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        <title>Environmental Health - Latest Articles</title>
        <link>http://www.ehjournal.net</link>
        <description>The latest research articles published by Environmental Health</description>
        <dc:date>2012-05-21T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/36" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/35" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/34" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/33" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/32" />
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                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/29" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/28" />
                                <rdf:li rdf:resource="http://www.ehjournal.net/content/11/1/27" />
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        <item rdf:about="http://www.ehjournal.net/content/11/1/36">
        <title>Effects of temperature on mortality in Chiang Mai city, Thailand: a time series study</title>
        <description>Background:
The association between temperature and mortality has been examined mainly in North America and Europe. However, less evidence is available in developing countries, especially in Thailand. In this study, we examined the relationship between temperature and mortality in Chiang Mai city, Thailand, during 1999-2008.MethodA time series model was used to examine the effects of temperature on cause-specific mortality (non-external, cardiopulmonary, cardiovascular, and respiratory) and age-specific non-external mortality (&lt;=64, 65-74, 75-84, and &gt; =85 years), while controlling for relative humidity, air pollution, day of the week, season and long-term trend. We used a distributed lag non-linear model to examine the delayed effects of temperature on mortality up to 21 days.
Results:
We found non-linear effects of temperature on all mortality types and age groups. Both hot and cold temperatures resulted in immediate increase in all mortality types and age groups. Generally, the hot effects on all mortality types and age groups were short-term, while the cold effects lasted longer. The relative risk of non-external mortality associated with cold temperature (19.35degreesC, 1st percentile of temperature) relative to 24.7degreesC (25th percentile of temperature) was 1.29 (95% confidence interval (CI): 1.16, 1.44) for lags 0-21. The relative risk of non-external mortality associated with high temperature (31.7degreesC, 99th percentile of temperature) relative to 28degreesC (75th percentile of temperature) was 1.11 (95% CI: 1.00, 1.24) for lags 0-21.
Conclusion:
This study indicates that exposure to both hot and cold temperatures were related to increased mortality. Both cold and hot effects occurred immediately but cold effects lasted longer than hot effects. This study provides useful data for policy makers to better prepare local responses to manage the impact of hot and cold temperatures on population health.</description>
        <link>http://www.ehjournal.net/content/11/1/36</link>
                <dc:creator>Yuming Guo</dc:creator>
                <dc:creator>Kornwipa Punnasiri</dc:creator>
                <dc:creator>Shilu Tong</dc:creator>
                <dc:source>Environmental Health 2012, null:36</dc:source>
        <dc:date>2012-05-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-36</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
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        <prism:startingPage>36</prism:startingPage>
        <prism:publicationDate>2012-05-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.ehjournal.net/content/11/1/35">
        <title>Childhood brain tumours and use of mobile phones: comparison of a case-control study with incidence data</title>
        <description>The first case-control study on mobile phone use and brain tumor risk among children and adolescents (CEFALO study) has recently been published. In a commentary published in Environmental Health, Soderqvist and colleagues argued that CEFALO suggests an increased brain tumor risk in relation to wireless phone use. In this article, we respond and show why consistency checks of case-control study results with observed time trends of incidence rates are essential, given the well described limitations of case-control studies and the steep increase of mobile phone use among children and adolescents during the last decade. There is no plausible explanation of how a notably increased risk from use of wireless phones would correspond to the relatively stable incidence time trends for brain tumours among children and adolescents observed in the Nordic countries. Nevertheless, an increased risk restricted to heavy mobile phone use, to very early life exposure, or to rare subtypes of brain tumors may be compatible with stable incidence trends at this time and thus further monitoring of childhood brain tumor incidence rate time trends is warranted.</description>
        <link>http://www.ehjournal.net/content/11/1/35</link>
                <dc:creator>Denis Aydin</dc:creator>
                <dc:creator>Maria Feychting</dc:creator>
                <dc:creator>Joachim Schuz</dc:creator>
                <dc:creator>Martin Roosli</dc:creator>
                <dc:source>Environmental Health 2012, null:35</dc:source>
        <dc:date>2012-05-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-35</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
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        <prism:startingPage>35</prism:startingPage>
        <prism:publicationDate>2012-05-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.ehjournal.net/content/11/1/34">
        <title>Mortality and morbidity study of petrochemical emplyees in a polluted site</title>
        <description>Background:
The area of Gela was included among the 57 Italian polluted sites of national interest for environmental remediation because of its widespread contamination from a petrochemical complex. The present study investigates mortality and morbidity of the cohort of Gela petrochemical workers with the aim of disentangling occupational from residential risk.
