years and older with complete IgG antibody data against 19 oral microorganisms. We used cluster analysis to classify the 19 antibody titers into 4 mutually exclusive groups called "Orange-Red," "Red-Green," "Yellow- Orange," and "Orange-Blue," and calculated cluster scores by summing antibody titer z-scores for each of the four groups. Physical activity was evaluated based on reported frequency and intensity of physical activity conducted in the last month. Participants were grouped into three categories: adequately physically active, inadequately physically active, and inactive. The outcomes were IgG cluster scores with physical activity as the predictor. Multivariable models adjusted for age, sex, race, smoking status, waist circumference, education, poverty-income-ratio, alcohol, and diabetes. RESULTS: In adjusted models, physical activity was positively associated with the antibodies in the Orange-Blue cluster (E. nodatum, A. naeslundii), a cluster that is associated with healthy periodontal states. The mean differences in cluster scores were 15.2 (95% CI -1.0, 31.4) for Model 3, and 7.0 (95% CI -8.3, 22.3) for Model 4 comparing the sufficiently active group to the inactive group. CONCLUSIONS: Antibody titers against periodontal microorganisms reflecting good oral health trended higher among physically active individuals, but the results were not statistically significant at the 0.05 level.

Risk factors associated with 30-day readmission and length of stay in patients with type 2 diabetes.

AIMS: Patients with type 2 diabetes mellitus (type 2 DM) are at greater risk of poor hospital outcomes. The purpose of this study was to determine the impact of type 2 DM on 30-day hospital readmission and length of stay (LOS). METHODS: We studied all inpatient admissions in Pennsylvania during 2011 using data from the Pennsylvania Health Care Cost Containment Council. Outcomes included 30-day readmission and inpatient LOS. We estimated the impact of type 2 DM on readmission and LOS, and identified risk factors for readmission and prolonged LOS. RESULTS: Among inpatient admissions, patients with diabetes were more likely to be readmitted (AOR=1.17, P<0.001) and have longer LOS (0.19days, P<0.001) compared to patients without diabetes. Among those with diabetes, several factors were associated with readmission, including demographics, source of admission, and comorbidities. Patients with diabetes were more likely to be readmitted for infectious complications (9.4% vs. 7.7%), heart failure (6.0% vs. 3.1%), and chest pain/MI (5.5% vs. 3.3%) than patients without diabetes. CONCLUSIONS: Diabetes is associated with risk of 30-day readmission and LOS, and several patient-specific factors are associated with outcomes for patients with diabetes. Future studies may target risk factors to develop strategies to reduce readmissions and LOS.

Risk of renal cell carcinoma following exposure to metalworking fluids among autoworkers.

OBJECTIVES: Metalworking fluids (MWF), used to cool and lubricate metal in occupational settings, are linked to several cancers but data on kidney cancer are limited. We examine how MWF influence the rate of renal cell carcinoma (RCC) in a large prospective study. METHODS: A cohort of Michigan autoworkers consisting of 33 421 individuals was followed from 1985 to 2009. The cohort was linked to the Michigan Cancer Registry to identify new cases of RCC. We analysed RCC in relation to cumulative exposure to each specific type of MWF (straight, soluble and synthetic) and all 3 types pooled into a single MWF variable, with a 15-year lag. Cox proportional hazards regression with splines were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), controlling for age, gender, race, calendar year, year hired, time since hire, plant and other MWF types. RESULTS: There were 135 incident cases. A linear increase in the log-HR was observed for RCC with increasing cumulative exposure to each MWF type and total MWF exposure. At the mean of total MWF exposure (18.80 mg/m(3)-year), the estimated HR was 1.11 (95% CI 1.04 to 1.19). CONCLUSIONS: Our results provide evidence for a dose-dependent association between MWF exposure and RCC. The influence of components of oil-based and water-based MWF needs further examination.

Relationship between serologic markers of periodontal bacteria and metabolic syndrome and its components.

BACKGROUND: Periodontitis is a result of a complex biologic alteration of the periodontal microenvironment and a distributional shift of key periodontal pathogens. Metabolic syndrome (MetS), a complex cluster of cardiovascular risk factors, has been linked to periodontal diseases; however, the contribution of periodontal bacteria to systemic conditions remains unclear. METHODS: The study population comprised 7,848 United States adults who participated in an interview, underwent a clinical oral-health examination, and had serum immunoglobulin G titers measured against 19 periodontal bacteria as part of the third National Health and Nutritional Examination Survey. The z-score antibody titers were clustered into four mutually exclusive groups and named after Socransky's classification of periodontal bacteria (Orange-Red, Red-Green, Yellow-Orange, and Orange-Blue). Survey logistic regression was used to investigate the independent associations between the cluster scores, and MetS and each component, including hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, central obesity, and elevated fasting glucose. RESULTS: The Orange-Red cluster score (that included Porphyromonas gingivalis and Prevotella spp.) was positively associated (odds ratio [OR] = 1.067, 95% confidence interval [CI] = 1.02 to 1.12) and the Orange-Blue cluster score (which included Actinomyces naeslundii and Eubacterium nodatum) was inversely associated (OR = 0.93, 95% CI = 0.88 to 0.97) with elevated fasting glucose (≥ 110 mg/dL) after adjustment for clusters and potential confounders. Neither MetS nor its other remaining MetS components were associated with a particular cluster score. CONCLUSIONS: The associations between specific antibody clusters (Orange-Red and Orange-Blue) against periodontal bacteria and elevated plasma glucose were in qualitatively opposite directions after multivariable adjustment in a large, adult population. The periodontal bacterial profile was not found to be associated with metabolic control other than a very moderate association with elevated plasma glucose.