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Research October 2014 | Volume 122 | Issue 10
Asthma in Inner-City Children at 5–11 Years of Age and Prenatal Exposure to Phthalates: The Columbia Center for Children's Environmental Health Cohort
Robin M. Whyatt,1 Matthew S. Perzanowski,1 Allan C. Just,2 Andrew G. Rundle,3 Kathleen M. Donohue,4 Antonia M. Calafat,5 Lori A. Hoepner,1 Frederica P. Perera,1 and Rachel L. Miller1,4,6
Background: Studies suggest that phthalate exposures may adversely affect child respiratory health.
Objectives: We evaluated associations between asthma diagnosed in children between 5 and 11 years of age and prenatal exposures to butylbenzyl phthalate (BBzP), di-n-butyl phthalate (DnBP), di(2-ethylhexyl) phthalate (DEHP), and diethyl phthalate (DEP).
Methods: Phthalate metabolites were measured in spot urine collected from 300 pregnant inner-city women. Children were examined by an allergist or pulmonologist based on the first parental report of wheeze, other respiratory symptoms, and/or use of asthma rescue/controller medication in the preceding 12 months on repeat follow-up questionnaires. Standardized diagnostic criteria were used to classify these children as either having or not having current asthma at the time of the physician examination. Children without any report of wheeze or the other asthma-like symptoms were classified as nonasthmatics at the time of the last negative questionnaire. Modified Poisson regression analyses were used to estimate relative risks (RR) controlling for specific gravity and potential confounders.
Results: Of 300 children, 154 (51%) were examined by a physician because of reports of wheeze, other asthma-like symptoms, and/or medication use; 94 were diagnosed with current asthma and 60 without current asthma. The remaining 146 children were classified as nonasthmatic. Compared with levels in nonasthmatics, prenatal metabolites of BBzP and DnBP were associated with a history of asthma-like symptoms (p < 0.05) and with the diagnosis of current asthma: RR = 1.17 (95% CI: 1.01, 1.35) and RR = 1.25 (95% CI: 1.04, 1.51) per natural log-unit increase, respectively. Risk of current asthma was > 70% higher among children with maternal prenatal BBzP and DnBP metabolite concentrations in the third versus the first tertile.
Conclusion: Prenatal exposure to BBzP and DnBP may increase the risk of asthma among inner-city children. However, because this is the first such finding, results require replication.
Citation: Whyatt RM, Perzanowski MS, Just AC, Rundle AG, Donohue KM, Calafat AM, Hoepner LA, Perera FP, Miller RL. 2014. Asthma in inner-city children at 5–11 years of age and prenatal exposure to phthalates: the Columbia Center for Children's Environmental Health Cohort. Environ Health Perspect 122:1141–1146; http://dx.doi.org/10.1289/ehp.1307670
Address correspondence to R.M. Whyatt, Department of Environmental Health Sciences, Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, 722 West 168th St., New York, NY 10032 USA. Telephone: (212) 304-5502. E-mail: email@example.com
We are grateful for the technical assistance of M. Silva, E. Samandar, J. Preau, X. Ye, R. Hennings, X. Zhou, and L. Jia in measuring phthalates and bisphenol A.
Funding was provided by the National Institute of Environmental Health Sciences (NIEHS) and the U.S. Environmental Protection Agency (EPA) (NIEHS/EPA P01 ES09600/RD83214101 and NIEHS R01ES014393, R01ES13163, and P30ES009089). This publication was made possible in part by U.S. EPA grants R82702701 and RD83214101.
The contents are solely the responsibility of the grantee and do not necessarily represent the official views of the U.S. EPA. Further, the U.S. EPA does not endorse the purchase of any commercial products or services mentioned in the publication. Findings expressed in this paper are the opinions of the authors and do not necessarily reflect the official opinion of the Centers for Disease Control and Prevention.
The authors declare they have no actual or potential competing financial interests.
Received: 19 September 2013
Accepted: 10 July 2014
Advance Publication: 17 September 2014
Final Publication: 1 October 2014
- Supplemental Material (138 KB) PDF
Phthalates are high-production chemicals widely used in consumer products (Sathyanarayana 2008). Exposures are ubiquitous, including among inner-city populations [Centers for Disease Control and Prevention (CDC) 2009; Whyatt et al. 2012]. Diet is thought to be the main source of exposure for di(2-ethylhexyl) phthalate (DEHP), although nondietary pathways also can be substantial for other phthalates (Carlstedt et al. 2013; Koch 2013). Phthalates have short biologic half-lives, with most metabolites eliminated within 24 hr (Wittassek and Angerer 2008). Measures of phthalate metabolites in the urine are informative as internal dosimeters of exposure because urinary enzymatic activity is negligible (Kato et al. 2004). Thus, metabolite concentrations in urine reflect an individual's internal exposure to phthalates, rather than phthalate contaminants introduced into their urine sample during collection and processing. Prior studies have shown moderate intraclass correlation coefficients (ICCs) for most phthalate metabolites in repeat urine samples indicating reasonable reliability (Hauser et al. 2004; Teitelbaum et al. 2008; Whyatt et al. 2012).
Preliminary epidemiologic findings suggest that phthalates may be associated with child asthma and other respiratory problems (Bornehag and Nanberg 2010; Kwak et al. 2009). Among Swedish children 3–8 years of age, house dust concentrations of DEHP were associated with physician-confirmed asthma, and concentrations of butylbenzyl phthalate (BBzP) were associated with child eczema and rhinitis (Bornehag et al. 2004). A follow-up study from Bulgaria reported that house dust DEHP concentrations were associated with child asthma (Kolarik et al. 2008). In cross-sectional analyses, urinary concentrations of diethyl phthalate (DEP) and di-n-butyl phthalate (DnBP) metabolites were associated with decreased forced expiratory volume in 1 sec (FEV1) in adult males but not adult females (Hoppin et al. 2004). We previously reported a statistically significant association between fractional exhaled nitric oxide (FeNO), a measure of airway inflammation, and concentrations of metabolites of DEP and BBzP, in urine collected from cohort children at 5–9 years of age (Just et al. 2012a). In addition, two studies have shown that polyvinyl chloride (PVC) materials in the home, exposure sources for BBzP and DEHP, are associated with child asthma and other respiratory symptoms (Bornehag and Nanberg 2010; Larsson et al. 2010).
Increasingly, it is becoming evident that the prenatal period is an important window of susceptibility when environmental exposures may affect lung development and respiratory health (Duijts 2012; Miller et al. 2001; Rosa et al. 2011). However, to our knowledge no prior studies have been published on effects of prenatal phthalate exposures and child asthma. The current study was designed to fill this gap. We hypothesized that maternal prenatal urinary metabolite concentrations of BBzP, DnBP, DEHP, and DEP would be associated with current asthma among inner-city children.
The study includes 300 inner-city women and their children, 5–11 years of age, participating in the Columbia Center for Children's Environmental Health (CCCEH) longitudinal birth cohort of 727 women enrolled between 1998 and 2006 while they were pregnant with the index child. Women 18–35 years old, who self-identified as African American or Dominican and had resided in northern Manhattan or the South Bronx for at least 1 year before pregnancy, were enrolled through prenatal clinics at Harlem and New York Presbyterian Hospital (Perera et al. 2003). Women were excluded from enrollment into the cohort if they reported active smoking, used other tobacco products or illicit drugs, had diabetes, hypertension, or known HIV, or had their first prenatal visit after 20 weeks gestation. The 300 children were included in the present analysis if phthalate metabolite concentrations had been measured in a maternal spot urine sample collected during pregnancy and data were available for model covariates and to classify the child's asthma status. Children were excluded from the present analysis if their mothers reported active smoking during pregnancy (n = 30), if prenatal maternal urine phthalate metabolite concentrations were not available (n = 281), if children were lost to follow-up (n = 89), or were missing covariate data (n = 27). The 300 children were similar to the other children in the CCCEH cohort with regard to their race/ethnicity, maternal prenatal marital status and education level, household income, household tobacco smoke exposure, maternal asthma, or maternal demoralization during pregnancy (see Supplemental Material, Table S1). All women signed an IRB-approved consent form and children signed an IRB-approved assent form beginning at age 7. The institutional review boards at the Columbia University Medical Center and the CDC approved the study.
Urine sample collection and phthalate measurements. A spot urine sample was collected from the women (n = 300) during the third trimester (mean ± SD, 34.0 ± 3.0 weeks gestation; median, 33.7 weeks) and from the children at ages 3 (n = 216), 5 (n = 270) and 7 years (n = 154). Samples were analyzed for the following four phthalate metabolites at the CDC using solid phase extraction coupled with high performance liquid chromatography–isotope dilution tandem spectrometry as described (Kato et al. 2005): mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), as a representative of the DEHP metabolites as described (Just et al. 2012a); monobenzyl phthalate (MBzP), a metabolite of BBzP; mono-n-butyl phthalate (MnBP), a metabolite of DnBP; and monoethyl phthalate (MEP), a metabolite of DEP. Bisphenol A (BPA) was measured in maternal and child urine samples using solid phase extraction coupled with high performance liquid chromatography-isotope tandem mass spectrometry (Ye et al. 2005). Specific gravity was measured in the urine samples using a handheld refractometer and was used to control for urinary dilution (Atago PAL 10-S; Bellevue, WA) (Hauser et al. 2004).
Diagnosis of child asthma. At child ages 5, 6, 7, 9, and 11 years, repeat questionnaires were administered to the mother or guardian to gather information on asthma-like symptoms in the child. The questionnaires were administered in English or Spanish by fully bilingual research workers. These included the well-validated International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire (Asher et al. 1995) and the Brief Respiratory Questionnaire (BRQ) (Bonner et al. 2006), as well as report of asthma rescue and/or controller medication. As described previously (Donohue et al. 2013), children were referred for physician evaluation for asthma based on the first report that the child had wheeze or whistling in the chest, a cough that lasted more than a week, other breathing problems, and/or use of asthma rescue or controller medication in the preceding 12 months on any of the follow-up study questionnaires. Examinations included a standardized history, physical examination, and prebronchodilator and postbronchodilator pulmonary function testing. Two allergists/pulmonologists independently reviewed the results of each examination and classified their asthma status according to the following pre-specified criteria: a) current asthma symptoms OR current asthma medication AND either a 12% increase in FEV1 or a 30% increase in FEF25–75 postbronchodilator; b) current asthma symptoms OR current asthma medication AND history of asthma symptoms on previous questionnaires; c) history of asthma symptoms on previous questionnaires AND wheeze on current exam.