Methods:
Mortality was assessed for 5,627 men hired from 1960, year of the plant start-up, to 1993; it was followed up for vital status in the period 1960-2002. Morbidity was analysed for 5,431 workers neither dead nor lost to follow-up from 1960 to 2001 and was based on Hospital Discharge Records in the period 2001-2006. The work experience was classified in terms of job categories such as blue collars, white collars, and both - workers who shifted from blue to white collar (95%) or vice versa. An ad hoc mobility model was applied to define qualitative categories of residence in Gela, as residents and commuters. Standardized Mortality Ratios (SMRs) and Mortality Rate Ratios (MRRs) were computed, the latter by using a Poisson regression model. Morbidity was analyzed in terms of Hospital Discharge Odds Ratios (HDORs) through a logistic regression model. While performing the internal comparisons, white collars was the reference category for the job analysis, and commuters was the reference category for the residential analysis.
Results:
In the light of epidemiological evidence about health risk from petrochemical industries in both occupational and environmental settings, and/or on the basis of information about occupational and residential contamination and health risk in the area of Gela, noteworthy results are shown for lung cancer [MRR: 2.11 (IC 90%; 0.96-4.63) in blue collars; 1.71 (1.09-2.69) in residents], respiratory diseases [HDOR: 2.0 (1.0-3.0) in blue collars; 1.4 (0.96-2.06) in residents] and genitourinary diseases [HDOR: 1.34 (1.06-1.68) in blue collars; 1.23 (1.04-1.45) in residents].
Conclusions:
The results support a role of the exposures in the occupational and residential settings, the latter due to the local ascertained contamination, in affecting the workers&apos; health. These results underline the urgent need of water, soil, air and food-chain monitoring programs, to discover active sources of exposure and consequently define public health interventions.</description>
        <link>http://www.ehjournal.net/content/11/1/34</link>
                <dc:creator>Roberto Pasetto</dc:creator>
                <dc:creator>Amerigo Zona</dc:creator>
                <dc:creator>Roberta Pirastu</dc:creator>
                <dc:creator>Achille Cernigliaro</dc:creator>
                <dc:creator>Gabriella Dardanoni</dc:creator>
                <dc:creator>Sebastiano Pollina Addario</dc:creator>
                <dc:creator>Salvatore Scondotto</dc:creator>
                <dc:creator>Pietro Comba</dc:creator>
                <dc:source>Environmental Health 2012, null:34</dc:source>
        <dc:date>2012-05-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-34</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
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        <prism:startingPage>34</prism:startingPage>
        <prism:publicationDate>2012-05-18T00:00:00Z</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/11/1/33">
        <title>A measure for quantifying the impact of housing quality on respiratory health: a cross-sectional study</title>
        <description>Background:
Damp and mould in homes have been established as risk factors for respiratory health. There is a need for a relatively straightforward assessment of the home that quantifies this risk.
Methods:
Using data from 891 New Zealand houses, the utility of a Respiratory Hazard Index quantifying key attributes related to damp and mould was tested by studying its associations with self-reported respiratory symptoms.
Results:
A dose-response relationship was found whereby each unit increase in the Respiratory Hazard Index was associated with an 11% increase in the odds of at least one episode of wheezing/whistling in the chest over the last 12 months (relative odds of 1.11 with a 95% CI 1.04%-1.20%). An 11% increase in the odds of an asthma attack over the last 12 months was estimated (relative odds of 1.11 with a 95% CI 1.01%-1.22%). These estimates were adjusted for household crowding levels, age, sex and smoking status. There was suggestive evidence of more steeply increasing odds of respiratory symptoms with increasing levels of the Respiratory Hazard Index for children aged under 7. In the worst performing houses according to the Index, a 33% reduction in the number of people experiencing respiratory symptoms (relative risk 0.67 with 95% CI 0.53 to 0.85) could be expected if people were housed in the best performing houses.
