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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1143?rss=1">
<title><![CDATA[Low Workplace Social Capital as a Predictor of Depression: The Finnish Public Sector Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1143?rss=1</link>
<description><![CDATA[
<p>In a prospective cohort study of Finnish public sector employees, the authors examined the association between workplace social capital and depression. Data were obtained from 33,577 employees, who had no recent history of antidepressant treatment and who reported no history of physician-diagnosed depression at baseline in 2000&ndash;2002. Their risk of depression was measured with two indicators: recorded purchases of antidepressants until December 31, 2005, and self-reports of new-onset depression diagnosed by a physician in the follow-up survey in 2004&ndash;2005. Multilevel logistic regression analysis was used to explore whether self-reported and aggregate-level workplace social capital predicted indicators of depression at follow-up. The odds for antidepressant treatment and physician-diagnosed depression were 20&ndash;50% higher for employees with low self-reported social capital than for those reporting high social capital. These associations were not accounted for by sex, age, marital status, socioeconomic position, place of work, smoking, alcohol use, physical activity, and body mass index. The association between social capital and self-reported depression attenuated but remained significant after further adjustment for baseline psychological distress (a proxy for undiagnosed mental health problems). Aggregate-level social capital was not associated with subsequent depression.</p>
]]></description>
<dc:creator><![CDATA[Kouvonen, A., Oksanen, T., Vahtera, J., Stafford, M., Wilkinson, R., Schneider, J., Vaananen, A., Virtanen, M., Cox, S. J., Pentti, J., Elovainio, M., Kivimaki, M.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn067</dc:identifier>
<dc:title><![CDATA[Low Workplace Social Capital as a Predictor of Depression: The Finnish Public Sector Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1151</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1143</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1152?rss=1">
<title><![CDATA[Invited Commentary: Social Capital, Social Contexts, and Depression]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1152?rss=1</link>
<description><![CDATA[
<p>The literature concerning social capital and health has grown exponentially during the past somewhat more than 10 years. The study by Kouvonen et al. (<I>Am J Epidemiol</I> 2008;167:1143&ndash;1151) is a longitudinal multilevel analysis of 33,577 public sector employees in Finland. The study shows a significant association between workplace social capital and depression, which is an interesting finding in a very new field of the study of social capital and health. However, the study also serves as an inspiration for further studies in important research areas. Workplace social capital may be investigated according to both horizontal, that is, social contacts and level of trust in relation to coworkers, and vertical, that is, relation with employer/supervisor across power gradients, dimensions. The fact that workplace social capital may affect social capital outside work and vice versa is also of interest. It is also important to define and identify the social context level in a correct way in multilevel studies. In the study by Kouvonen et al., the social context is not a geographic entity but an entity defined according to place of work, and the definition of such a social context entails several difficulties. This study presents interesting findings and provides a basis for future studies.</p>
]]></description>
<dc:creator><![CDATA[Lindstrom, M.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn070</dc:identifier>
<dc:title><![CDATA[Invited Commentary: Social Capital, Social Contexts, and Depression]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1154</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1152</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1155?rss=1">
<title><![CDATA[Determinants and Outcomes of Serious Attempted Suicide: A Nationwide Study in Finland, 1996-2003]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1155?rss=1</link>
<description><![CDATA[
