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        <title>Environmental Health - Most accessed articles</title>
        <link>http://www.ehjournal.net</link>
        <description>The most accessed research articles published by Environmental Health</description>
        <dc:date>2012-05-02T00:00:00Z</dc:date>
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        <item rdf:about="http://www.ehjournal.net/content/4/1/6">
        <title>The Bhopal disaster and its aftermath: a review</title>
        <description>On December 3 1984, more than 40 tons of methyl isocyanate gas leaked from a pesticide plant in Bhopal, India, immediately killing at least 3,800 people and causing significant morbidity and premature death for many thousands more. The company involved in what became the worst industrial accident in history immediately tried to dissociate itself from legal responsibility. Eventually it reached a settlement with the Indian Government through mediation of that country&apos;s Supreme Court and accepted moral responsibility. It paid $470 million in compensation, a relatively small amount of based on significant underestimations of the long-term health consequences of exposure and the number of people exposed. The disaster indicated a need for enforceable international standards for environmental safety, preventative strategies to avoid similar accidents and industrial disaster preparedness.Since the disaster, India has experienced rapid industrialization. While some positive changes in government policy and behavior of a few industries have taken place, major threats to the environment from rapid and poorly regulated industrial growth remain. Widespread environmental degradation with significant adverse human health consequences continues to occur throughout India.</description>
        <link>http://www.ehjournal.net/content/4/1/6</link>
                <dc:creator>Edward Broughton</dc:creator>
                <dc:source>Environmental Health 2005, null:6</dc:source>
        <dc:date>2005-05-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-4-6</dc:identifier>
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        <prism:startingPage>6</prism:startingPage>
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        <item rdf:about="http://www.ehjournal.net/content/8/1/2">
        <title>Mercury from chlor-alkali plants: measured concentrations in food product sugar</title>
        <description>Mercury cell chlor-alkali products are used to produce thousands of other products including food ingredients such as citric acid, sodium benzoate, and high fructose corn syrup. High fructose corn syrup is used in food products to enhance shelf life. A pilot study was conducted to determine if high fructose corn syrup contains mercury, a toxic metal historically used as an anti-microbial. High fructose corn syrup samples were collected from three different manufacturers and analyzed for total mercury. The samples were found to contain levels of mercury ranging from below a detection limit of 0.005 to 0.570 micrograms mercury per gram of high fructose corn syrup. Average daily consumption of high fructose corn syrup is about 50 grams per person in the United States. With respect to total mercury exposure, it may be necessary to account for this source of mercury in the diet of children and sensitive populations.</description>
        <link>http://www.ehjournal.net/content/8/1/2</link>
                <dc:creator>Renee Dufault</dc:creator>
                <dc:creator>Blaise LeBlanc</dc:creator>
                <dc:creator>Roseanne Schnoll</dc:creator>
                <dc:creator>Charles Cornett</dc:creator>
                <dc:creator>Laura Schweitzer</dc:creator>
                <dc:creator>Lyn Patrick</dc:creator>
                <dc:creator>Jane Hightower</dc:creator>
                <dc:creator>David Wallinga</dc:creator>
                <dc:creator>Walter Lukiw</dc:creator>
                <dc:source>Environmental Health 2009, null:2</dc:source>
        <dc:date>2009-01-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-8-2</dc:identifier>
                            <dc:title>Hidden mercury lurking in sweetner</dc:title>
                            <dc:description>High fructose corn syrup, produced using mercury cell chlor-alkali products, can contain up to 0.57 micrograms mercury per gram and this source may need to be considered when accounting for mercury in the diet.</dc:description>
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        <prism:startingPage>2</prism:startingPage>
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        <item rdf:about="http://www.ehjournal.net/content/6/1/23">
        <title>Near-highway pollutants in motor vehicle exhaust: A review of epidemiologic evidence of cardiac and pulmonary health risks</title>
        <description>There is growing evidence of a distinct set of freshly-emitted air pollutants downwind from major highways, motorways, and freeways that include elevated levels of ultrafine particulates (UFP), black carbon (BC), oxides of nitrogen (NOx), and carbon monoxide (CO). People living or otherwise spending substantial time within about 200 m of highways are exposed to these pollutants more so than persons living at a greater distance, even compared to living on busy urban streets. Evidence of the health hazards of these pollutants arises from studies that assess proximity to highways, actual exposure to the pollutants, or both. Taken as a whole, the health studies show elevated risk for development of asthma and reduced lung function in children who live near major highways. Studies of particulate matter (PM) that show associations with cardiac and pulmonary mortality also appear to indicate increasing risk as smaller geographic areas are studied, suggesting localized sources that likely include major highways. Although less work has tested the association between lung cancer and highways, the existing studies suggest an association as well. While the evidence is substantial for a link between near-highway exposures and adverse health outcomes, considerable work remains to understand the exact nature and magnitude of the risks.</description>
