<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.ehjournal.net/feeds/latestarticles/journal?quantity=&amp;format=rss&amp;version=">
        <title>Environmental Health - Latest Articles</title>
        <link>http://www.ehjournal.net</link>
        <description>The latest research articles published by Environmental Health</description>
        <dc:date>2013-05-09T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/41" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/40" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/39" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/38" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/37" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/36" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/35" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/34" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/33" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/12/1/32" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.ehjournal.net/content/12/1/41">
        <title>Prenatal and perinatal analgesic exposure and autism: an ecological link</title>
        <description>Background:
Autism and Autism Spectrum Disorder (ASD) are complex neurodevelopmental disorders. Susceptibility is believed to be the interaction of genetic heritability and environmental factors. The synchronous rises in autism/ASD prevalence and paracetamol (acetaminophen) use, as well as biologic plausibility have led to the hypothesis that paracetamol exposure may increase autism/ASD risk.
Methods:
To explore the relationship of antenatal paracetamol exposure to ASD, population weighted average autism prevalence rates and paracetamol usage rates were compared. To explore the relationship of early neonatal paracetamol exposure to autism/ASD, population weighted average male autism prevalence rates for all available countries and U.S. states were compared to male circumcision rates -- a procedure for which paracetamol has been widely prescribed since the mid-1990s. Prevalence studies were extracted from the U.S. Centers for Disease Control and Prevention Summary of Autism/ASD Prevalence Studies database. Maternal paracetamol usage and circumcision rates were identified by searches on Pub Med.
Results:
Using all available country-level data (n = 8) for the period 1984 to 2005, prenatal use of paracetamol was correlated with autism/ASD prevalence (r = 0.80). There was a strong correlation between country-level (n = 9) autism/ASD prevalence in males and a country&apos;s circumcision rate (r = 0.98). A very similar pattern was seen among U.S. states and when comparing the 3 main racial/ethnic groups in the U.S. The country-level correlation between autism/ASD prevalence in males and paracetamol was considerably weaker before 1995 when the drug became widely used during circumcision.
Conclusions:
This ecological analysis identified country-level correlations between indicators of prenatal and perinatal paracetamol exposure and autism/ASD. State level correlation was also identified for the indicator of perinatal paracetamol exposure and autism/ASD. Like all ecological analyses, these data cannot provide strong evidence of causality. However, biologic plausibility is provided by a growing body of experimental and clinical evidence linking paracetamol metabolism to pathways shown to be important in autism and related developmental abnormalities. Taken together, these ecological findings and mechanistic evidence suggest the need for formal study of the role of paracetamol in autism.</description>
        <link>http://www.ehjournal.net/content/12/1/41</link>
                <dc:creator>Ann Bauer</dc:creator>
                <dc:creator>David Kriebel</dc:creator>
                <dc:source>Environmental Health 2013, null:41</dc:source>
        <dc:date>2013-05-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-41</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-41-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>41</prism:startingPage>
        <prism:publicationDate>2013-05-09T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/40">
        <title>PM2.5, oxidant defence and cardiorespiratory health: a review</title>
        <description>Airborne fine particle mass concentrations (PM2.5) are used for ambient air quality management worldwide based in part on known cardiorespiratory health effects. While oxidative stress is generally thought to be an important mechanism in determining these effects, relatively few studies have specifically examined how oxidant defence may impact susceptibility to particulate air pollution. Here we review studies that explore the impact of polymorphisms in anti-oxidant related genes or anti-oxidant supplementation on PM2.5-induced cardiorespiratory outcomes in an effort to summarize existing evidence related to oxidative stress defence and the health effects of PM2.5. Recent studies of PM-oxidative burden were also examined. In total, nine studies were identified and reviewed and existing evidence generally suggests that oxidant defence may modify the impact of PM2.5 exposure on various health outcomes, particularly heart rate variability (a measure of autonomic function) which was the most common outcome examined in the studies reviewed. Few studies examined interactions between PM2.5 and oxidant defence for respiratory outcomes, and in general studies focused primarily on acute health effects. Therefore, further evaluation of the potential modifying role of oxidant defence in PM2.5-induced health effects is required, particularly for chronic outcomes. Similarly, while an exposure metric that captures the ability of PM2.5 to cause oxidative stress may offer advantages over traditional mass concentration measurements, little epidemiological evidence is currently available to evaluate the potential benefits of such an approach. Therefore, further evaluation is required to determine how this metric may be incorporated in ambient air quality management.</description>
        <link>http://www.ehjournal.net/content/12/1/40</link>
                <dc:creator>Scott Weichenthal</dc:creator>
                <dc:creator>Krystal Godri-Pollitt</dc:creator>
                <dc:creator>Paul Villeneuve</dc:creator>
                <dc:source>Environmental Health 2013, null:40</dc:source>
        <dc:date>2013-05-04T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-40</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-40-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>40</prism:startingPage>
        <prism:publicationDate>2013-05-04T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/39">
        <title>Particulate matter components and subclinical atherosclerosis: common approaches to estimating exposure in a Multi-Ethnic Study of Atherosclerosis cross-sectional study</title>
        <description>Background:
Concentrations of outdoor fine particulate matter (PM2.5) have been associated with cardiovascular disease. PM2.5 chemical composition may be responsible for effects of exposure to PM2.5.