<p>Suicide is among the 10 leading causes of death. Attempted suicide is 10&ndash;40 times more frequent than completed suicide and is the strongest single predictor of subsequent suicide. The current study population included all persons in Finland who were hospitalized with a diagnosis of attempted suicide between 1996 and 2003 (<I>N</I> = 18,199). Information on background variables and mortality was obtained by register linkage. The risk of repeated attempted suicide was 30% and the risk of suicide was 10%. The risks of repeated attempted suicide, completed suicide, and death from any cause were high immediately after discharge from the hospital. Analysis of competing causes of death revealed that while alcohol-related disorder was not associated with suicide, it markedly increased the risk of other violent death: The subdistribution hazards rate (SHR) was 2.61 (95% confidence interval (CI): 2.12, 3.21). Schizophrenia-related disorders (SHR = 1.87, 95% CI: 1.57, 2.21) and mood disorders (SHR = 1.72, 95% CI: 1.47, 2.01) were associated with the risk of suicide. The risks of suicide and all-cause mortality were extremely high immediately after hospitalization for attempted suicide.</p>
]]></description>
<dc:creator><![CDATA[Haukka, J., Suominen, K., Partonen, T., Lonnqvist, J.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn017</dc:identifier>
<dc:title><![CDATA[Determinants and Outcomes of Serious Attempted Suicide: A Nationwide Study in Finland, 1996-2003]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1163</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1155</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1164?rss=1">
<title><![CDATA[Maternal Dietary Intake of Vitamin A and Risk of Orofacial Clefts: A Population-based Case-Control Study in Norway]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1164?rss=1</link>
<description><![CDATA[
<p>A population-based case-control study was carried out in Norway between 1996 and 2001. The aim was to evaluate the association between maternal intake of vitamin A from diet and supplements and risk of having a baby with an orofacial cleft. Data on maternal dietary intake were available from 535 cases (188 with cleft palate only and 347 with cleft lip with or without cleft palate) and 693 controls. The adjusted odds ratio for isolated cleft palate only was 0.47 (95% confidence interval: 0.24, 0.94) when comparing the fourth and first quartiles of maternal intake of total vitamin A. In contrast, there was no appreciable association of total vitamin A with isolated cleft lip with or without cleft palate. An intake of vitamin A above the 95th percentile was associated with a lower estimated risk of all isolated clefts compared with the 40th&ndash;60th percentile (adjusted odds ratio = 0.48, 95% confidence interval: 0.20, 1.14). Maternal intake of vitamin A is associated with reduced risk of cleft palate only, and there is no evidence of increased risk of clefts among women in our study with the highest 5% of vitamin A intake.</p>
]]></description>
<dc:creator><![CDATA[Johansen, A. M. W., Lie, R. T., Wilcox, A. J., Andersen, L. F., Drevon, C. A.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn035</dc:identifier>
<dc:title><![CDATA[Maternal Dietary Intake of Vitamin A and Risk of Orofacial Clefts: A Population-based Case-Control Study in Norway]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1170</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1164</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1171?rss=1">
<title><![CDATA[Maternal Fish Intake during Pregnancy, Blood Mercury Levels, and Child Cognition at Age 3 Years in a US Cohort]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1171?rss=1</link>
<description><![CDATA[
<p>The balance of contaminant risk and nutritional benefit from maternal prenatal fish consumption for child cognitive development is not known. Using data from a prospective cohort study of 341 mother-child pairs in Massachusetts enrolled in 1999&ndash;2002, the authors studied associations of maternal second-trimester fish intake and erythrocyte mercury levels with children's scores on the Peabody Picture Vocabulary Test (PPVT) and Wide Range Assessment of Visual Motor Abilities (WRAVMA) at age 3 years. Mean maternal total fish intake was 1.5 (standard deviation, 1.4) servings/week, and 40 (12%) mothers consumed &gt;2 servings/week. Mean maternal mercury level was 3.8 (standard deviation, 3.8) ng/g. After adjustment using multivariable linear regression, higher fish intake was associated with better child cognitive test performance, and higher mercury levels with poorer test scores. Associations strengthened with inclusion of both fish and mercury: effect estimates for fish intake of &gt;2 servings/week versus never were 2.2 (95% confidence interval (CI): &ndash;2.6, 7.0) for the PPVT and 6.4 (95% CI: 2.0, 10.8) for the WRAVMA; for mercury in the top decile, they were &ndash;4.5 (95% CI: &ndash;8.5, &ndash;0.4) for the PPVT and &ndash;4.6 (95% CI: &ndash;8.3, &ndash;0.9) for the WRAVMA. Fish consumption of &le;2 servings/week was not associated with a benefit. Dietary recommendations for pregnant women should incorporate the nutritional benefits as well as the risks of fish intake.</p>
]]></description>
<dc:creator><![CDATA[Oken, E., Radesky, J. S., Wright, R. O., Bellinger, D. C., Amarasiriwardena, C. J., Kleinman, K. P., Hu, H., Gillman, M. W.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn034</dc:identifier>