The physician examination was conducted once during study follow-up, and the children were classified as having current asthma or as not having current asthma based on their status at the time of the examination. Children whose parents or guardians did not report wheeze or the other asthma-like symptoms or asthma medication use on any of the follow-up questionnaires were classified as nonasthmatics at the time of the last negative questionnaire.
Statistical analyses. Phthalate metabolite concentrations were right-skewed and transformed using the natural logarithm (ln). Concentrations that were below the limit of detection (LOD) were assigned a value of 0.5 × LOD. Variables assessed as potential confounders were selected from those known or suspected of being associated with phthalate concentrations or asthma (Just et al. 2012a; Miller et al. 2004; Whyatt et al. 2012). Variables were retained in the models if they were associated with the outcome (p ≤ 0.10) and/or addition or removal changed the coefficient for the exposure (phthalate metabolite) to outcome relationship by > 10%. Variables assessed included race/ethnicity, prenatal and postnatal household tobacco smoke exposure, maternal history of asthma, maternal education, maternal marital status, material hardship (lack of food, housing, gas, or electricity, clothing, or medicine during pregnancy), sex of the child, and child age at diagnosis (age at diagnosis as either current asthma or not current asthma for children with a history of the asthma-like symptoms seen by the physician, or age at classification as nonasthmatic at the last negative questionnaire for children without history of the asthma-like symptoms). Maternal prenatal demoralization also was assessed by validated questionnaire (Dohrenwend et al. 1978) because it previously has been associated with wheeze among children in the cohort (Reyes et al. 2011). Models were also adjusted for maternal prenatal BPA urinary concentrations (Donohue et al. 2013) but not child postnatal BPA concentrations because inclusion caused < 10% change in the phthalate exposure–outcome relationship. In addition, we assessed whether child postnatal urinary phthalate concentrations acted as a confounder using the phthalates measured at child ages 3, 5, and 7 years (2 children who had phthalates measured in urine collected at age 7 but whose asthma status was determined before age 7 were removed from the age 7 analyses). However, none of the postnatal phthalate metabolite concentrations were associated with child asthma (see Supplemental Material, Table S2), and inclusion caused < 10% change in effect size of predictor variables. The maternal phthalate urinary concentrations were included in models as ln-transformed variables, and also were categorized into tertiles and modeled using indicator variables to estimate relative risks comparing the second and third tertiles to the first tertile (referent). Metabolite concentrations were adjusted for specific gravity before categorizing using the formula described previously (Hauser et al. 2004). Consistent with our prior approach (Just et al. 2012a), relative risks were estimated using Poisson regression with robust standard error estimation using the generalized estimating equations based method of Zou (2004) (see also Lovasi et al. 2012; Spiegelman and Hertzmark 2005). Analyses were conducted using SPSS version 21 (SPSS, IBM, Chicago, IL). Results were considered significant at p < 0.05.
Table 1 provides subject characteristics. Self-reported ethnicity was African American (35.7%) or Domincan (64.3%). Educational attainment was low (35.7% had not completed high school), and the majority (68%) reported never having been married. Table 2 shows the distribution of the urinary phthalate metabolite concentrations measured in maternal prenatal spot urine. All phthalate metabolites were detected in 100% of maternal prenatal urine samples except for MBzP in one sample (assigned a value of 0.11 ng/mL). Concentrations were generally comparable with those of a representative sample of the U.S. population sampled over roughly the same time period (1999–2004) (CDC 2009). Table 3 shows the correlations between the (ln)maternal prenatal phthalate metabolite concentrations adjusted for specific gravity. All metabolites were positively correlated, with correlation coefficients ranging from 0.16 (for MEP and MnBP) to 0.50 (for MnBP and MBzP) (all p-values < 0.01).
Table 1 – Characteristics of children (n = 300) from the CCCEH birth cohort.
Table 2 – Distribution of phthalate metabolites in maternal prenatal urine during pregnancy (ng/mL).
Table 3 – Correlationa between prenatal phthalate metabolite concentrations adjusted for specific gravity (n = 300).
A total of 1,013 repeat questionnaires on wheeze and other asthma-like symptoms were administered between ages 5 and 11 years (mean, 3.7 ± 1.1 questionnaires per child). The children were 8.1 ± 1.9 years on average at the time of the last questionnaire administration. Of the 300 children, 154 had a history of the following asthma-like symptoms on one or more questionnaires between 5 and 11 years: a report in the preceding 12 months of wheeze or whistling in the chest, a cough that lasted more than a week, other breathing problems, and/or reported use of asthma rescue or controller medication. These 154 children met our screening criteria for the physician diagnosis of asthma based on the first report of any of these symptoms. At the time of the physician exam, 94 children were diagnosed with current asthma and 60 were diagnosed as not having current asthma. A greater proportion of African-American than Dominican children were classified as having current asthma (36% vs. 29%, chi-square p = 0.11). The remaining 146 children had no history of any of the asthma-like symptoms on repeat questionnaires and were classified as nonasthmatic at the time of the last negative questionnaire.
We estimated relative risks (RRs) for three different outcome groups relative to the children classified as nonasthmatic (n = 146) as a common referent group: a) children with any report of symptoms and/or medication use, regardless of the outcome of their asthma examination (n = 154); b) children diagnosed with current asthma at the time of their physician examination (n = 94); and c) children with a history of symptoms but diagnosed as not having current asthma at the time of the physician examination (n = 60). Linear results are presented in Figures 1–3 and categorical results in Table 4.
Figure 1 – Association between maternal prenatal (ln)phthalate metabolite concentrations and presence (n = 154) compared with the absence (n = 146) of a history of asthma-like symptoms on repeat questionnaires administered between child ages 5 and 11 years. RRs were estimated using Poisson regression with robust standard error estimation using the generalized estimating equations controlling for maternal asthma, household tobacco smoke exposure, maternal prenatal BPA, maternal prenatal demoralization, and maternal prenatal specific gravity.
*p < 0.05.
Figure 2 – Association between maternal prenatal (ln)phthalate metabolite concentrations and diagnosis of current asthma (n = 94) compared with nonasthmatic (n = 146) between child ages 5 and 11 years. RRs were estimated using Poisson regression with robust standard error estimation using the generalized estimating equations controlling for maternal asthma, household tobacco smoke exposure, maternal prenatal BPA, maternal prenatal demoralization, child age, and maternal prenatal specific gravity.
*p < 0.05.
Figure 3 – Association between maternal prenatal (ln)phthalate metabolites concentrations and diagnosis as not current asthma among children with a history of the asthma-like symptoms (n = 60) compared with children without any history of asthma-like symptoms classified as nonasthmatics (n = 146). RRs were estimated using Poisson regression with robust standard error estimation using the generalized estimating equations controlling for maternal asthma, household tobacco smoke exposure, maternal prenatal BPA, maternal prenatal demoralization, child age, and maternal prenatal specific gravity.
*p < 0.05.
Table 4 – RR (95% CI) for history of asthma-like symptoms (group 1, n = 154), diagnosis of current asthma (group 2, n = 94), and diagnosis of not current asthma (group 3, n = 60) compared with nonasthmatics (n = 146) by tertiles of phthalate metabolites.
Report of asthma-like symptoms regardless of the outcome of the asthma examination. Compared with nonasthmatic children, a significant association was seen between maternal prenatal urinary MBzP and MnBP concentrations and children with a history of asthma-like symptoms: RR = 1.12 (95% CI: 1.01, 1.24) and RR = 1.16 (95% CI: 1.02, 1.33) per ln-unit increase, respectively (Figure 1). Compared with children of mothers with MBzP and MnBP concentrations in the first tertile, the RRs for a history of asthma-like symptoms among those in the second tertile were 1.25 (95% CI: 0.94, 1.65) and 1.39 (95% CI: 1.06, 1.82), respectively, and among those in the third tertile the RRs were 1.39 (95% CI: 1.05, 1.86) and 1.44 (95% CI: 1.09, 1.90, respectively (Table 4). There was no significant increase in risk of asthma-like symptoms in the linear models associated with either maternal MEP or MEHHP concentrations (Figure 1). However, in the categorical models (Table 4) compared with children of mothers with MEP in the first tertile, a significant increase in risk of asthma-like symptoms was seen among those in the second tertile (RR = 1.33; 95% CI: 1.03, 1.73) but not among those in the third tertile (RR = 1.08; 95% CI: 0.82, 1.42). There was no increase in risk of asthma-like symptoms across tertiles of MEHHP concentrations (Table 4).
Diagnosis of current asthma at physician examination. Compared with nonasthmatic children, maternal prenatal MBzP and MnBP concentrations, but not the other phthalate metabolites, were associated with the diagnosis of the child with current asthma at the physician examination in the linear models: RR = 1.17 (95% CI: 1.01, 1.35) and RR = 1.25 (95% CI: 1.04, 1.51) per ln-unit increase, respectively (Figure 2). In the categorical models (Table 4), compared with children of mothers with MBzP and MnBP concentrations in the first tertile, RRs for current asthma among those in the second tertile were 1.31 (95% CI: 0.87, 1.96) and 1.87 (95% CI: 1.28, 2.67), respectively, and among those in the third tertile RRs were 1.72 (95% CI: 1.15, 2.59) and 1.78 (95% CI: 1.18, 2.70), respectively. There were no significant associations between diagnosis of current asthma and maternal prenatal MEP or MEHHP concentrations in either linear (Figure 2) or categorical (Table 4) models.
History of symptoms but diagnosis of not current asthma at physician examination. Compared with nonasthmatic children, maternal prenatal MnBP concentrations were associated with a history of asthma-like symptoms but diagnosis of not current asthma at the physician examination: RR = 1.33 (95% CI: 1.05, 1.70) per ln-unit increase (Figure 3). In the categorical models (Table 4), compared with mothers with MnBP concentrations in the first tertile, the RR for not current asthma for those in the second tertile was 1.46 (95% CI: 0.81, 2.65) and in the third tertile was 1.71 (1.02, 2.88). The association between maternal prenatal MBzP concentrations and diagnosis of not current asthma among those with a history of the asthma-like symptoms was of borderline significance in the linear model: RR 1.17 (95% CI: 0.98, 1.41) per ln-unit increase (Figure 3). However, there was no increase in risk across tertiles of maternal MBzP concentration, and there were no significant associations between diagnosis of not current asthma and maternal prenatal MEP or MEHHP concentrations in either linear (Figure 3) or categorical (Table 4) models.