Methods:
Using data from the Multi-Ethnic Study of Atherosclerosis (MESA) collected in 2000--2002 on 6,256 US adults without clinical cardiovascular disease in six U.S. metropolitan areas, we investigated cross-sectional associations of estimated long-term exposure to total PM2.5 mass and PM2.5 components (elemental carbon [EC], organic carbon [OC], silicon and sulfur) with measures of subclinical atherosclerosis (coronary artery calcium [CAC] and right common carotid intima-media thickness [CIMT]). Community monitors deployed for this study from 2007 to 2008 were used to estimate exposures at baseline addresses using three commonly-used approaches: (1) nearest monitor (the primary approach), (2) inverse-distance monitor weighting and (3) city-wide average.
Results:
Using the exposure estimate based on nearest monitor, in single-pollutant models, increased OC (effect estimate [95% CI] per IQR: 35.1mum [26.8, 43.3]), EC (9.6mum [3.6,15.7]), sulfur (22.7mum [15.0,30.4]) and total PM2.5 (14.7mum [9.0,20.5]) but not silicon (5.2mum [-9.8,20.1]), were associated with increased CIMT; in two-pollutant models, only the association with OC was robust to control for the other pollutants. Findings were generally consistent across the three exposure estimation approaches. None of the PM measures were positively associated with either the presence or extent of CAC. In sensitivity analyses, effect estimates for OC and silicon were particularly sensitive to control for metropolitan area.
Conclusion:
Employing commonly-used exposure estimation approaches, all of the PM2.5 components considered, except silicon, were associated with increased CIMT, with the evidence being strongest for OC; no component was associated with increased CAC. PM2.5 chemical components, or other features of the sources that produced them, may be important in determining the effect of PM exposure on atherosclerosis. These cross-sectional findings await confirmation in future work employing longitudinal outcome measures and using more sophisticated approaches to estimating exposure.</description>
        <link>http://www.ehjournal.net/content/12/1/39</link>
                <dc:creator>Min Sun</dc:creator>
                <dc:creator>Joel Kaufman</dc:creator>
                <dc:creator>Sun-Young Kim</dc:creator>
                <dc:creator>Timothy Larson</dc:creator>
                <dc:creator>Timothy Gould</dc:creator>
                <dc:creator>Joseph Polak</dc:creator>
                <dc:creator>Matthew Budoff</dc:creator>
                <dc:creator>Ana Diez Roux</dc:creator>
                <dc:creator>Sverre Vedal</dc:creator>
                <dc:source>Environmental Health 2013, null:39</dc:source>
        <dc:date>2013-05-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-39</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-39-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>39</prism:startingPage>
        <prism:publicationDate>2013-05-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/38">
        <title>Association of air pollution and use of glyceryl trinitrate against angina pectoris: a population-based case-crossover study</title>
        <description>Background:
Ambient air pollution has been associated with increased cardiovascular morbidity and mortality. In Reykjavik, Iceland, air pollutant concentrations exceed official health limits several times every year. The aim was to study the association of concentrations of NO2, O3, PM10, and H2S in the Reykjavik capital area with the dispensing of anti-angina pectoris medication, glyceryl trinitrate to the inhabitants.