<dc:title><![CDATA[Maternal Fish Intake during Pregnancy, Blood Mercury Levels, and Child Cognition at Age 3 Years in a US Cohort]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1181</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1171</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1182?rss=1">
<title><![CDATA[Eczema, Birth Order, and Infection]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1182?rss=1</link>
<description><![CDATA[
<p>The association between infections occurring in the first 2 years of life and development of eczema was investigated in 1,782 control children from a national population-based case-control study in the United Kingdom conducted over the period 1991&ndash;1996. Dates of eczema and infectious diagnoses were ascertained from contemporaneously collected primary care records. Children diagnosed with eczema before the age of 2 years had more prior clinically diagnosed infections recorded than did children without eczema (rate ratio = 1.26, 95% confidence interval (CI): 1.18, 1.36). The difference in infection rates between children with and without eczema was apparent from birth and throughout the first 2 years of life. As expected, compared with children of second or higher birth order, those firstborn were at increased risk of eczema (<I>p</I> = 0.020); however, the relation between eczema and prior infection was evident only among children of second or higher birth order and not among firstborn children (rate ratio = 1.45, 95% CI: 1.32, 1.59, and rate ratio = 1.08, 95% CI: 0.98, 1.20, respectively). The authors' results are consistent with the notion that the association between birth order and eczema is unlikely to be attributable to variations in early infectious exposure.</p>
]]></description>
<dc:creator><![CDATA[Hughes, A. M., Crouch, S., Lightfoot, T., Ansell, P., Simpson, J., Roman, E.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn042</dc:identifier>
<dc:title><![CDATA[Eczema, Birth Order, and Infection]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1187</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1182</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1188?rss=1">
<title><![CDATA[Domestic Violence and Chronic Malnutrition among Women and Children in India]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1188?rss=1</link>
<description><![CDATA[
<p>Domestic violence has harmful physical and psychological health correlates, but there is little evidence regarding a relation between domestic violence and malnutrition. To investigate this relation, the authors analyzed data from 69,072 women aged 15&ndash;49 years and 14,552 children aged 12&ndash;35 months in the 1998&ndash;1999 Indian National Family Health Survey. Physical domestic violence victimization was self-reported by the women. Aspects of nutritional status included in this study were anemia and underweight. Anemia was measured with a blood test for hemoglobin. Underweight was calculated from anthropometric measurements and was determined as body mass index for women, and it included stunting and wasting for children. Results indicate associations of multiple incidents of domestic violence in the previous year with anemia (odds ratio = 1.11, 95% confidence interval: 1.04, 1.18) and underweight (odds ratio = 1.21, 95% confidence interval: 1.13, 1.29) in women and a suggested relation among children. Possible mechanisms for this relation include withholding of food as a form of abuse and stress-mediated influences of domestic violence on nutritional outcomes. These findings indicate that reducing domestic violence is important not only from a moral and intrinsic perspective but also because of the instrumental health benefits likely to accrue.</p>
]]></description>
<dc:creator><![CDATA[Ackerson, L. K., Subramanian, S. V.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn049</dc:identifier>
<dc:title><![CDATA[Domestic Violence and Chronic Malnutrition among Women and Children in India]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1196</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1188</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1197?rss=1">
<title><![CDATA[A Prospective Study of Multivitamin Supplement Use and Risk of Breast Cancer]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1197?rss=1</link>
<description><![CDATA[