We observed a significant association between concentrations of MBzP, the BBzP metabolite, and MnBP, the DnBP metabolite, in maternal urine collected during the third trimester of pregnancy and diagnosis of current asthma among CCCEH cohort children 5–11 years of age. Risk of current asthma was > 70% higher among children whose mothers had BBzP and DnBP metabolite concentrations during pregnancy in the third versus first tertile. This work extends our previous CCCEH findings in cross-sectional analyses that increases in concentrations of metabolites of BBzP, as well as DEP, in child urine were associated with increases in FeNO, an indicator of airway inflammation and asthma (Just et al. 2012a). Although prior research has shown associations between other phthalates and child asthma, only one prior cross-sectional study reported evidence of a dose–response relationship between MBzP and child asthma but was limited by small sample size (n = 101) (Hsu et al. 2012). Other cross-sectional studies in Sweden (n = 400 children ages 3–8 years) and Bulgaria (n = 102 children ages 2–7 years) have reported associations between house dust concentrations of DEHP and child asthma, and of BBzP and child eczema and rhinitis, but not BBzP and child asthma (Bornehag et al. 2004; Kolarik et al. 2008). A recent cross-sectional study reported a significant association between child asthma and mono(carboxyoctyl) phthalate and mono(carboxynonyl) phthalate in first morning void urine collected from 623 10-year-old Norwegian children, but did not observe any association between asthma and urinary concentrations of the BBzP or DnBP metabolites (Bertelsen et al. 2013). Another recent cross-sectional study conducted among participants in NHANES (National Health and Nutrition Examination Study) found urinary concentrations of MBzP, but not MnBP, to be significantly associated with current asthma, wheeze, hay fever, and rhinitis in adults (n = 1,546) but not in children 6–17 years of age (n = 779) (Hoppin et al. 2013).
Consistent with our prior findings (Whyatt et al. 2012), significant correlations were seen between prenatal urinary concentrations of MBzP and MnBP adjusted for specific gravity (Spearman's rho = 0.50). This may reflect common sources of exposure and/or similar metabolic pathways. Consumer products including personal care products and home materials are sources of exposure to both of these phthalates (Buckley et al. 2012; Carlstedt et al. 2013). In addition, MnBP is a minor metabolite of BBzP, accounting for approximately 6% (Anderson et al. 2001). Nonetheless, most MnBP in urine is attributable to DnBP exposures. Several studies, including findings in the CCCEH cohort, suggest that PVC materials in the home are likely a substantial source of BBzP exposure, as indicated by measures in maternal and child urine and residential and personal air samples (Adibi et al. 2008; Carlstedt et al. 2013). Although DEHP is also a constituent of PVC, evidence suggests that exposure to this phthalate occurs primarily through the diet, likely as a result of use in food packaging (Koch 2013; Rudel et al. 2011). Prior cross-sectional studies also have found PVC materials in the home to be associated with child asthma and other respiratory symptoms (Bornehag and Nanberg 2010), and these results provide at least some corroboration for the current findings. For example, in a prospective study of 4,779 children in Sweden without asthma or respiratory symptoms at child ages 1–3 years, PVC flooring at baseline was associated with parental report of child asthma at the 5- and 10-year follow-up (Larsson et al. 2010; Shu et al. 2014).
The significant association seen in our present study between MnBP and MBzP urinary concentrations and asthma-like symptoms, regardless of whether or not the child received a diagnosis of current asthma, was not anticipated. These findings may imply that prenatal exposure to some phthalates has effects on transient wheeze and/or nonspecific airway hyperresponsiveness. It is possible that the respiratory consequences of prenatal exposure to phthalates mimic what has been observed following prenatal exposure to cigarette smoke, where several large cohort studies have essentially established its role in recurrent wheeze in very young children (Magnusson et al. 2005). Alternatively, prenatal phthalate exposure may induce a nonspecific airway hyperresponsiveness, manifested as report of wheeze, use of asthma medication, cough, or other breathing problems, that develops into clinical asthma during childhood only in a subset of children. The development of airway hyperresponsiveness is believed to have an environmental component (Lund et al. 2007; Riley et al. 2012), and develops at a very early age (Lesouef et al. 1989). Further prospective studies are needed to resolve these important clinical questions.
Research on mechanisms whereby phthalates might induce asthma or asthma-like symptoms is extremely limited [reviewed by (Kwak et al. 2009)]. Several phthalates have shown adjuvant effects on proallergic T helper 2 differentiation and immunoglobulin (Ig) G1 and IgE production when administered via subcutaneous or intraperitoneal injection to BALB/c mice sensitized by ovalbumin (Bornehag and Nanberg 2010; Guo et al. 2012). Our prior research in the CCCEH cohort did not find any association between maternal prenatal urinary MBzP concentrations and child seroatopy, although we did observe an association between maternal prenatal MBzP concentrations and early-onset eczema (Just et al. 2012b). In addition, as discussed above, when we used a repeated-measures design, we saw a significant association between MBzP concentrations in child urine and FeNO, suggesting that MBzP induces airway inflammation (Just et al. 2012a). In cross-sectional analyses, urinary concentrations of MBzP also have been shown to be associated with C-reactive protein, a nonspecific marker of systemic inflammation, and both MBzP and MnBP have been associated with biomarkers of oxidative stress (Ferguson et al. 2011, 2012). However, the relevance of these findings to the potential effect of the phthalates on respiratory health remains unclear. Mechanistic data explaining why the prenatal period of exposure may be deleterious also are limited, but our group has provided evidence of epigenetic regulation following prenatal exposure to several environmental exposures in human and mouse studies on asthma (Kundakovic 2013; Liu et al. 2008; Niedzwiecki et al. 2012; Perera et al. 2009; Tang et al. 2012).
Strengths of the current study include the standardized physician diagnosis of child asthma that is an improvement over most prior research, which used parental report of child asthma as the outcome. Additionally, this is the first study to evaluate associations between prenatal phthalate exposure and asthma during early to mid-childhood in a longitudinal birth cohort. This is a strength because most prior studies of phthalates and asthma have been cross-sectional. The rate of both maternal and child asthma in our cohort is high (31.8% and 25.2%, respectively). Asthma prevalence among New York City children ranges from 3% to 25% (Nicholas et al. 2005), with some inner-city communities having triple the asthma prevalence of their bordering neighborhoods. Although family history of asthma or atopy were not required inclusion criteria for the current cohort, pregnant mothers were informed at enrollment that the research was evaluating environmental risk factors in child asthma development, and this may have been an incentive for mothers whose children were at higher risk to participate.
Limitations also should be noted. We used as our exposure dosimeters the measurements of the phthalate metabolite concentrations in a single prenatal spot urine sample, and this could result in exposure misclassification, especially for some phthalate metabolites. Controlling for urinary dilution, we previously reported that the ICCs for phthalate metabolites in repeat prenatal spot urine samples (n = 135) collected biweekly over the last 6 weeks of pregnancy from 48 women in the CCCEH cohort were 0.77 for MBzP, 0.64 for MnBP, 0.27 for MEHHP, and 0.19 for MEP (Whyatt et al. 2012), indicating that reliability of the phthalate biomarkers differs across the phthalates. We would expect the exposure misclassification for these phthalates to be nondifferential with respect to asthma and could thus reduce our power to observe an effect for either MEP or MEHHP on asthma risk, because they had the lower ICCs. However, this is less likely to be a problem with MBzP and MnBP due to the higher ICCs in repeat prenatal urine samples, coupled with the relatively high correlations seen previously in the CCCEH cohort between BBzP concentrations in maternal 48-hr prenatal personal air samples and 2-week integrated indoor air samples (Spearman's rho = 0.67) and between BBzP in maternal personal and indoor air samples and MBzP concentrations in maternal prenatal urine (Spearman's rho = 0.48 and 0.71, respectively) (Adibi et al. 2008). However, the correlations between DnBP concentration in maternal prenatal personal and indoor air samples and MnBP concentrations in maternal prenatal urine were considerably lower (Spearman's rho = 0.05 and 0.27, respectively) (Adibi et al. 2008). Missing data and loss to follow-up, as often occurs in a long-term prospective study, could also bias study results (Kurukulaaratchy et al. 2003; Matricardi et al. 2008). However, 97% of the children in the current study had questionnaire data on ISAAC wheeze and other respiratory symptoms collected at least twice, and 86% of the children had questionnaire data collected three or more times. In addition, maternal urine samples were collected during the third trimester of pregnancy, and this is another potential limitation given that the critical window of susceptibility is not known but may well be earlier in pregnancy. Additionally, the research was conducted in an inner-city cohort, with high rates of maternal and child asthma and was restricted to nonsmoking mothers during pregnancy. Therefore, results may well not be generalizable to other populations. Further, noncausal associations (e.g., due to confounding by some other factor associated with phthalates and asthma) cannot be ruled out. For all of these reasons, the findings should be interpreted with caution before replication in other cohorts that include evaluation of associations between child asthma and exposures during other trimesters of pregnancy.
These results suggest that prenatal exposure to BBzP and DnBP may increase risk of childhood asthma. The findings raise new concerns that the presence of relatively ubiquitous environmental exposures may have deleterious respiratory effects. However, because, to our knowledge, this is the first study to evaluate associations between prenatal phthalate exposures and child asthma risk, results require replication.
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Clarivate Analytics released the 2018 Journal Citation Reports, which tracks citations for articles published in 2015 and 2016. EHP's new Journal Impact Factor is 8.31, with a 5-Year Journal Impact Factor of 9.81. (more…)
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Via Scoop.it – Heal Or Die: Healthy Eating 1. Berries. If I took the time to break them down, they would take up all five slots on my list. Blueberries top this "sublist" in that they contain 14 mg of Vitamin C in one cup and are filled with antioxidants. Then there's strawberries, blackberries, [...]
Posts Tagged 'Parkinson'
Heal Or Die: 5 Power Fruits THAT YOU MUST Eat Everyday
January 25th, 2012 AniseSmithHeal