Conclusions:
This study showed that increased evidence of housing conditions supporting dampness and mould was associated with increased odds of respiratory symptoms. A valid housing assessment tool can provide a rational basis for investment in improved housing quality to improve respiratory health.</description>
        <link>http://www.ehjournal.net/content/11/1/33</link>
                <dc:creator>Michael Keall</dc:creator>
                <dc:creator>Julian Crane</dc:creator>
                <dc:creator>Michael Baker</dc:creator>
                <dc:creator>Kristin Wickens</dc:creator>
                <dc:creator>Philippa Howden-Chapman</dc:creator>
                <dc:creator>Malcolm Cunningham</dc:creator>
                <dc:source>Environmental Health 2012, null:33</dc:source>
        <dc:date>2012-05-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-33</dc:identifier>
                                <prism:require>/content/figures/1476-069X-11-33-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>2012-05-14T00:00:00Z</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/11/1/32">
        <title>The acceptability of rat trap use over pesticides for rodent control in two poor urban communities in South Africa</title>
        <description>Background:
Rodent infestations are a public health problem in poor urban communities. The use of illegal street pesticides to control rodent infestations with resulting poisonings is an additional public health concern receiving limited attention in many developing countries, including South Africa.
Methods:
Participants in a household intervention in two poor urban areas of Cape Town, South Africa, received two high quality rat traps. Reported in this article are the results of a follow-up survey conducted six months after distribution to assess community perceived acceptability of using rat traps instead of toxic pesticides (N = 175).
Results:
Of the 175 respondents that were followed up, 88% used the traps and only 35% continued using pesticides after the intervention. The analysis identified perceived effectiveness of the traps (prevalence odds ratio 18.00, 95% confidence interval 4.62 to 70.14), being male (prevalence odds ratio 8.86, 95% confidence interval 1.73 to 45.19), and the willingness to buy traps from an informal market (prevalence odds ratio 17.75, 95% confidence interval 4.22 to 74.57) as significantly associated with the acceptance of trap use.
Conclusions:
Rat traps, when introduced to poor urban communities, are acceptable as an alternative to toxic pesticides for rodent control. Sustainability of trap use, however, needs to be researched, especially cost and cost-benefit.</description>
        <link>http://www.ehjournal.net/content/11/1/32</link>
                <dc:creator>Rifqah Roomaney</dc:creator>
                <dc:creator>Rodney Ehrlich</dc:creator>
                <dc:creator>Hanna-Andrea Rother</dc:creator>
                <dc:source>Environmental Health 2012, null:32</dc:source>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-32</dc:identifier>
                                <prism:require>/content/figures/1476-069X-11-32-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>2012-05-03T00:00:00Z</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/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:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>31</prism:startingPage>
        <prism:publicationDate>2012-05-02T00:00:00Z</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/11/1/30">
        <title>Portrait of the journal as a young adult</title>
        <description>Since its founding a decade ago, Environmental Health has received more than one thousand manuscripts. Last year marked the first time we published over 100 articles. The journal web site currently receives over 60,000 unique visitors every month, and the steady increase suggests that the number will soon exceed 100,000 monthly. Individual articles are usually accessed several thousand times within a few years of publication, the highest number for a single paper being close to 100,000. The access numbers suggest that the journal has a reach that goes much beyond narrow academic circles as represented by numbers of citations in scholarly journals. To further the goal of reaching the wider public health community and linking to environmental health promotion, we ask prospective Environmental Health authors to highlight the findings that are new or different along with the implications for future research and in terms of prevention of environmental hazards.</description>
        <link>http://www.ehjournal.net/content/11/1/30</link>
                <dc:creator>Philippe Grandjean</dc:creator>
                <dc:creator>David Ozonoff</dc:creator>
                <dc:source>Environmental Health 2012, null:30</dc:source>
        <dc:date>2012-05-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-30</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>30</prism:startingPage>
        <prism:publicationDate>2012-05-02T00:00:00Z</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/11/1/29">
        <title>Correcting for the influence of sampling conditions on biomarkers of exposure to phenols and phthalates: a 2-step standardization method based on regression residuals</title>
        <description>Background:
Environmental epidemiology and biomonitoring studies typically rely on biological samples to assay the concentration of non-persistent exposure biomarkers. Between-participant variations in sampling conditions of these biological samples constitute a potential source of exposure misclassification. Few studies attempted to correct biomarker levels for this error. We aimed to assess the influence of sampling conditions on concentrations of urinary biomarkers of select phenols and phthalates, two widely-produced families of chemicals, and to standardize biomarker concentrations on sampling conditions.
Methods:
Urine samples were collected between 2002 and 2006 among 287 pregnant women from Eden and Pelagie cohorts, from which phthalates and phenols metabolites levels were assayed. We applied a 2-step standardization method based on regression residuals. First, the influence of sampling conditions (including sampling hour, duration of storage before freezing) and of creatinine levels on biomarker concentrations were characterized using adjusted linear regression models. In the second step, the model estimates were used to remove the variability in biomarker concentrations due to sampling conditions and to standardize concentrations as if all samples had been collected under the same conditions (e.g., same hour of urine collection).