<p>The authors evaluated the association between multivitamin supplement use and breast cancer risk in a completed trial. At baseline (1992&ndash;1995), 37,920 US women aged &ge;45 years and free of cancer provided detailed information on multivitamin supplement use. During an average of 10 years of follow-up, 1,171 cases of invasive breast cancer were documented. Multivitamin use was not significantly associated with overall risk of breast cancer. Compared with the risk for never users, the multivariable relative risks were 0.97 (95% confidence interval: 0.81, 1.16) for past users and 0.99 (95% confidence interval: 0.82, 1.19) for current users. Current multivitamin use for &ge;20 years or &ge;6 times/week was also not significantly associated with risk. Multivitamin use was nonsignificantly inversely associated with risk of breast cancer among women consuming &ge;10 g/day of alcohol and with risk of estrogen receptor negative&ndash;progesterone receptor negative breast cancer. Multivitamin use was nonsignificantly associated with a reduced risk of developing &le;2-cm breast tumors but an increased risk of &gt;2-cm tumors. The authors' data indicate no overall association between multivitamin use and breast cancer risk but suggest that multivitamin use might reduce risk for women consuming alcohol or decrease risk of estrogen receptor negative&ndash;progesterone receptor negative breast cancer.</p>
]]></description>
<dc:creator><![CDATA[Ishitani, K., Lin, J., Manson, J. E., Buring, J. E., Zhang, S. M.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn027</dc:identifier>
<dc:title><![CDATA[A Prospective Study of Multivitamin Supplement Use and Risk of Breast Cancer]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1206</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1197</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1207?rss=1">
<title><![CDATA[Estrogen Plus Progestin Therapy and Breast Cancer in Recently Postmenopausal Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1207?rss=1</link>
<description><![CDATA[
<p>The Women's Health Initiative trial found a modestly increased risk of invasive breast cancer with daily 0.625-mg conjugated equine estrogens plus 2.5-mg medroxyprogesterone acetate, with most evidence among women who had previously received postmenopausal hormone therapy. In comparison, observational studies mostly report a larger risk increase. To explain these patterns, the authors examined the effects of this regimen in relation to both prior hormone therapy and time from menopause to first use of postmenopausal hormone therapy ("gap time") in the Women's Health Initiative trial and in a corresponding subset of the Women's Health Initiative observational study. Postmenopausal women with a uterus enrolled at 40 US clinical centers during 1993&ndash;1998. The authors found that hazard ratios agreed between the two cohorts at a specified gap time and time from hormone therapy initiation. Combined trial and observational study data support an adverse effect on breast cancer risk. Women who initiate use soon after menopause, and continue for many years, appear to be at particularly high risk. For example, for a woman who starts soon after menopause and adheres to this regimen, estimated hazard ratios are 1.64 (95% confidence interval: 1.00, 2.68) over a 5-year period of use and 2.19 (95% confidence interval: 1.56, 3.08) over a 10-year period of use.</p>
]]></description>
<dc:creator><![CDATA[Prentice, R. L., Chlebowski, R. T., Stefanick, M. L., Manson, J. E., Pettinger, M., Hendrix, S. L., Hubbell, F. A., Kooperberg, C., Kuller, L. H., Lane, D. S., McTiernan, A., Jo O'Sullivan, M., Rossouw, J. E., Anderson, G. L.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn044</dc:identifier>
<dc:title><![CDATA[Estrogen Plus Progestin Therapy and Breast Cancer in Recently Postmenopausal Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1216</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1207</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1217?rss=1">
<title><![CDATA[Estrogen Receptor Alpha and Matrix Metalloproteinase 2 Polymorphisms and Age-related Maculopathy in Older Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1217?rss=1</link>
<description><![CDATA[
<p>In this study, the authors sought to determine whether single nucleotide polymorphisms in the estrogen receptor alpha (<I>ESR1</I>) and matrix metalloproteinase 2 (<I>MMP2</I>) genes are associated with age-related maculopathy (ARM) in older women. Subjects comprised a random sample of Caucasian women aged &ge;74 years participating in the Study of Osteoporotic Fractures year 10 follow-up (<I>n</I> = 906) in 1997&ndash;1998. Fundus photographs were graded for ARM using a modification of the Wisconsin Age-Related Maculopathy Grading System. The prevalences of early ARM and late ARM were 46% and 4%, respectively. The <I>MMP2 rs2287074</I> single nucleotide polymorphism (G-&gt;A) was associated with ARM. The A allele was present in 47%, 43%, and 30% of subjects with no, early, and late ARM, respectively (<I>p</I> = 0.01), and was associated with lower odds of any ARM (for AG vs. GG, odds ratio = 0.80, 95% confidence interval: 0.65, 0.99; for AA vs. GG, odds ratio = 0.64, 95% confidence interval: 0.42, 0.98). An interaction with use of postmenopausal hormone therapy was significant (<I>p</I> = 0.02). The <I>MMP2 rs2287074</I> A allele may be associated with a lower likelihood of ARM in older Caucasian women, particularly those who have never used hormone therapy. The role of <I>MMP2 rs2287074</I> in ARM should be further elucidated.</p>
]]></description>