subset: commoncrawl


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May 12, 2012
12:00 pm
As cofounder of Soundbuzz, Simon Lower was the king of iteration: the company went from online to mobile, ringtones to 3G downloads, and B2C to B2B. But this "trial by fire" turned out well, with Soundbuzz getting acquired by Motorola in 2008.
Much the wiser, Lower is now cofounder of venture accelerator Greencloud Labs and cofounder of a spinoff called Beepmo, an app for connecting with professionals nearby. The app made its big debut this week at Next Bank Asia, a premier banking conference in Singapore.
With all the buzz about social discovery apps at SXSW, Beepmo focuses on one of their most useful and non-creepy applications: networking. As with other apps, you can discover what you have in common with people and connect directly. Beepmo is targeting Southeast Asia, India, and Australia.
When I spoke to Lower in February, he told me that partnerships with event organizers would make or break Beepmo – so this is definitely a good sign. He also reflected on his 8-year experience at Soundbuzz and offered these lessons for other entrepreneurs:
Simon Lower: Probably the biggest mistake that we made from day 1 was not having a CTO, or not having someone technical as a founder and thinking we could outsource it and build it externally, or just hire people to do it. And so technology was a continual problem. We were great in terms of relationships with operators and relationships with the recording industry, but in terms of technology, that was always something that we struggled with. To this day, I won't start anything or I won't invest in anything that doesn't have a strong technical lead as a founder, especially at the seed stage….
When you start any business with other partners and founders, you need to be very clear what the roadmap's going to be and have those hard conversations at the beginning, rather than trying to figure them out when people want to leave and move on. That's something that we learned. That's something that, when we invest in a business or if we look at any business, we make that very clear up front. You need to know what your roles and responsibilities are, and know that … everyone needs to contribute. If one guy doesn't contribute but feels they have some life stake to this ownership, that's always where issues ensue and that can be very detrimental to any business. And often that's why a lot of these businesses don't work – it's more internal problems rather than the business model or the idea….
Getting out of Singapore – we learned that really quickly. You can't have a startup in Southeast Asia that's single market, unless maybe you're in Indonesia, or India, or China, of course. The markets are just not big enough, so we just had to scale very quickly and hire great local people.
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Reiki Master Teacher Course
Saturday, April 28, 2018 at 9:30 AM - Sunday, April 29, 2018 at 5:30 PM (UTC)
Event Details
This course intensifies your connection to Reiki and empowers you to work with energy at Reiki Master level for you rself and in treating others. It also teaches you how to teach Reiki. For further information follow this link.
The course costs £450, to reserve your place you pay £150 deposit today and then £300 on the weekend of the course. There is also an instalment payment option if you want to spread the payments, contact me on firstname.lastname@example.com for further information.
When & Where
The Complete Wellness Centre
18 Leicester Road, Uppingham
LE15 9SD Rutland
United Kingdom
Saturday, April 28, 2018 at 9:30 AM - Sunday, April 29, 2018 at 5:30 PM (UTC)
Add to my calendar
Website: http://www.happyinmyskin.co.uk/organizer/faiy/
Phone: 07974 739 743