Methods:
Data on daily dispensing of glyceryl trinitrate, were retrieved from the Icelandic Medicines Registry. Data on hourly concentrations of NO2, O3, PM10, and H2S were obtained from the Environment Agency of Iceland. A case-crossover design was used, based on the dispensing of glyceryl trinitrate to 5,246 individuals (&gt;=18 years) between 2005 and 2009.
Results:
For every 10 mug/m3 increase of NO2 and O3 3-day mean concentrations, the odds ratio (OR) for daily dispensing of glyceryl trinitrates was 1.136 (95% confidence intervals (CI) 1.069-1.207) and 1.094 (95% CI 1.029-1.163) at lag 0, and OR was 1.096 (95% CI 1.029-1.168) and 1.094 (95% CI 1.028-1.166) at lag 1, respectively.
Conclusions:
These findings suggest that NO2 and O3 ambient air concentrations may adversely affect cardiovascular health, as measured by the dispensing of glyceryl trinitrates for angina pectoris. Further, the findings suggest that data on the dispensing of medication may be a valuable health indicator when studying the effect of air pollution on cardiovascular morbidity.</description>
        <link>http://www.ehjournal.net/content/12/1/38</link>
                <dc:creator>Ragnhildur Finnbjornsdottir</dc:creator>
                <dc:creator>Helga Zoëga</dc:creator>
                <dc:creator>Orn Olafsson</dc:creator>
                <dc:creator>Throstur Thorsteinsson</dc:creator>
                <dc:creator>Vilhjalmur Rafnsson</dc:creator>
                <dc:source>Environmental Health 2013, null:38</dc:source>
        <dc:date>2013-04-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-38</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-38-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>38</prism:startingPage>
        <prism:publicationDate>2013-04-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/37">
        <title>Association of urinary monomethylated arsenic concentration and risk of hypertension: a cross-sectional study from arsenic contaminated areas in northwestern China</title>
        <description>Background:
Although some studies mainly from Taiwan, Bangladesh and the United States, have suggested a consistent dose&#8211;response increase in the prevalence of hypertension with increasing arsenic exposure, the association between chronic environmental arsenic exposure and the risk of hypertension is still inconclusive. Most of the studies discussed the association from the point of view of arsenic concentration in drinking water or cumulative arsenic exposure (CAE), few involved arsenic speciation into the discussion. In this cross-sectional study, we evaluated the potential association between environmental arsenic exposure through drinking water and the prevalence of hypertension by analyzing not only CAE but also urinary arsenic speciation, and provided data on arsenic exposure and hypertension from mainland of China.
Methods:
A cross-sectional study was conducted in one of the arsenic contaminated areas in the northwest of China. Among a total of 1005 residents who voluntarily participated in the study, 604 of eligible subjects were confirmed and interviewed door to door. Standing height, body weight, and blood pressure were measured. First void urine was collected and measured for the concentration of urinary arsenic speciation. CAE was calculated in a subpopulation of 360 subjects with detailed water consumption history. The association between urinary arsenic speciation, CAE and the risk of hypertension were analyzed by multiple logistic regressions.
Results:
We found that the levels of urinary arsenic species of inorganic arsenic (iAs), monomethylated arsenic (MMA), dimethylated arsenic (DMA) and total arsenic (tAs) were significantly correlated with systolic or pulse blood pressure. A positive relationship was found between the highest tertile of CAE and hypertension in a dose-dependent manner. Subjects with higher concentration of urinary MMA or lower percentage of DMA tended to be liable to suffer from hypertension. A significant increasing trend of the risk of hypertension with increasing tertiles of MMA concentration was also observed in the logistic regression models both before and after adjustment for confounders.