<dc:creator><![CDATA[Seitzman, R. L., Mahajan, V. B., Mangione, C., Cauley, J. A., Ensrud, K. E., Stone, K. L., Cummings, S. R., Hochberg, M. C., Hillier, T. A., Sinsheimer, J. S., Yu, F., Coleman, A. L., for the Study of Osteoporotic Fractures Research Group]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn024</dc:identifier>
<dc:title><![CDATA[Estrogen Receptor Alpha and Matrix Metalloproteinase 2 Polymorphisms and Age-related Maculopathy in Older Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1225</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1217</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1226?rss=1">
<title><![CDATA[Glomerular Filtration Rate, Albuminuria, and Risk of Cardiovascular and All-Cause Mortality in the US Population]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1226?rss=1</link>
<description><![CDATA[
<p>Decreased glomerular filtration rate (GFR) and albuminuria are used in combination to define chronic kidney disease, but their separate and combined effects on cardiovascular and all-cause mortality have not been studied in the general population. The linked mortality file of the Third National Health and Nutrition Examination Survey includes data from 13 years of follow-up (1988&ndash;2000) for 14,586 US adults. The authors estimated GFR from standardized serum creatinine levels. Albuminuria was defined by the urinary albumin:creatinine ratio. Incidence rate ratios (IRRs) were adjusted for major cardiovascular disease risk factors and C-reactive protein. Lower estimated GFR was associated with higher risks of cardiovascular and all-cause mortality overall and within every albuminuria category. Likewise, increasing albuminuria was associated with higher risk of estimated GFR overall and within every category. When estimated GFR and albuminuria were examined simultaneously, a 10-ml/minute/1.73 m<sup>2</sup> lower estimated GFR (among persons with estimated GFR &lt;60 ml/minute/1.73 m<sup>2</sup>) was associated with an IRR of 1.29 (95% confidence interval: 1.06, 1.55) for cardiovascular mortality and a doubling of albuminuria was associated with an IRR of 1.06 (95% confidence interval: 1.04, 1.08) for cardiovascular mortality. The authors conclude that moderately decreased estimated GFR and albuminuria independently predict cardiovascular and all-cause mortality in the general population. These data support recent recommendations defining chronic kidney disease and stratifying subsequent risks based on both decreased GFR and albuminuria.</p>
]]></description>
<dc:creator><![CDATA[Astor, B. C., Hallan, S. I., Miller, E. R., Yeung, E., Coresh, J.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn033</dc:identifier>
<dc:title><![CDATA[Glomerular Filtration Rate, Albuminuria, and Risk of Cardiovascular and All-Cause Mortality in the US Population]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1234</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1226</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1235?rss=1">
<title><![CDATA[Incident Diabetes and Pesticide Exposure among Licensed Pesticide Applicators: Agricultural Health Study, 1993-2003]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1235?rss=1</link>
<description><![CDATA[
<p>Exposure to certain environmental toxicants may be associated with increased risk of developing diabetes. The authors' aim was to investigate the relation between lifetime exposure to specific agricultural pesticides and diabetes incidence among pesticide applicators. The study included 33,457 licensed applicators, predominantly non-Hispanic White males, enrolled in the Agricultural Health Study. Incident diabetes was self-reported in a 5-year follow-up interview (1999&ndash;2003), giving 1,176 diabetics and 30,611 nondiabetics for analysis. Lifetime exposure to pesticides and covariate information were reported by participants at enrollment (1993&ndash;1997). Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively. The observed association of organochlorine and organophosphate insecticides with diabetes is consistent with results from previous human and animal studies. Long-term exposure from handling certain pesticides, in particular, organochlorine and organophosphate insecticides, may be associated with increased risk of diabetes.</p>
]]></description>
<dc:creator><![CDATA[Montgomery, M. P., Kamel, F., Saldana, T. M., Alavanja, M. C. R., Sandler, D. P.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn028</dc:identifier>
<dc:title><![CDATA[Incident Diabetes and Pesticide Exposure among Licensed Pesticide Applicators: Agricultural Health Study, 1993-2003]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1246</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1235</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1247?rss=1">
<title><![CDATA[Use of Recovery Biomarkers to Calibrate Nutrient Consumption Self-Reports in the Women's Health Initiative]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1247?rss=1</link>