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Growing up, I never doubted that I would someday become a mother.
But over the past few years, I have begun to question whether or not I should ever have children.
It has nothing to do with anxiety about supporting a child on a writer's income -- that could be overcome with help and hard work. It has nothing to do with a lack of maternal urges -- my uterus twinges every time I smell a baby's hair. It has everything to do with my fears about climate change and how different my child's life will be from my own.
I am not exactly an environmental crusader. I turn off the lights whenever I leave a room. I use public transportation. I recycle. For a long time, I thought this was enough.
It's not.
No decent parent would knowingly put his or her child in situations where they would experience fear, discomfort and pain. But this is exactly what we are doing by not acting immediately to lessen our impact on this planet.
In the latest issue of Rolling Stone, leading environmental journalist Bill McKibben uses the undeniable power of numbers to explain that we are quickly marching into doomsday. He writes:
We have five times as much oil and coal and gas on the books as climate scientists think is safe to burn. We'd have to keep 80 percent of those reserves locked away underground to avoid that fate. Before we knew those numbers, our fate had been likely. Now, barring some massive intervention, it seems certain.
I am beginning to understand that "alarmism" is a word people like to use when they would prefer not to think about inconvenient truths.
We must understand and accept is that climate change is not happening at some unspecified time in the future. From droughts and wildfires across the United States to the breaking off of an iceberg twice the size of Manhattan just last week, climate change is here. We are all bearing witness to it. It is happening.
What will it take to spur action from world leaders? Do we need an environmental Pearl Harbour? Will it take New York City under water? Smog alerts on Christmas Eve? How about a failed North American corn crop that will spike food prices to astronomical levels and make widespread hunger a reality for those of us who have never truly felt it?
When you are speeding towards a brick wall, it's a bad idea to wait until the last possible second to slam on the brakes.
Fossil fuels are very much the enemy. President Obama squandered a golden opportunity by giving the automobile industry bailouts without this disclaimer: they would receive the billions of public dollars only if General Motors, Ford and Chrysler acted in the interests of our children -- by creating and implementing vehicles using only sustainable fuel sources.
But every day, world leaders are choosing the economy over the environment. As McKibben puts it, you can't have both.
Personally, I choose unemployment over extinction.
We need decisive leadership and action now. It will not come from the Canadian prime minister, as Stephen Harper is unashamedly bedfellows with Big Oil. It will not come from our minister of the environment, Peter Kent, a vocal proponent of the oil sands. Oh, Canada! Stephen Leacock himself could not have penned a parody this absurd.
I look to President OBama and other world leaders to make this change. I ask for an emergency environmental summit in exchange for our votes this November.
As a species, we must adapt or die. World leaders must scrap our current system by penalizing and taxing the fossil fuel industry within an inch of its life and using that money to grow the sustainable energy economies. By continuing on as we have always done, we are digging ourselves into an ever-deeper hole that our children will never be able to climb out from.
Sixteen years from now (Malia will be 30 and Sasha will be 27), I cannot look into the eyes of my suffering child and tell her, when there was still time to alter the course of her future, that we sat back and did nothing.
And that is why I'm still not certain that I can ever become a mother.
My voice is the only weapon I have. You have one, too.


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#Weekly Video: B.D. ft. KGE THE SHADOWMEN, MIKRIS – "NINJA TUNE"
Forest Ninja ^^
Senpai – They Say Just Wait Till Morning EP
Petals on Fire [Short Video]
Impressive work from Kodai Tanaka & Shing02
If you wanna to show your art skills, don't be shy, email me ^_^
Figub Brazlevič – Inner City Tribe
Audio Dope correct sentence ^^
The Krekpek crew has different backgrounds which melt into each other. Krekpek maintains a high standard in its developing of ideas.
It cooperates between producers and artists and bring them together to realize ideas in music and graphics.
Thank you to all beatmakers from the Netherlands, Canada, Belgium and Germany.
Shout outs to Pierre Dixsaut for the permission to use the type for the artwork.
Regards to all supporters of that project who helped us to bring it to success.
This Beattape wouldn't be possible without the support of your great work we put together to this compilation — enjoy this great first issue called AUDIØDOPE.
instrumental / beats / hip-hop


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In one week, we will have been in the UK for one year. And yesterday marked our tenth completed month in Scotland. I haven't been able to really put my thoughts into words until tonight…so bear with me as this starts bad and ends somewhat better.
Since July, we've had numerous difficult things happen, and I get it that life is made up of difficult things with lots of mundane and good things in the middle. Life happens no matter where you live. For most of the summer, I think I was in the worst of culture shock and difficult things felt magnified. Then after much prayer, things shifted in a positive direction in the middle of August, and I could see with a new perspective. I think my view of Scotland became very balanced and real, but at the same time, I had numerous conversations in which people told us that we have to be in this for the long haul as that's what's needed for effective ministry in Scotland. And reality hit harder. On top of it, Mark is heavily preparing for a new career and the unknown of how and what is coming for him and us is pressing at times. Will he have a three hour round trip commute by bus, will he need us to drive him to work which requires a new boldness in my driving, will he get a full time, good paying job right when the other job ends??? And even though we haven't verbally worried, these times of transition are never easy. We've done enough transition to last us the next ten years, and so I think I've been off kilter a bit for a while.
Edinburgh and Scotland itself are not easy environments to live in. Yes, it's beautiful and there are some truly kind and wonderful people here. I think we have the best set of neighbors in all the world, and so I'm very aware that there are lots of good things here. Yet for an outsider, there's also a lot that I struggle with. The top one being that the government is very socialist, and politics matter to me. The socialist mindset and all it entails has infiltrated everything. We, Americans, take so much in the States for granted. I could write a whole book on this, but I won't. It's just very evident once you're away for some time. I will say though that we, as a team, are learning how much we need Jesus in order to thrive here. We've left churches that we loved and that were home for us, and while there are solid, good churches here, they're not what we left. My heart has been crying as there's no freedom here to dance or cry or get yourself where you need to be during worship at church. And many of you will be like what?! Yes, this quiet, reserved, white girl needs worship time to express my heart; I need the freedom to worship in my unique expression of that. Therefore, I have felt like my right arm is missing at church, so last week, I did it anyway, danced for just two minutes, and avoided all eye contact!! LOL! If we cannot be free to worship God in church, then what are we doing?!? So I'm telling you that to lead to this…the spiritual atmosphere is tough. It is dry; it is filled with stuff that is not Godly. And as much as we welcome talking to anyone who will talk to us, it can get old to always stand out in your beliefs, your politics, your accent, etc. Sometimes, I have to catch myself as I feel that all I'm doing is defending myself when instead I just need to be me. It's also hard to hear about all the ministries that have come and gone. Yet we know nothing about why they came and left. All we know is that if we're here for the long haul, then we'd better just get on with being who God made us to be…even in all the uncomfortable, awkward moments. So I've been wrestling and struggling with just not wanting to commit to the long haul with this government and this atmosphere.
And then it got worse….I (driving myself and two kids) bravely ventured to the nearest town to run some errands. It's a bit of a rough town; it's not posh or wealthy. It's real life. It's not in a Jane Austen film. As we're running errands, Ryder had an emergency bathroom urge, and British public toilets are rough. Cleanliness is lacking, so I tend to avoid them at all costs. Because I had Eden in a stroller, I sent him in and waited by the door with Eden. He then needed help, so Eden, the stroller, and I went in and I just completely freaked as someone had left an STD test + urine + packaging/instructions spread out all over the bathroom sink right next to where my son had just been sitting. I immediately thought "Lord, I cannot do this! I can't raise my kids here!! I'm struggling with child laws I don't agree with, mean kids in the neighborhood, dirty bathrooms, super markets where kids are fighting in line, people working in those stores who don't care and don't try, terrible customer service, and now STDs on the toilet that my son has been sitting on!!" and my mind just shouted all the ugliness I could think of. Not a proud moment. And Mark had to talk me down from crazy, upset mama mode. But it was the straw that broke the camel's back.
And I tend to crash, and God comes in and calmly, lovingly teaches me. Over the past year, I have fought so much fear about raising my kids here. I've fought massive insecurity about homeschooling and parenting in this culture. Our neighbor kids know nothing about Jesus. Absolutely nothing, and yes, that's why we are here. But I'm also sending my kids out there to play with these kids every single day while I trust them to the Lord. I have no idea what's talked about unless they tell me, and this is new for us. We went from having them in Christian schools and church to a very different environment here. This is real life, but my kids are young and this hurts my heart. And so honestly, I have to give my children and my parenting to Him every day. Ryder ran in yesterday to say that the neighbor kid gave him the finger, and it actually became a good moment for us as we had a great discussion about it. It's not what I want my 7, 5, and 3 year olds seeing, but I am there to talk them through it. I thank God for that. And I realize that American kids swear, give the finger, deal with STDs, etc. This is where the cultural gap is unexplainable because I can't visibly give you a comparison of the two countries and all that I'm seeing and explaining. Both countries are flawed; both countries have high points and low points. Both countries have lovers of Jesus and those that are lost. The things that I'm experiencing now are things that I can't explain to you until you've been there and then come here. You just have to read this and hopefully hear my heart.
Scotland is a beautiful country filled with history and strong, independent people. I do think this is one of the most beautiful places on earth, and I wish the Scottish as a whole took care of it. I know that God adores these people, and He is building a strong Church here. So even though I do not know how to reach or love those I encounter here, I know that I can confidently rest and go about my day being led by Him as He perfectly knows how to love those I meet. However, to learn His ways and His heart, I have to spend more time with Him. I already feel like I'm juggling too much, but my heart is saying that it's time to make much more room for Him. If we are here to fulfill our part and are staying here, we need much more of Him. So whatever I need to do to make that happen, it has to happen. Just as I have to be super intentional in teaching my children about Jesus, I have to be super intentional in renewing my mind and in seeking His heart.
And so this is an ugly post written by a tired and very human missionary living very far from home. I pray that God sees my heart and sees my rough days and uses them to just teach me more. I want more of Him. The next time I encounter a situation that takes me totally off guard, I want to react by praying for that one who is dealing with the results of an STD test. I want to meet the neighbor kid who thinks she can just wave her middle finger at little ones and talk to her about why she's doing it. I want to say a kind word to the mom whose sons are smacking each other in the line at the grocery store. I want to see the Scots free to dance or shout or do whatever they need to worship Jesus in their own expression. I want to just be a vessel that flows in His leading. So I'm totally okay to be the awkward American if it helps someone to realize they can get out of the norm and be who God made them. And God will provide and be all we need Him to no matter if we're here 10 or 50 years. He is always enough, and He is more than enough for my kids and their future.