        <link>http://www.ehjournal.net/content/6/1/23</link>
                <dc:creator>Doug Brugge</dc:creator>
                <dc:creator>John Durant</dc:creator>
                <dc:creator>Christine Rioux</dc:creator>
                <dc:source>Environmental Health 2007, null:23</dc:source>
        <dc:date>2007-08-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-6-23</dc:identifier>
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        <prism:startingPage>23</prism:startingPage>
        <prism:publicationDate>2007-08-09T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/5/1/25">
        <title>Obesity, physical activity, and the urban environment: public health research needs</title>
        <description>Persistent trends in overweight and obesity have resulted in a rapid research effort focused on built environment, physical activity, and overweight. Much of the focus of this research has been on the design and form of suburbs. It suggests that several features of the suburban built environment such as low densities, poor street connectivity and the lack of sidewalks are associated with decreased physical activity and an increased risk of being overweight. But compared to suburban residents, inner city populations have higher rates of obesity and inactivity despite living in neighborhoods that are dense, have excellent street connectivity and who&apos;s streets are almost universally lined with sidewalks.We suggest that the reasons for this apparent paradox are rooted in the complex interaction of land use, infrastructure and social factors affecting inner city populations. Sometimes seemingly similar features are the result of very different processes, necessitating different policy responses to meet these challenges. For example, in suburbs, lower densities can result from government decision making that leads to restrictive zoning and land use issues. In the inner city, densities may be lowered because of abandonment and disinvestment. In the suburbs, changes in land use regulations could result in a healthier built environment. In inner cities, increasing densities will depend on reversing economic trends and investment decisions that have systematically resulted in distressed housing, abandoned buildings and vacant lots.These varying issues need to be further studied in the context of the totality of urban environments, incorporating what has been learned from other disciplines, such as economics and sociology, as well as highlighting some of the more successful inner city policy interventions, which may provide examples for communities working to improve their health.Certain disparities among urban and suburban populations in obesity and overweight, physical activity and research focus have emerged that are timely to address. Comparable research on the relationship of built environment and health is needed for urban, especially inner city, neighborhoods.</description>
        <link>http://www.ehjournal.net/content/5/1/25</link>
                <dc:creator>Russell Lopez</dc:creator>
                <dc:creator>H. Patricia Hynes</dc:creator>
                <dc:source>Environmental Health 2006, null:25</dc:source>
        <dc:date>2006-09-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-5-25</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
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        <prism:startingPage>25</prism:startingPage>
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        <item rdf:about="http://www.ehjournal.net/content/11/1/28">
        <title>Complex organochlorine pesticide mixtures as determinant factor for breast cancer risk: a population-based case-control study in the Canary Islands (Spain)</title>
        <description>Background:
All the relevant risk factors contributing to breast cancer etiology are not fully known. Exposure to organochlorine pesticides has been linked to an increased incidence of the disease, although not all data have been consistent. Most published studies evaluated the exposure to organochlorines individually, ignoring the potential effects exerted by the mixtures of chemicals.
Methods:
This population-based study was designed to evaluate the profile of mixtures of organochlorines detected in 103 healthy women and 121 women diagnosed with breast cancer from Gran Canaria Island, and the relation between the exposure to these compounds and breast cancer risk.
Results:
The most prevalent mixture of organochlorines among healthy women was the combination of lindane and endrin, and this mixture was not detected in any affected women. Breast cancer patients presented more frequently a combination of aldrin, dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane (DDD), and this mixture was not found in any healthy woman. After adjusting for covariables, the risk of breast cancer was moderately associated with DDD (OR = 1.008, confidence interval 95% 1.001-1.015, p = 0.024).