<description><![CDATA[
<p>Underreporting of energy consumption by self-report is well-recognized, but previous studies using recovery biomarkers have not been sufficiently large to establish whether participant characteristics predict misreporting. In 2004&ndash;2005, 544 participants in the Women's Health Initiative Dietary Modification Trial completed a doubly labeled water protocol (energy biomarker), 24-hour urine collection (protein biomarker), and self-reports of diet (assessed by food frequency questionnaire (FFQ)), exercise, and lifestyle habits; 111 women repeated all procedures after 6 months. Using linear regression, the authors estimated associations of participant characteristics with misreporting, defined as the extent to which the log ratio (self-reported FFQ/nutritional biomarker) was less than zero. Intervention women in the trial underreported energy intake by 32% (vs. 27% in the comparison arm) and protein intake by 15% (vs. 10%). Younger women had more underreporting of energy (<I>p</I> = 0.02) and protein (<I>p</I> = 0.001), while increasing body mass index predicted increased underreporting of energy and overreporting of percentage of energy derived from protein (<I>p</I> = 0.001 and <I>p</I> = 0.004, respectively). Blacks and Hispanics underreported more than did Caucasians. Correlations of initial measures with repeat measures (<I>n</I> = 111) were 0.72, 0.70, 0.46, and 0.64 for biomarker energy, FFQ energy, biomarker protein, and FFQ protein, respectively. Recovery biomarker data were used in regression equations to calibrate self-reports; the potential application of these equations to disease risk modeling is presented. The authors confirm the existence of systematic bias in dietary self-reports and provide methods of correcting for measurement error.</p>
]]></description>
<dc:creator><![CDATA[Neuhouser, M. L., Tinker, L., Shaw, P. A., Schoeller, D., Bingham, S. A., Horn, L. V., Beresford, S. A. A., Caan, B., Thomson, C., Satterfield, S., Kuller, L., Heiss, G., Smit, E., Sarto, G., Ockene, J., Stefanick, M. L., Assaf, A., Runswick, S., Prentice, R. L.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn026</dc:identifier>
<dc:title><![CDATA[Use of Recovery Biomarkers to Calibrate Nutrient Consumption Self-Reports in the Women's Health Initiative]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1259</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1247</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1260?rss=1">
<title><![CDATA[Buccal Swabs and Treated Cards: Methodological Considerations for Molecular Epidemiologic Studies Examining Pediatric Populations]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1260?rss=1</link>
<description><![CDATA[
<p>Self-collection of buccal cells provides a noninvasive method for obtaining biologic samples for genetic analyses in pediatric studies. Nevertheless, low yields, microbial contamination, and degradation of buccal samples present challenges for epidemiologic studies incorporating genetic investigations. The aims of this study were to compare the quality and yield of DNA extracted from buccal specimens with BuccalAmp swabs (Epicenter BioTechnologies, Madison, Wisconsin) or FTA cards (Whatman, Inc., Clifton, New Jersey) and to investigate the use of whole-genome amplification (WGA) for increasing DNA yields for single nucleotide polymorphism analyses. Buccal specimens were collected from 55 children with acute lymphoblastic leukemia and 52 control children without acute lymphoblastic leukemia in New South Wales, Australia, in 2003&ndash;2004. Real-time polymerase chain reaction was used to evaluate polymorphisms in the genes encoding the cytochrome p450 enzyme CYP3A4 (<I>CYP3A4</I> A392G, also known as <I>CYP3A4*1B</I>) and the steroid xenobiotic receptor (<I>SXR</I> C25385T). Results showed that DNA could be isolated from buccal specimens collected by use of both methods and that yields could be substantially improved with WGA without introducing genotyping error. However, DNA quality was poorer in samples collected by BuccalAmp swabs, and the presence of polymerase chain reaction inhibitors in these samples reduced the sensitivity of quantitative real-time PCR analysis. These findings show that different methods for collecting buccal samples impact on the downstream success of genetic investigations and influence DNA quality after WGA.</p>
]]></description>
<dc:creator><![CDATA[Beckett, S. M., Laughton, S. J., Pozza, L. D., McCowage, G. B., Marshall, G., Cohn, R. J., Milne, E., Ashton, L. J.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn012</dc:identifier>
<dc:title><![CDATA[Buccal Swabs and Treated Cards: Methodological Considerations for Molecular Epidemiologic Studies Examining Pediatric Populations]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1267</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1260</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1268?rss=1">