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How Did the Moon Form?
The night sky just wouldn't feel right without the Moon. Where did our our friendly, familiar satellite come from?
Scientists and philosophers have been wondering about this for centuries.
Once Copernicus gave us our current model of the Solar System, with the Earth as just another planet and the Sun at the centre of the Solar System, this gave us a new way of looking at the Moon.
The first modern idea about the formation of the Moon was called the fission theory, and it came from George Darwin, the son of Charles Darwin.
He reasoned the Moon must have broken away from our planet, when the Earth was still a rapidly rotating ball of molten rock.
His theory lasted from the 1800s right up until the space age.
Another idea is that the Earth captured the Moon after its formation.
Usually, these kinds of gravitational interactions don't go well.
Models predict that either the Moon would collide with the Earth, or get flung out into a different orbit.
It's possible that the early Earth's atmosphere was much larger and thicker, and acted like a brake, modifying the Moon's trajectory into a stable orbit around the Earth.
Or the Earth and Moon formed together in their current positions as a binary object, with Earth taking most of the mass and the Moon forming from the leftovers.
The most widely accepted theory is that the Moon was formed when a Mars-sized object slammed into the Earth, billions of years ago.
This collision turned the newly formed Earth into a molten ball of rock again, and ejected material into orbit.
Most of the material crashed back into the Earth, but some collected together from mutual gravity to form the Moon we have today.
This theory was first conceived in 1946 by Reginald Aldworth Daly from Harvard University. He challenged Darwin's theory, calculating that just a piece of Earth breaking off couldn't actually allow the Moon to get to its current position. He suggested an impact could do the trick though.
This idea wasn't given much thought until a 1974 paper by Dr. William K. Hartmann and Dr. Donald R. Davis was published in the Journal Icarus. They suggested that the early Solar System was still filled with leftover moon-sized objects which were colliding with the planets.
The impact theory explained many of the challenges about the formation of the Moon. For example, one question was: why do the Earth and Moon have very different-sized cores.
After an impact from a Mars-sized planet, the lighter outer layers of the Earth would have been ejected into orbit and coalesced into the Moon, while the denser elements collected back together into the Earth.
It also helps explain how the Moon is on an inclined plane to the Earth. If the Earth and Moon formed together, they'd be perfectly lined up with the Sun.
But an impactor could come from any direction and carve out a moon. One surprising idea is that the impact actually created two moons for the Earth.
The second, smaller object would have been unstable and eventually slammed into the far side of the Moon, explaining why the surface on the far side of the Moon is so different from the near side.
Even though we don't know for sure how the Moon formed, the giant impact theory holds the most promise, and you can bet that scientists are continuing to look for clues to tell us more.
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1 Response
The latest iteration I know of is that better computer modeling has opened up the parameter space, and varied models align better with the various similarities that exist between Earth and Moon.
The most exciting scenario IMO is that Tellus, the geohistorically proposed name for the preimpact protoplanet that mostly made up Earth, and Theia, the astronomically proposed name for the preimpact protoplanet that mostly made up Moon, was roughly equally massed but impacted at low velocities and rotation.
That would make direct comparison to Pluto-Charon, which is the most analogous system today and is also believed to have been the result of a low velocity impact event, and to Vesta, which first impact in the large Rheasilvia is believed to have been a low rotation impact.
Similar massed Tellus and Theia protoplanets is also apriori most likely as contemporary results of accretion.
Finally, the low velocity impact reminds of the constraints of the old hypothesis of Theia as an orbital resonance parked impactor that was disturbed and later hit Tellus. I dunno if that scenario works with equal massed protoplanets though.


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It's been that kind of day, gang. We weren't lying when we said we were stacked with people tips and in this particular case, we can confirm that Keith Cartwright is no longer with the Martin Agency. Cartwright joined Martin 15 months ago as a GCD and subsequently served as creative lead on campaigns including the "Dragee" social/digital work for Mentos.
Prior to Martin Agency, Cartwright spent three years at W+K New York and worked on accounts including Nike's Jordan Brand. Oddly enough, his LinkedIn states that he's currently a CD at W+K, though this could just be an error as said agency tells us that Cartwright has NOT returned to the Wieden network. In the meantime, we're trying to find out exactly why Cartwright and Martin Agency parted ways (one tipster claims that he "abruptly left").