Conclusions:
Our findings suggested that arsenic exposure, especially high level of CAE, was positively associated with the prevalence of hypertension, and that higher concentration of urinary MMA might be related to the increased susceptibility to hypertension.</description>
        <link>http://www.ehjournal.net/content/12/1/37</link>
                <dc:creator>Xin Li</dc:creator>
                <dc:creator>Bing Li</dc:creator>
                <dc:creator>Shuhua Xi</dc:creator>
                <dc:creator>Quanmei Zheng</dc:creator>
                <dc:creator>Da Wang</dc:creator>
                <dc:creator>Guifan Sun</dc:creator>
                <dc:source>Environmental Health 2013, null:37</dc:source>
        <dc:date>2013-04-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-37</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-37-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>37</prism:startingPage>
        <prism:publicationDate>2013-04-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/36">
        <title>Diesel exhaust but not ozone increases fraction of exhaled nitric oxide in a randomized controlled experimental exposure study of healthy human subjects</title>
        <description>Background:
Fraction of exhaled nitric oxide (FENO) is a promising non-invasive index of airway inflammation that may be used to assess respiratory effects of air pollution. We evaluated FENO as a measure of airway inflammation after controlled exposure to diesel exhaust or ozone.
Methods:
Healthy volunteers were exposed to either diesel exhaust (particle concentration 300 &#956;g/m3) and filtered air for one hour, or ozone (300 ppb) and filtered air for 75 minutes. FENO was measured in duplicate at expiratory flow rates of 10, 50, 100 and 270 mL/s before, 6 and 24 hours after each exposure.
Results:
Exposure to diesel exhaust increased FENO at 6 hours compared with air at expiratory flow rates of 10 mL/s (p&#8201;=&#8201;0.01) and at 50 mL/s (p&#8201;=&#8201;0.011), but FENO did not differ significantly at higher flow rates. Increases in FENO following diesel exhaust were attenuated at 24 hours. Ozone did not affect FENO at any flow rate or time point.
Conclusions:
Exposure to diesel exhaust, but not ozone, increased FENO concentrations in healthy subjects. Differences in the induction of airway inflammation may explain divergent responses to diesel exhaust and ozone, with implications for the use of FENO as an index of exposure to air pollution.</description>
        <link>http://www.ehjournal.net/content/12/1/36</link>
                <dc:creator>Stefan Barath</dc:creator>
                <dc:creator>Nicholas Mills</dc:creator>
                <dc:creator>Ellinor Ädelroth</dc:creator>
                <dc:creator>Anna-Carin Olin</dc:creator>
                <dc:creator>Anders Blomberg</dc:creator>
                <dc:source>Environmental Health 2013, null:36</dc:source>
        <dc:date>2013-04-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-36</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-36-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>36</prism:startingPage>
        <prism:publicationDate>2013-04-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/35">
        <title>Immunotoxicity of perfluorinated alkylates: calculation of benchmark doses based on serum concentrations in children</title>
        <description>Background:
Immune suppression may be a critical effect associated with exposure to perfluorinated compounds (PFCs), as indicated by recent data on vaccine antibody responses in children. Therefore, this information may be crucial when deciding on exposure limits.
Methods:
Results obtained from follow-up of a Faroese birth cohort were used. Serum-PFC concentrations were measured at age 5&#160;years, and serum antibody concentrations against tetanus and diphtheria toxoids were obtained at age 7&#160;years. Benchmark dose results were calculated in terms of serum concentrations for 431 children with complete data using linear and logarithmic curves, and sensitivity analyses were included to explore the impact of the low-dose curve shape.
Results:
Under different linear assumptions regarding dose-dependence of the effects, benchmark dose levels were about 1.3&#160;ng/mL serum for perfluorooctane sulfonic acid and 0.3&#160;ng/mL serum for perfluorooctanoic acid at a benchmark response of 5%. These results are below average serum concentrations reported in recent population studies. Even lower results were obtained using logarithmic dose&#8211;response curves. Assumption of no effect below the lowest observed dose resulted in higher benchmark dose results, as did a benchmark response of 10%.
