For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
95
views
70
references
 Top references
cited by
55
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      56
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Systematic evaluation of environmental factors: persistent pollutants and nutrients correlated with serum lipid levels

      article-commentary

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background Both genetic and environmental factors contribute to triglyceride, low-density lipoprotein-cholesterol (LDL-C), and high-density lipoprotein-cholesterol (HDL-C) levels. Although genome-wide association studies are currently testing the genetic factors systematically, testing and reporting one or a few factors at a time can lead to fragmented literature for environmental chemical factors. We screened for correlation between environmental factors and lipid levels, utilizing four independent surveys with information on 188 environmental factors from the Centers of Disease Control, National Health and Nutrition Examination Survey, collected between 1999 and 2006.

          Methods We used linear regression to correlate each environmental chemical factor to triglycerides, LDL-C and HDL-C adjusting for age, age 2, sex, ethnicity, socio-economic status and body mass index. Final estimates were adjusted for waist circumference, diabetes status, blood pressure and survey. Multiple comparisons were controlled for by estimating the false discovery rate and significant findings were tentatively validated in an independent survey.

          Results We identified and validated 29, 9 and 17 environmental factors correlated with triglycerides, LDL-C and HDL-C levels, respectively. Findings include hydrocarbons and nicotine associated with lower HDL-C and vitamin E (γ-tocopherol) associated with unfavourable lipid levels. Higher triglycerides and lower HDL-C were correlated with higher levels of fat-soluble contaminants (e.g. polychlorinated biphenyls and dibenzofurans). Nutrients and vitamin markers (e.g. vitamins B, D and carotenes), were associated with favourable triglyceride and HDL-C levels.

          Conclusions Our systematic association study has enabled us to postulate about broad environmental correlation to lipid levels. Although subject to confounding and reverse causality bias, these findings merit evaluation in additional cohorts.

          Related collections

          Most cited references70

          • Record: found
          • Abstract: found
          • Article: not found

          Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

          C. Pope, Richard Burnett, George Thurston … (2004)
          Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
          Article 0 comments Cited 585 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Systematic Review of the Empirical Evidence of Study Publication Bias and Outcome Reporting Bias

            Kerry Dwan, Douglas G. Altman, Juan A. Arnaiz … (2008)
            Background The increased use of meta-analysis in systematic reviews of healthcare interventions has highlighted several types of bias that can arise during the completion of a randomised controlled trial. Study publication bias has been recognised as a potential threat to the validity of meta-analysis and can make the readily available evidence unreliable for decision making. Until recently, outcome reporting bias has received less attention. Methodology/Principal Findings We review and summarise the evidence from a series of cohort studies that have assessed study publication bias and outcome reporting bias in randomised controlled trials. Sixteen studies were eligible of which only two followed the cohort all the way through from protocol approval to information regarding publication of outcomes. Eleven of the studies investigated study publication bias and five investigated outcome reporting bias. Three studies have found that statistically significant outcomes had a higher odds of being fully reported compared to non-significant outcomes (range of odds ratios: 2.2 to 4.7). In comparing trial publications to protocols, we found that 40–62% of studies had at least one primary outcome that was changed, introduced, or omitted. We decided not to undertake meta-analysis due to the differences between studies. Conclusions Recent work provides direct empirical evidence for the existence of study publication bias and outcome reporting bias. There is strong evidence of an association between significant results and publication; studies that report positive or significant results are more likely to be published and outcomes that are statistically significant have higher odds of being fully reported. Publications have been found to be inconsistent with their protocols. Researchers need to be aware of the problems of both types of bias and efforts should be concentrated on improving the reporting of trials.
            Article 0 comments Cited 433 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The effect of fruit and vegetable intake on risk for coronary heart disease.

              Kaumudi Joshipura, Frank Hu, JoAnn Manson … (2001)
              Many constituents of fruits and vegetables may reduce the risk for coronary heart disease, but data on the relationship between fruit and vegetable consumption and risk for coronary heart disease are sparse. To evaluate the association of fruit and vegetable consumption with risk for coronary heart disease. Prospective cohort study. The Nurses' Health Study and the Health Professionals' Follow-Up Study. 84 251 women 34 to 59 years of age who were followed for 14 years and 42 148 men 40 to 75 years who were followed for 8 years. All were free of diagnosed cardiovascular disease, cancer, and diabetes at baseline. The main outcome measure was incidence of nonfatal myocardial infarction or fatal coronary heart disease (1127 cases in women and 1063 cases in men). Diet was assessed by using food-frequency questionnaires. After adjustment for standard cardiovascular risk factors, persons in the highest quintile of fruit and vegetable intake had a relative risk for coronary heart disease of 0.80 (95% CI, 0.69 to 0.93) compared with those in the lowest quintile of intake. Each 1-serving/d increase in intake of fruits or vegetables was associated with a 4% lower risk for coronary heart disease (relative risk, 0.96 [CI, 0.94 to 0.99]; P = 0.01, test for trend). Green leafy vegetables (relative risk with 1-serving/d increase, 0.77 [CI, 0.64 to 0.93]), and vitamin C-rich fruits and vegetables (relative risk with 1-serving/d increase, 0.94 [CI, 0.88 to 0.99]) contributed most to the apparent protective effect of total fruit and vegetable intake. Consumption of fruits and vegetables, particularly green leafy vegetables and vitamin C-rich fruits and vegetables, appears to have a protective effect against coronary heart disease.
              Article 0 comments Cited 256 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Epidemiol
                Journal ID (iso-abbrev): Int J Epidemiol
                Journal ID (publisher-id): ije
                Journal ID (hwp): intjepid
                Title: International Journal of Epidemiology
                Publisher: Oxford University Press
                ISSN (Print): 0300-5771
                ISSN (Electronic): 1464-3685
                Publication date (Print): June 2012
                Publication date (Electronic): 12 March 2012
                Publication date PMC-release: 12 March 2012
                Volume: 41
                Issue: 3
                Pages: 828-843
                Affiliations
                1Department of Pediatrics, Division of Systems Medicine, Stanford University School of Medicine, Stanford, CA, USA, 2Lucile Packard Children's Hospital, Palo Alto, CA, USA, 3Department of Medicine, Division of General Medical Disciplines, Stanford University School of Medicine, Stanford, CA, USA, 4Department of Medicine, Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA, USA, 5Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA, USA and 6Department of Statistics, Stanford University School of Humanities and Sciences, Stanford, CA USA
                Author notes
                *Corresponding author. Department of Pediatrics, Stanford School of Medicine, 1265 Welch Road, Stanford, CA 94305, USA. E-mail: abutte@ 123456stanford.edu
                Article
                Publisher ID: dys003
                DOI: 10.1093/ije/dys003
                PMC ID: 3396318
                PubMed ID: 22421054
                SO-VID: 7d6373b7-f0b1-43f0-9031-c4256a476615
                Copyright © Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2012; all rights reserved.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 5 January 2012
                Page count
                Pages: 16
                Categories
                Subject: Other Original Articles

                ScienceOpen disciplines: Public health
                Keywords: pollutants,environment,nutrients,ewas,cholesterol,lipids,gwas
                Data availability:
                ScienceOpen disciplines: Public health
                Keywords: pollutants, environment, nutrients, ewas, cholesterol, lipids, gwas

                Comments

                Comment on this article

                scite_

                Similar content56

                See all similar

                Cited by50

                See all cited by

                Most referenced authors2,634

                See all reference authors