Conclusions:
This study indicates that healthy women show a very different profile of organochlorine pesticide mixtures than breast cancer patients, suggesting that organochlorine pesticide mixtures could play a relevant role in breast cancer risk.</description>
        <link>http://www.ehjournal.net/content/11/1/28</link>
                <dc:creator>Luis Boada</dc:creator>
                <dc:creator>Manuel Zumbado</dc:creator>
                <dc:creator>Luis Alberto Henriquez-Hernandez</dc:creator>
                <dc:creator>Maira Almeida-Gonzalez</dc:creator>
                <dc:creator>Eva Alvarez-Leon</dc:creator>
                <dc:creator>Lluis Serra-Majem</dc:creator>
                <dc:creator>Octavio Luzardo</dc:creator>
                <dc:source>Environmental Health 2012, null:28</dc:source>
        <dc:date>2012-04-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-28</dc:identifier>
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        <prism:startingPage>28</prism:startingPage>
        <prism:publicationDate>2012-04-25T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/10/1/9">
        <title>Knowns and unknowns on burden of disease due to chemicals: a systematic review</title>
        <description>Background:
Continuous exposure to many chemicals, including through air, water, food, or other media and products results in health impacts which have been well assessed, however little is known about the total disease burden related to chemicals. This is important to know for overall policy actions and priorities. In this article the known burden related to selected chemicals or their mixtures, main data gaps, and the link to public health policy are reviewed.
Methods:
A systematic review of the literature for global burden of disease estimates from chemicals was conducted. Global disease due to chemicals was estimated using standard methodology of the Global Burden of Disease.
Results:
In total, 4.9 million deaths (8.3% of total) and 86 million Disability-Adjusted Life Years (DALYs) (5.7% of total) were attributable to environmental exposure and management of selected chemicals in 2004. The largest contributors include indoor smoke from solid fuel use, outdoor air pollution and second-hand smoke, with 2.0, 1.2 and 0.6 million deaths annually. These are followed by occupational particulates, chemicals involved in acute poisonings, and pesticides involved in self-poisonings, with 375,000, 240,000 and 186,000 annual deaths, respectively.
Conclusions:
The known burden due to chemicals is considerable. This information supports decision-making in programmes having a role to play in reducing human exposure to toxic chemicals. These figures present only a number of chemicals for which data are available, therefore, they are more likely an underestimate of the actual burden. Chemicals with known health effects, such as dioxins, cadmium, mercury or chronic exposure to pesticides could not be included in this article due to incomplete data and information. Effective public health interventions are known to manage chemicals and limit their public health impacts and should be implemented at national and international levels.</description>
        <link>http://www.ehjournal.net/content/10/1/9</link>
                <dc:creator>Annette Pruss-Ustun</dc:creator>
                <dc:creator>Carolyn Vickers</dc:creator>
                <dc:creator>Pascal Haefliger</dc:creator>
                <dc:creator>Roberto Bertollini</dc:creator>
                <dc:source>Environmental Health 2011, null:9</dc:source>
        <dc:date>2011-01-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-10-9</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2011-01-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/10/1/78">
        <title>Health Effects and Wind Turbines: A Review of the Literature</title>
        <description>Background:
Wind power has been harnessed as a source of power around the world. Debate is ongoing with respect to the relationship between reported health effects and wind turbines, specifically in terms of audible and inaudible noise. As a result, minimum setback distances have been established world-wide to reduce or avoid potential complaints from, or potential effects to, people living in proximity to wind turbines. People interested in this debate turn to two sources of information to make informed decisions: scientific peer-reviewed studies published in scientific journals and the popular literature and internet.
Methods:
The purpose of this paper is to review the peer-reviewed scientific literature, government agency reports, and the most prominent information found in the popular literature. Combinations of key words were entered into the Thomson Reuters Web of KnowledgeSM and the internet search engine Google. The review was conducted in the spirit of the evaluation process outlined in the Cochrane Handbook for Systematic Reviews of Interventions.
Results:
Conclusions of the peer reviewed literature differ in some ways from those in the popular literature. In peer reviewed studies, wind turbine annoyance has been statistically associated with wind turbine noise, but found to be more strongly related to visual impact, attitude to wind turbines and sensitivity to noise. To date, no peer reviewed articles demonstrate a direct causal link between people living in proximity to modern wind turbines, the noise they emit and resulting physiological health effects. If anything, reported health effects are likely attributed to a number of environmental stressors that result in an annoyed/stressed state in a segment of the population. In the popular literature, self-reported health outcomes are related to distance from turbines and the claim is made that infrasound is the causative factor for the reported effects, even though sound pressure levels are not measured.