Conclusions:
The benchmark dose results obtained are in accordance with recent data on toxicity in experimental models. When the results are converted to approximate exposure limits for drinking water, current limits appear to be several hundred fold too high. Current drinking water limits therefore need to be reconsidered.</description>
        <link>http://www.ehjournal.net/content/12/1/35</link>
                <dc:creator>Philippe Grandjean</dc:creator>
                <dc:creator>Esben Budtz-Jørgensen</dc:creator>
                <dc:source>Environmental Health 2013, null:35</dc:source>
        <dc:date>2013-04-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-35</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-35-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>35</prism:startingPage>
        <prism:publicationDate>2013-04-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/34">
        <title>Residential proximity to major roads and adverse birth outcomes: a hospital-based study</title>
        <description>Background:
Exposure to air pollution has been demonstrated to increase the risk of preterm birth and low birth weight (LBW). Although evidence has accumulated on characteristics associated with increased risk of air pollution-related health effects, most studies have been conducted in the adult population and evidence on reproductive outcomes is limited. We examined whether socio-economic position (SEP) and parental characteristics (parental behavior and co-morbidity) modified the relationship between air pollution and adverse birth outcomes.
Methods:
Data were extracted from a perinatal hospital database based in Shizuoka, Japan. We restricted the analysis to mothers who delivered live-born single births from January 1997 to December 2010 (n&#8201;=&#8201;16,615). Each birth was assigned proximity to major roads. Multivariate adjusted odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated for the outcomes of preterm birth and term LBW. We stratified subjects by individual/area-level SEP and parental characteristics. We then measured interactions on the additive scale between the respective factors and exposure.
Results:
Lower SEP at both individual and area levels was associated with the increased occurrence of adverse birth outcomes. Living within 200&#160;m from a major road increased the risk of preterm birth by 1.5 times (95% CI: 1.3-1.9) and LBW by 1.2 times (95% CI: 0.9-1.6). Mothers with lower individual SEP defined by household occupation experienced higher ORs for term LBW (OR&#8201;=&#8201;3.1, 95% CI: 1.2-8.2) compared with those with higher individual SEP. In contrast, mothers who lived in the highest area-level SEP region (i.e., affluent areas) showed slightly higher point estimates compared with those who lived in middle or poor areas. In addition, maternal diabetic and hypertensive status modified the association between proximity and preterm birth, while maternal smoking status modified the association between proximity and term LBW.
Conclusions:
The present study demonstrated that air pollution is an independent risk factor for adverse birth outcomes. Mothers with lower individual SEP and mothers living in higher SEP region may be susceptible to the adverse effect of air pollution. Maternal diabetic, hypertensive, and smoking status may also increase susceptibility to this air pollution-related health effect.</description>
        <link>http://www.ehjournal.net/content/12/1/34</link>
                <dc:creator>Takashi Yorifuji</dc:creator>
                <dc:creator>Hiroo Naruse</dc:creator>
                <dc:creator>Saori Kashima</dc:creator>
                <dc:creator>Soshi Takao</dc:creator>
                <dc:creator>Takeshi Murakoshi</dc:creator>
                <dc:creator>Hiroyuki Doi</dc:creator>
                <dc:creator>Ichiro Kawachi</dc:creator>
                <dc:source>Environmental Health 2013, null:34</dc:source>
        <dc:date>2013-04-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-34</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-34-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>34</prism:startingPage>
        <prism:publicationDate>2013-04-18T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/33">
        <title>Bisphenol A-associated epigenomic changes in prepubescent girls: a cross-sectional study in Gharbiah, Egypt</title>
        <description>Background:
There is now compelling evidence that epigenetic modifications link adult disease susceptibility to environmental exposures during specific life stages, including pre-pubertal development. Animal studies indicate that bisphenol A (BPA), the monomer used in epoxy resins and polycarbonate plastics, may impact health through epigenetic mechanisms, and epidemiological data associate BPA levels with metabolic disorders, behavior changes, and reproductive effects. Thus, we conducted an environmental epidemiology study of BPA exposure and CpG methylation in pre-adolescent girls from Gharbiah, Egypt hypothesizing that methylation profiles exhibit exposure-dependent trends.
Methods:
Urinary concentrations of total (free plus conjugated) species of BPA in spot samples were quantified for 60 girls aged 10 to 13. Genome-wide CpG methylation was concurrently measured in bisulfite-converted saliva DNA using the Infinium HumanMethylation27 BeadChip (N&#8201;=&#8201;46). CpG sites from four candidate genes were validated via quantitative bisulfite pyrosequencing.