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In academic environments, for instance, the precedent is given as bliss; a surplus, yes, but one that must be embraced as a literal source: a spring, a birthplace, a cradle, a home. Being with the source (and at the source) is, here, a being-home. And indeed, it is only in the formulation of the precedent that one can find one's home. According to this logic, to be without a precedent (which is to say, to be original) is to be homeless, in the most fundamental sense of the word.
Because this homelessness is hard to bear, an entire project has been created for the elimination of the predecessor. Indeed, there is no such thing as poetry without the rejection of the forerunner. As Robert Pinsky has pointed out somewhere, poetry is always what it is not, insofar as poetry can only say something that doesn't already exist. In order for poetry to be creative it has to formulate something from scratch. Otherwise it is mere epigonism, unproductive repetition, pleonastic nonsense. So here we have the to-be-or-not-to-be of creativity: to be with a predecessor, and therefore redundant, or not to be with a predecessor, and therefore acknowledged as original.
Of course, we are familiar with this project of the rejection of precedence, because we are citizens of postmodernity, and its discourse of demythification is familiar to us. It has given us plenty of space to think of precedence as something we might be better without.
Whacking the forerunner
There is a "contamination anxiety" shaping the artistic choices of writers in general. Jonathan Lethem says it is a symptom of modernism. If what one fears in relation to the source is its ability to contaminate (to impose itself as a necessary repetition), then the source is in truth not venerated but abhorred. The source needs to be buried under the weight of its own significance, never to see the light of day again. If such is the case, then the original/initial is a parasite: one that parasitizes literature – insofar as we think of literature as a domain that renews itself all the time, instead of accepting to be caught up in the continuous loop of reiteration.
|Source: Alcalde
The parasitical original/initial stands there, in the middle of everything (whence it can radiate its venom) like an inconvenience. It upsets the natural flow of things. It grows like a boil about to burst. And because of that it needs to be evicted, excised, operated out; removed like a gangrene. Any discussion of precedence needs to employ this language of repugnance if the writer were to be liberated from the terror of antecedence.
This aspect becomes apparent when the predecessor has grown to a size where it cannot be avoided. When it has become an automatic reference, a mental trick the role of which is to sort out the inconvenience of creativity, this source (this precedence that exceeds) disturbs purely and simply. It has no other function than that of inhibition. And its shadow is cast so thickly upon all acts of creation that no exercise can ever come out immaculate, unaltered, un-referenced. Take the example of the Bible, of Shakespeare, of the Classics. When they come up in any context they take the shape of 'it goes without saying.' It's this 'without saying' that is troublesome to the writer who is striving to make a name for him/herself. This writer arrives at the feast of recognition already burdened by a name that is not their own. Their very name has already been worn by others, hijacked by them, stolen before the acknowledgment of any presence (their own presence most importantly).
So the ideal situation for a beginner would be to ignore this precedence that obstructs his development. To ignore it, i.e. to make it seem invisible. One would have to write, therefore, with the only intention of hiding the traces of the forerunner. Every instance of writing will have to be an affirmation of one's originality, even when that originality is a figment of one's imagination.
But this project would be forever obstructed by the affirmative presence of the discourse that stands behind writing. The discourse, the overwhelming precedent of all forms of creative action, poses the precedent as necessary. Only someone growing in the shadow of a precedent can be counted as significant to a discourse. They would have to acknowledge the shadow even in the most original of their moments. Because there is no situation worse than that of a poet without precedents. That's what the Academia will argue.
The foreigner that speaks better
The fear of the one-without-precedent is the typical fear of originality, insofar as the original is terrible. Let us say it again: the original is impolite, distinctive; in other words, the original is truly foreign.
The antidote to barbarism is subjection to familiarity. And here is where the precedent is in its most powerful state. The precedent is a guarantor. Without it, the city may crumble. Without it, there will be no rules. Without it (to embody a seventeenth-century fear of John Locke), humanity is likely to return to its state of pre-humanity: a state without laws, without governing bodies, and therefore without foreigners.
|Source: www.twainquotes.com
In the land of the precedent everything must fall under the rubric of domestic familiarity. The whole family, down to the newborn, needs to know perfectly well the extent of the precedent in order to reconstruct the entire genealogical tree of the family's 'romance.' And so, the problem of the precedent isn't quite a problem of the poet alone, but one that transgresses professional or artistic boundaries.
But the poet is the figure we are interested in, because in the poet it is easier to trace the trajectory of thoughts; because the poet writes or memorizes, and therefore, brings along with him/herself the specter of the predecessor. With his (inherited – how else?) ability to inscribe, a poet materializes this specter better than any other sign-maker, because it's in the case of the poet that the dependence on the precedent appears in the form of an artistic culpability. I take this from Harold Bloom, who mentions "the only guilt that matters to a poet, the guilt of indebtedness."
A poet cannot speak without speaking the language of someone who spoke before. And the antecedence of this speech act is sure to (im)pose the precedent as a guest: a foreigner, someone who comes from outside the current event, like a specter that haunts.
So the precedent is a foreigner who speaks. And one whose speech is taken to be a better form of expression. The cult of ancestors depends on this better-saying in order to assert a tradition whose sole purpose is to salvage the future from its straying away from the source.
A battle against redundancy
The project of writing-after-the-precedent takes shape under the spasms caused by the fear of tautology. Tautology, i.e. the thing already said and which can't be said again because saying-again is punishable by law (the law of grammar or that of logic, it matters not).
Tautology comes about as an interdiction in its own right, one rhetorical in nature but which poses precisely the problem of the precedent as a necessary absence. In order for the precedent to be acknowledged it has to be obliterated. It has to be acknowledged as non-presence. Pure absence, as Jacques Derrida has pointed out, is not exactly the way to put the problem in relation to the trace. A trace is not a lack. A trace is always already present, always already formulating the present event, the present utterance.
|Source: Write Right
A trace, i.e. a presence of the precedent as an absence-that-matters, is something akin to inscriptions, where what is being inscribed is always already there in the form of a discourse that returns. Of course, this discourse is pushed to the margins all the time, minimized, reduced to an apparent absence, in order to maximize its efficiency. Discourses are productive only if they are well hidden; if their subjects don't get a glimpse of the game that is being played in the background. That's why Derrida insists on the absent presence that characterizes a trace. With the trace in full sight, the discourse would be exposed (and therefore lose its efficiency). Without it, the discourse would thrive, because it is the absence that articulates its power, its very possibility to be. So in order to avoid discursive suicide, the trace (the precedent) has to go; it has to be as though it had never been. But this is far from being a killing of the precedent. On the contrary, it marks the consolidation of its position. A precedent that isn't perceived as present is a precedent capable of influence. One can see this in the case of truisms, where the impossibility to locate the precedent is truly frustrating, but where one knows that the precedent exists because one can see its effects.


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Exploring Hydrocarbon Depletion
Page added on May 27, 2014
Despite increased spending, oil majors are seeing flat or declining production as they struggle to replace reserves, according to a recent analyst report.
Exxon Mobil Corp., Chevron Corp., Royalty Dutch Shell plc and BP plc recorded declines in their 2013 production. ExxonMobil reported an average production of 4,175 million barrels of oil equivalent per day (MMboepd), down 1.5 percent from 2012, and Chevron saw its production decline by .5 percent from 2012 to 2013 to 2,597 MMboepd. Shell's average 3,199 MMboepd of production for 2013 was down 1.9 percent from 2012 levels, while BP saw its production volumes fall to 2,256 MMboepd, or 2.7 percent, from 2012 to 2013.
France's Total S.A. was the only company to buck the trend in declining production, with average hydrocarbon production in 2013 of 2,299 MMboepd, Zacks Equity research analyst Nilanjan Choudhury said in a May 16 report.
"But overall, most 'Big Oil' is suffering from marginal or falling returns even as crude prices stay strong, reflecting their struggle to replace reserves, as access to new energy resources becomes more difficult," said Choudhury. "As it is, given their large base, achieving growth in oil and natural gas production has been a challenge for these companies over the last many years."
Rising capital expenses also are hurting the oil majors. Despite capital budgets of anywhere from $25 billion for BP and Total each to the $37 billion and $40 billion that Shell, ExxonMobil and Chevron plan to spend this year, these expenditures are not augmenting output.
Choudhury recommended that oil majors such as ExxonMobil and Shell curb their future spending, noting that indications are appearing that drilling expenditures have peaked, with huge budgetary jumps "likely to be a thing of the past."
The inability of these firms to generate enough cash from operations to address their rising spending and shareholder payouts has forced most of them to take on more debt.
"Though the situation is no cause for alarm, it does raise some questions regarding the companies' ability to finance shareholder returns," Choudhury commented. "Notwithstanding the fact that almost all components of Big Oil hiked their dividends recently, there is no doubt their balance sheets are under pressure from spiraling capital spending and shareholder distributions."
To maintain production rates, oil companies have had to race to find new reserves faster than the old ones dry up, Bloomberg reported in January of this year. That essentially puts them on a treadmill at which they must run faster just to keep pace – a horrible problem in any business. As a result, majors are making significant investments in costly megaprojects such as Shell's Prelude floating liquefied natural gas.
The fact that the oil and gas majors entered U.S. shale plays late also has contributed to the problem, according to Bloomberg. Many companies pulled out of the United States to explore in places such as Africa and Asia, leaving smaller companies positioned to acquire North America's shale assets cheaply. The timing of shale deals has proved difficult for the majors such as ExxonMobil, who acquired XTO Energy Inc. for $41 billion in 2010, right before natural gas prices declined.
Shell announced earlier this month that it would sell its Eagle Ford asset stake to Sanchez Energy. The company has also divested interests in other North American shale plays, with planned divestments for 2014 and 2015 to reach $15 billion, as it seeks to restructure its North America portfolio to enhance profitability.
8 Comments on "Big Oil Spending More, Getting Less in Production"
Kenz300 on Tue, 27th May 2014 6:27 pm
It is time for BIG OIL to diversify away from sole reliance on oil to a more balanced energy strategy.
Oil companies need to change their business models and transform themselves into "energy" companies and begin to embrace alternative energy sources.
It is time to move "Beyond Petroleum" as BP once said….then forget to implement it.
Harquebus on Tue, 27th May 2014 6:56 pm
Most in the energy business are smarter than you Kenz300. Renewable generators do not return the total energy used in their manufacture and construction. If they could and then some, the planet would already be covered in them.
Get an education mate, you need one.
Makati1 on Tue, 27th May 2014 8:30 pm
So the costs are increasing. That only means we are approaching peak oil consumption. Bring it on! The sooner the whole BAU system fails, the more of the earth's ecology will be left to rebuild by those who survive.
Simon on Wed, 28th May 2014 3:39 am
EROEI – is not used to determine profitability so really is not relevant to whether renewables are covering the planet
Also what figures do you have to backup your assertion on renewable energy forms not returning 100% of the energy used in manufacture and distribution
meld on Wed, 28th May 2014 6:21 am
@ Harquebus – this has always been my argument. If renewables are so much better than Fossil fuels then the oil companies would have diversified into them years ago and the oil world would be over with. They know renewables are worth squat and so they are sticking with what they know work, even if it's for a limited time. They also know that humans will always want oil, even if that oil is $1000 a barrel, someone somewhere is going to pay it so they can jet around the world.
The future is a place where billionaires still have access to the tech we have today but the 99% collapse into neo feudalism. Then the wars come.
Davy, Hermann, MO on Wed, 28th May 2014 6:37 am
Watch out Meld future predicting is hazardess. The best we can do is a range of predictions and short term ones at that. It is reasonable to see warlords, nobles, and strongmen returning in a localized setting with serfs and a small artesian class. I imagine the clergy will remain in some form. I also see large groups like Genghis Kahn fighting and migrating living of the production of others a possibility although in the BAU scorched earth we may not see enough to support large armies
peterjames on Wed, 28th May 2014 8:44 am
Meld, I suspect at $1000 a barrel, the list of billionaires will decrease quite considerably. I am going to be sucking up more to my neighbour who has stored 500 cans of baked beans in his back shed, than the "billionaire" down the road who has 500 kilos of gold stored in his back shed, or who has 30 cars in his driveway. Well thats after I break into his house one night, to siphon the petrol from his cars. At $10 for a litre of petrol, I could imagine the function of a car would be severly diminished, you certainly would not leave it unattended at the local shops.
Simon on Wed, 28th May 2014 8:48 am
I think we are mixing up profitability with energy returns.
Whether renewables will exist in a total collapse is also not a function of the energy they create, as there are also a lot of materials involved that may or may not be available, this would determine whether or not they would be widely produced.
If we look at Libya as an example of mad max'ness, after about a year we already have a consolidation of groups and negotiations going on between them, I suspect a form of plutocracy in the next few years.