Conclusions:
What both types of studies have in common is the conclusion that wind turbines can be a source of annoyance for some people. The difference between both types is the reason for annoyance. While it is acknowledged that noise from wind turbines can be annoying to some and associated with some reported health effects (e.g., sleep disturbance), especially when found at sound pressure levels greater than 40 db(A), given that annoyance appears to be more strongly related to visual cues and attitude than to noise itself, self reported health effects of people living near wind turbines are more likely attributed to physical manifestation from an annoyed state than from wind turbines themselves. In other words, it appears that it is the change in the environment that is associated with reported health effects and not a turbine-specific variable like audible noise or infrasound. Regardless of its cause, a certain level of annoyance in a population can be expected (as with any number of projects that change the local environment) and the acceptable level is a policy decision to be made by elected officials and their government representatives where the benefits of wind power are weighted against their cons. Assessing the effects of wind turbines on human health is an emerging field and conducting further research into the effects of wind turbines (and environmental changes) on human health, emotional and physical, is warranted.</description>
        <link>http://www.ehjournal.net/content/10/1/78</link>
                <dc:creator>Loren Knopper</dc:creator>
                <dc:creator>Christopher Ollson</dc:creator>
                <dc:source>Environmental Health 2011, null:78</dc:source>
        <dc:date>2011-09-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-10-78</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
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        <prism:startingPage>78</prism:startingPage>
        <prism:publicationDate>2011-09-14T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/8/1/47">
        <title>The impact of transportation infrastructure on bicycling injuries and crashes: a review of the literature</title>
        <description>Background:
Bicycling has the potential to improve fitness, diminish obesity, and reduce noise, air pollution, and greenhouse gases associated with travel. However, bicyclists incur a higher risk of injuries requiring hospitalization than motor vehicle occupants. Therefore, understanding ways of making bicycling safer and increasing rates of bicycling are important to improving population health. There is a growing body of research examining transportation infrastructure and the risk of injury to bicyclists.
Methods:
We reviewed studies of the impact of transportation infrastructure on bicyclist safety. The results were tabulated within two categories of infrastructure, namely that at intersections (e.g. roundabouts, traffic lights) or between intersections on &quot;straightaways&quot; (e.g. bike lanes or paths). To assess safety, studies examining the following outcomes were included: injuries; injury severity; and crashes (collisions and/or falls).
Results:
The literature to date on transportation infrastructure and cyclist safety is limited by the incomplete range of facilities studied and difficulties in controlling for exposure to risk. However, evidence from the 23 papers reviewed (eight that examined intersections and 15 that examined straightaways) suggests that infrastructure influences injury and crash risk. Intersection studies focused mainly on roundabouts. They found that multi-lane roundabouts can significantly increase risk to bicyclists unless a separated cycle track is included in the design. Studies of straightaways grouped facilities into few categories, such that facilities with potentially different risks may have been classified within a single category. Results to date suggest that sidewalks and multi-use trails pose the highest risk, major roads are more hazardous than minor roads, and the presence of bicycle facilities (e.g. on-road bike routes, on-road marked bike lanes, and off-road bike paths) was associated with the lowest risk.
Conclusion:
Evidence is beginning to accumulate that purpose-built bicycle-specific facilities reduce crashes and injuries among cyclists, providing the basis for initial transportation engineering guidelines for cyclist safety. Street lighting, paved surfaces, and low-angled grades are additional factors that appear to improve cyclist safety. Future research examining a greater variety of infrastructure would allow development of more detailed guidelines.</description>
        <link>http://www.ehjournal.net/content/8/1/47</link>
                <dc:creator>Conor Reynolds</dc:creator>
                <dc:creator>M Anne Harris</dc:creator>
                <dc:creator>Kay Teschke</dc:creator>
                <dc:creator>Peter Cripton</dc:creator>
                <dc:creator>Meghan Winters</dc:creator>
                <dc:source>Environmental Health 2009, null:47</dc:source>
        <dc:date>2009-10-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-8-47</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
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        <prism:startingPage>47</prism:startingPage>
        <prism:publicationDate>2009-10-21T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.ehjournal.net/content/11/1/25">
        <title>Exposures to fine particulate air pollution and respiratory outcomes in adults using two national datasets: a cross-sectional study</title>
        <description>Background:
Relationships between chronic exposures to air pollution and respiratory health outcomes have yet to be clearly articulated for adults. Recent data from nationally representative surveys suggest increasing disparity by race/ethnicity regarding asthma-related morbidity and mortality. The objectives of this study are to evaluate the relationship between annual average ambient fine particulate matter (PM2.5) concentrations and respiratory outcomes for adults using modeled air pollution and health outcome data and to examine PM2.5 sensitivity across race/ethnicity.
Methods:
Respondents from the 2002-2005 National Health Interview Survey (NHIS) were linked to annual kriged PM2.5 data from the USEPA AirData system. Logistic regression was employed to investigate increases in ambient PM2.5 concentrations and self-reported prevalence of respiratory outcomes including asthma, sinusitis and chronic bronchitis. Models included health, behavioral, demographic and resource-related covariates. Stratified analyses were conducted by race/ethnicity.