Results:
CpG methylation varied widely among girls, and higher urinary BPA concentrations were generally associated with less genomic methylation. Based on pathway analyses, genes exhibiting reduced methylation with increasing urinary BPA were involved in immune function, transport activity, metabolism, and caspase activity. In particular, hypomethylation of CpG targets on chromosome X was associated with higher urinary BPA. Using the Comparative Toxicogenomics Database, we identified a number of candidate genes in our sample that previously have been associated with BPA-related expression change.
Conclusions:
These data indicate that BPA may affect human health through specific epigenomic modification of genes in relevant pathways. Thus, epigenetic epidemiology holds promise for the identification of biomarkers from previous exposures and the development of epigenetic-based diagnostic strategies.</description>
        <link>http://www.ehjournal.net/content/12/1/33</link>
                <dc:creator>Jung Kim</dc:creator>
                <dc:creator>Laura Rozek</dc:creator>
                <dc:creator>Amr Soliman</dc:creator>
                <dc:creator>Maureen Sartor</dc:creator>
                <dc:creator>Ahmed Hablas</dc:creator>
                <dc:creator>Ibrahim Seifeldin</dc:creator>
                <dc:creator>Justin Colacino</dc:creator>
                <dc:creator>Caren Weinhouse</dc:creator>
                <dc:creator>Muna Nahar</dc:creator>
                <dc:creator>Dana Dolinoy</dc:creator>
                <dc:source>Environmental Health 2013, null:33</dc:source>
        <dc:date>2013-04-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-33</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-33-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>33</prism:startingPage>
        <prism:publicationDate>2013-04-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/12/1/32">
        <title>Health effects of the September 2009 dust storm in Sydney, Australia: did emergency department visits and hospital admissions increase?</title>
        <description>Background:
During September 2009, a large dust storm was experienced in Sydney, New South Wales, Australia. Extremely high levels of particulate matter were recorded, with daily average levels of coarse matter (&lt;10 &#956;m) peaking over 11,000 &#956;g/m3 and fine (&lt;2.5 &#956;m) over 1,600 &#956;g/m3. We conducted an analysis to determine whether the dust storm was associated with increases in all-cause, cardiovascular, respiratory and asthma-related emergency department presentations and hospital admissions.
Methods:
We used distributed-lag Poisson generalized models to analyse the emergency department presentations and hospital admissions adjusted for pollutants, humidity, temperature and day of week and seasonal effects to obtain estimates of relative risks associated with the dust storm.
Results:
The dust storm period was associated with large increases in asthma emergency department visits (relative risk 1.23, 95% confidence interval 1.10-1.38, p&#8201;&lt;&#8201;0.01), and to a lesser extent, all emergency department visits (relative risk 1.04, 95% confidence interval 1.03-1.06, p&#8201;&lt;&#8201;0.01) and respiratory emergency department visits (relative risk 1.20, 95% confidence interval 1.15-1.26, p&#8201;&lt;&#8201;0.01). There was no significant increase in cardiovascular emergency department visits (p&#8201;=&#8201;0.09) or hospital admissions for any reason. Age-specific analyses showed the dust storm was associated with increases in all-cause and respiratory emergency department visits in the &#8805;65 year age group; the &#8804;5 year group had higher risks of all-cause, respiratory and asthma-related emergency department presentations.
Conclusions:
We recommend public health measures, especially targeting asthmatics, should be implemented during future dust storm events.</description>
        <link>http://www.ehjournal.net/content/12/1/32</link>
                <dc:creator>Alistair Merrifield</dc:creator>
                <dc:creator>Suzanne Schindeler</dc:creator>
                <dc:creator>Bin Jalaludin</dc:creator>
                <dc:creator>Wayne Smith</dc:creator>
                <dc:source>Environmental Health 2013, null:32</dc:source>
        <dc:date>2013-04-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-12-32</dc:identifier>
                                <prism:require>/content/figures/1476-069X-12-32-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>32</prism:startingPage>
        <prism:publicationDate>2013-04-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>