Results:
Sampling hour was associated with concentrations of several exposure biomarkers. After standardization for sampling conditions, median concentrations differed by 38 % for 2,5-dichlorophenol to +80 % for a metabolite of diisodecyl phthalate. However, at the individual level, standardized biomarker levels were strongly correlated (correlation coefficients above 0.80) with unstandardized measures.
Conclusions:
Sampling conditions, such as sampling hour, should be systematically collected in biomarker-based studies, in particular when the biomarker half-life is short. The 2-step standardization method based on regression residuals that we proposed in order to limit the impact of heterogeneity in sampling conditions could be further tested in studies describing levels of biomarkers or their influence on health.</description>
        <link>http://www.ehjournal.net/content/11/1/29</link>
                <dc:creator>Marion Mortamais</dc:creator>
                <dc:creator>Cecile Chevrier</dc:creator>
                <dc:creator>Claire Philippat</dc:creator>
                <dc:creator>Claire Petit</dc:creator>
                <dc:creator>Antonia Calafat</dc:creator>
                <dc:creator>Xiaoyun Ye</dc:creator>
                <dc:creator>Manori Silva</dc:creator>
                <dc:creator>Christian Brambilla</dc:creator>
                <dc:creator>Marinus Eijkemans</dc:creator>
                <dc:creator>Marie-Aline Charles</dc:creator>
                <dc:creator>Sylvaine Cordier</dc:creator>
                <dc:creator>Remy Slama</dc:creator>
                <dc:source>Environmental Health 2012, null:29</dc:source>
        <dc:date>2012-04-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-29</dc:identifier>
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                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
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        <prism:startingPage>29</prism:startingPage>
        <prism:publicationDate>2012-04-26T00:00:00Z</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/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:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
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        <prism:startingPage>28</prism:startingPage>
        <prism:publicationDate>2012-04-25T00:00:00Z</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/11/1/27">
        <title>Perceived annoyance from environmental odors and association with atmospheric ammonia levels in non-urban residential communities: a cross-sectional study</title>
        <description>ObjectiveOdor exposure is an environmental stressor that is responsible of many citizens complains about air pollution in non-urban areas. However, information about the exposure-response relation is scarce. One of the main challenges is to identify a measurable compound that can be related with odor annoyance responses. We investigated the association between regional and temporal variation of ammonia (NH3) concentrations in five Danish non-urban regions and environmental odor annoyance as perceived by the local residents.
Methods:
A cross-sectional study where NH3 concentration was obtained from the national air quality monitoring program and from emission-dispersion modelling, and odor pollution perception from questionnaires. The exposure-response model was a sigmoid model. Linear regression analyses were used to estimate the model constants after equation transformations. The model was validated using leave-one-out cross validation (LOOCV) statistical method.
Results:
About 45% of the respondents were annoyed by odor pollution at their residential areas. The perceived odor was characterized by all respondents as animal waste odor. The exposure-annoyance sigmoid model showed that the prevalence of odor annoyance was significantly associated with NH3 concentrations (measured and estimated) at the local air quality monitoring stations (p &lt; 0.01,R2 = 0.99; and p &lt; 0.05,R2 = 0.93; respectively). Prediction errors were below 5.1% and 20% respectively. The seasonal pattern of odor perception was associated with the seasonal variation in NH3 concentrations (p &lt; 0.001, adjusted R2 = 0.68).
Conclusion:
The results suggest that atmospheric NH3 levels at local air quality stations could be used as indicators of prevalence of odor annoyance in non-urban residential communities.</description>
        <link>http://www.ehjournal.net/content/11/1/27</link>
                <dc:creator>Victoria Blanes-Vidal</dc:creator>
                <dc:creator>Esmaeil Nadimi</dc:creator>
                <dc:creator>Thomas Ellermann</dc:creator>
                <dc:creator>Helle Andersen</dc:creator>
                <dc:creator>Per Løfstrøm</dc:creator>
                <dc:source>Environmental Health 2012, null:27</dc:source>
        <dc:date>2012-04-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-11-27</dc:identifier>
                                <prism:require>/content/figures/1476-069X-11-27-toc.gif</prism:require>
                <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>27</prism:startingPage>
        <prism:publicationDate>2012-04-18T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
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