Results:
Of nearly 110,000 adult respondents, approximately 8,000 and 4,000 reported current asthma and recent attacks, respectively. Overall, odds ratios (OR) for current asthma (0.97 (95% Confidence Interval: 0.87-1.07)) and recent attacks (0.90 (0.78-1.03)) did not suggest an association with a 10 mug/m3 increase in PM2.5. Stratified analyses revealed significant associations for non-Hispanic blacks [OR = 1.73 (1.17-2.56) for current asthma and OR = 1.76 (1.07-2.91) for recent attacks] but not for Hispanics and non-Hispanic whites. Significant associations were observed overall (1.18 (1.08-1.30)) and in non-Hispanic whites (1.31 (1.18-1.46)) for sinusitis, but not for chronic bronchitis.
Conclusions:
Non-Hispanic blacks may be at increased sensitivity of asthma outcomes from PM2.5 exposure. Increased chronic PM2.5 exposures in adults may contribute to population sinusitis burdens.</description>
        <link>http://www.ehjournal.net/content/11/1/25</link>
                <dc:creator>Keeve Nachman</dc:creator>
                <dc:creator>Jennifer Parker</dc:creator>
                <dc:source>Environmental Health 2012, null:25</dc:source>
        <dc:date>2012-04-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-25</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
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        <prism:startingPage>25</prism:startingPage>
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        <item rdf:about="http://www.ehjournal.net/content/11/1/31">
        <title>Effects of arsenic exposure on DNA methylation in cord blood samples from newborn babies and in a human lymphoblast cell line</title>
        <description>Background:
Accumulating evidence indicates that in utero exposure to arsenic is associated with congenital defects and long-term disease consequences including cancers. Recent studies suggest that arsenic carcinogenesis results from epigenetic changes, particularly in DNA methylation. This study aimed to investigate DNA methylation changes as a result of arsenic exposure in utero and in vitro.
Methods:
For the exposure in utero study, a total of seventy-one newborns (fifty-five arsenic-exposed and sixteen unexposed newborns) were recruited. Arsenic concentrations in the drinking water were measured, and exposure in newborns was assessed by measurement of arsenic concentrations in cord blood, nails and hair by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). In the in vitro study, human lymphoblasts were treated with arsenite at 0-100 muM for two, four and eight hours (short-term) and at 0, 0.5 and 1.0 muM for eight-weeks period (long-term). DNA methylation was analyzed in cord blood lymphocytes and lymphoblasts treated with arsenite in vitro. Global DNA methylation was determined as LINE-1 methylation using combined bisulfite restriction analysis (COBRA) and total 5-methyldeoxycytidine (5MedC) content which was determined by HPLC-MS/MS. Methylation of p53 was determined at the promoter region using methylation-specific restriction endonuclease digestion with MspI and HpaII.
Results:
Results showed that arsenic-exposed newborns had significantly higher levels of arsenic in cord blood, fingernails, toenails and hair than those of the unexposed subjects and a slight increase in promoter methylation of p53 in cord blood lymphocytes which significantly correlated with arsenic accumulation in nails (p &lt; 0.05) was observed, while LINE-1 methylation was unchanged. Short-term in vitro arsenite treatment in lymphoblastoid cells clearly demonstrated a significant global hypomethylation, determined as reduction in LINE-1 methylation and total 5-MedC content, and p53 hypermethylation (p &lt; 0.05). However, a slight LINE-1 hypomethylation and transient p53 promoter hypermethylation were observed following long-term in vitro treatment.
Conclusions:
This study provides an important finding that in utero arsenic exposure affects DNA methylation, particularly at the p53 promoter region, which may be linked to the mechanism of arsenic carcinogenesis and the observed increased incidence of cancer later in life.</description>
        <link>http://www.ehjournal.net/content/11/1/31</link>
                <dc:creator>Ponpat Intarasunanont</dc:creator>
                <dc:creator>Panida Navasumrit</dc:creator>
                <dc:creator>Somchamai Woraprasit</dc:creator>
                <dc:creator>Krittinee Chaisatra</dc:creator>
                <dc:creator>William Suk</dc:creator>
                <dc:creator>Chulabhorn Mahidol</dc:creator>
                <dc:creator>Mathuros Ruchirawat</dc:creator>
                <dc:source>Environmental Health 2012, null:31</dc:source>
        <dc:date>2012-05-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-31</dc:identifier>
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        <prism:startingPage>31</prism:startingPage>
        <prism:publicationDate>2012-05-02T00:00:00Z</prism:publicationDate>
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