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So, you are a single mother of a growing boy? Sure you know your boy is going through major changes. Here a lowdown.
The Changes
Nature has made boys very aggressive. When a boy changes into a man, the first thing that changes is his ego. He may want to ask for help, but may feel a little hesitant. There are a lot of hormonal changes taking place in his body too. They make him moody, depressed and very agitated at all times. He struggled with a growing sense of identity. He expresses his feelings more by actions than by words. He realizes that his parents are not perfect. He therefore looks for new people in addition to his family. His voice changes; he gets a moustache and of course is attracted to girls.
As your boy grows he will surely take interest in sex and women. This is very normal and you should let him be, only ensure that it is not abnormal. He will be very concerned about his own sexual attractiveness. There will be obvious feelings of love and passion in him and he might get into relationships with other sex. Though you should treat all this as normal, you must be very careful too. In a study done by an NGO in mumbai, most schoolboys visit brothels to use the services of a commercial sex worker. This is very unhealthy and should be avoided at all costs. Teach him about the dangers of such a sexual alliance. Also keep an eye on him to check his sexual preference. If your son is not interested in girls at this age, it is cause of concern. As an adult you much realise that though homosexuality is not accepted in out society it is natural. If your child is such a case be very careful and deal it with great sensitivity and respect.
Read Up and Seek Help
It might be difficult for you to deal with your growing kid. Read up books and more importantly take help from people. Uncles, friends, brothers, doctors, whomever you think your child will feel comfortable with.
The bottom line is, help your child grow up. This is the time when you should learn to accept your child as a friend. Learn to respect him/her from now on. Or else you are not going to get respect from them too!


text: It's getting to be the time of year when retailers lower their prices in hopes of luring in consumers to splurge for the holidays. It's not just physical items on sale, though. Apps and games are on sale for Black Friday as well. This roundup is your one-stop-shop for all the discounted apps and games fit for purchase. We'll keep this post updated throughout the holiday weekend, so check back on occasion.Read More


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Adult Children Of Alcoholics
PO Box 33165, Juneau, AK 99803
(907) 789-0965
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New Member!
Hello! I joined a while back but haven't posted since! I'm four weeks away from finishing my 5-month long CNA program. I finished my second clinical last night at a local nursing home, and it went very well! I'm really enjoying the deep level of patient involvement, and the work isn't nearly as scary as I thought it would be. I'm looking forward to getting a job at the hospital after I pass my state exam.
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Dear arresting wear, passenger severe. Orchard of the faint. Foreign to the clear.
Of distance how to focus now? Regaling the sub-conscience.
Hark there's a spark in the dark there's a spark in the sleeping beauty.
Slumber of the in between. Tunnel vision, gray displace.
Restless wander slush mislead. Pause ahead in muzzy grace.
Dear arresting wear, narcoleptic seer. Welcome every dawn with an angry yawn.
Of distance how to focus now? Regaling the subconscience.
Pillow biting. Snort, Snore, Snort, Snore.
Dancing with the obtuse phony, extinguish my face in fatigue and desire.
Relax... Relax. Oh god, I can't feel my fucking hands. Lagomorph, concentrate.
Sour the eager miniatures, anticipating the clear.
Lyrics taken from http://www.lyricsmode.com/lyrics/p/pt_grimm_the_dead_puppies/the_somnambule.html


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North American Doctors in Spain (Marbella)
I'm a Canadian and a recent international medical graduate (studied in the Cayman Islands, graduated with an American degree [M.D.]). I am curious about opportunities to do my residency training in Spain (family medicine/ GP), particularly in Andalucia and the Costa del Sol region. I know very little about how it all works here. I know that I need to have my credentials evaluated & verified by the government of Spain, but beyond that I'm a little lost.
Are there any Canadian or American physicians practicing here that might be able to offer any kind of advice or guidance? Perhaps suggestions on where to start or any helpful resources? Any help would be extremely appreciated.
Chris Lewis


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Tri-C JazzFest: Three Days Packed with Dozens of Performances
Intimate jam sessions. Soul-soothing solos. Classic quartets. Big band bopping. Dramatic divas.
That's the sound of Cleveland for three solid days during the 36th Annual Tri-C Jazzfest July 9 - 11. Experience nine performances, as well as numerous free concerts featuring the best of blues, big band, zydeco, gypsy swing, Latin, calypso, bop and straight-ahead and smooth jazz.
It all happens inside the opulent theaters and outdoor performance plaza at Playhouse Square. And, don't be surprised if you see some serious swing dancing action while in town. Check out the schedule of ticketed performances and free concerts.
Topping this year's line-up are performances by Pete Escovedo Latin Jazz Orchestra featuring the glamorous Sheila E. and brother Juan Escovedo. Additionally, there'll be a centennial celebration of the immortal music of Robert Lockwood Jr. and a tribute to Ray Brown featuring Benny Green, John Clayton and Jeff Hamilton.
Other performing artists include the Warren Wolf Quartet, Creole Joe, Cyrille Aimee and Wycliffe Gordon and His International All-Stars, Dominick Farinacci Quintet/Clayton-Hamilton Jazz Orchestra with special guest Take 6, and more.
Want to make it to all the performances? Consider purchasing a Festival Pass for only $200, which grants you access to all nine performances, as well as the opening night fete. Individual tickets can be purchased in advance by visiting www.playhousesquare.org. For accommodations, JazzFest partners with the Wyndham Cleveland at Playhouse Square.
Live Jazz in CLE
While in town, make sure to check out some of the city's best venues for jazz, blues and big band sounds. Each venue features shows happening throughout the JazzFest weekend.
Found on Cleveland's west side, Brothers Lounge is an historic club where you can catch anything from big bands and 80s covers inside the music hall to jazz quartets and acoustic crooners inside the wine bar.
Owned and operated by the prestigious Cleveland Music Settlement, which boasts more than a century of musical expertise, BOP STOP is quickly reemerging as one of the best venues to catch live jazz music several days of the week.
Jazz and blues will be the theme July 9 -11 at this quintessential Cleveland music venue located on East 4th Street downtown. And, don't forget to book your spot at the Kirk Franklin Gospel Sunday Brunch on July 12.
One of the newest spots to catch some tunes is the Music Box Supper Club on the West Bank of the Flats. The owners - who have decades of cred in the music biz -book tons of genres including blues, jazz, soul, Americana, rock, punk, roots and country.
Cleveland Heights' Nighttown was voted one of the top jazz clubs in the world by Down Beat magazine with live music nearly every night. With a variety of dining rooms and intimate performance settings, Nighttown has topped Cleveland's jazz scene since 1965, and it only gets better with age.
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Question: What other hotspots should JazzFest attendees hit up while in town?


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Date: February 4, 2018
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We Salute You Pines Village Retirement Communities hosts a complimentary monthly meet and gather over a hearty breakfast buffet for all Veterans The Rise & Shine Veterans Breakfast Club, is held the third Thursday of each month at 8:30 a.m. Thursday, February 15th | 8:30 am 3303 Pines Village Circle, Valparaiso Call 219.465.1591 to make your reservation Senator Joe Donnelly invites you to participate in the Veterans History Project Thursday, February 15 10 am-12 pm at Pines Village Share and record your military story that will be archived in the permanent collections of the US Library of Congress. lections of the US Library of Congress. Please contact Ryan Wiegand at 317.226.5555 if you would like to provide an oral history or interview a veteran. Independence Day Cmplell St Cafe Pises Vilg Livisg PINES VILLAGE RETIREMENTICOM MUNITIES PinesVillage.org