<title><![CDATA[Epidemiological Methods in Life Course Research: Edited by Andrew Pickles, Barbara Maughan, and Michael Wadsworth]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1268?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Faerstein, E.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn054</dc:identifier>
<dc:title><![CDATA[Epidemiological Methods in Life Course Research: Edited by Andrew Pickles, Barbara Maughan, and Michael Wadsworth]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1268</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1268</prism:startingPage>
<prism:section>BOOK-REVIEW</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1017?rss=1">
<title><![CDATA[How Much of the Data Published in Observational Studies of the Association between Diet and Prostate or Bladder Cancer Is Usable for Meta-Analysis?]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1017?rss=1</link>
<description><![CDATA[
<p>Epidemiologic investigations often report dose-response associations, which may be combined in meta-analyses. The authors examined how often the log odds, risk, or hazard ratio per unit increase in exposure, and its standard error, can be estimated from results reported from observational studies of diet and prostate or bladder cancer so that results are usable in meta-analyses estimating dose-response associations. Eight electronic databases were searched for studies reporting on the association of diet, nutrition, or physical activity with these cancers. A total of 767 papers reported 3,284 results; 1,999 (61%) results, reported in 545 (71%) papers, were usable in dose-response meta-analyses. The most important reason that results were not usable was the absence of sufficient information on exposure levels in the different groups. The proportion of results usable in "high-low" meta-analyses (comparisons of extreme categories) was similar (62%). Results that showed evidence of an association were more likely to be usable than results that found no such evidence. Insufficient detail in reporting of results of observational studies can lead to exclusion of these results from meta-analyses and is an important threat to the validity of systematic reviews of such research. Results providing evidence of associations may be overrepresented in meta-analyses of observational studies.</p>
]]></description>
<dc:creator><![CDATA[Bekkering, G. E., Harris, R. J., Thomas, S., Mayer, A.-M. B., Beynon, R., Ness, A. R., Harbord, R. M., Bain, C., Smith, G. D., Sterne, J. A. C.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn005</dc:identifier>
<dc:title><![CDATA[How Much of the Data Published in Observational Studies of the Association between Diet and Prostate or Bladder Cancer Is Usable for Meta-Analysis?]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1026</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1017</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1027?rss=1">
<title><![CDATA[Age-specific Trends in Mammographic Density: The Minnesota Breast Cancer Family Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1027?rss=1</link>
<description><![CDATA[
<p>Mammographic density is a strong risk factor for breast cancer, yet few studies have evaluated density trends, and associated factors, over time. The authors retrieved and digitized mammograms (&ge;1 per woman) imaged in 1990&ndash;2003 to evaluate percent density (PD) in the Minnesota Breast Cancer Family cohort. Multivariable-adjusted, mixed-effects, repeated-measures models incorporating a natural cubic spline provided estimates of nonlinear trends in PD with age and were used to examine association with covariates. Overall, 5,698 mammograms from 1,689 women with covariate information were digitized. In descriptive analyses, the highest median PD was 33.1% (interquartile range, 21.8%; <I>n</I> = 230) among premenopausal women, 31.0% (interquartile range, 23.2%; <I>n</I> = 175) among women who transitioned from pre- to postmenopause, and 18.7% (interquartile range, 22.2%; <I>n</I> = 1,284) among postmenopausal women. On average, premenopausal compared with postmenopausal women had 1.9% (<I>p</I> = 0.001) higher PD. In repeated-measures analyses, greater declines in PD occurred with menopause and among women with higher baseline PD; current postmenopausal hormone use and higher body mass index modified these declines (<I>p</I> interaction &lt; 0.001). No significant modification of the density change with age was seen with parity/age at first birth, age at menarche, oral contraceptive use, family history of breast or ovarian cancer in a first- or second-degree relative, educational level, smoking status, or alcohol intake were observed. These data suggest that menopause, baseline PD, postmenopausal hormone use, and body mass index predict changes in mammographic density trends during adult life.</p>
]]></description>
<dc:creator><![CDATA[Kelemen, L. E., Pankratz, V. S., Sellers, T. A., Brandt, K. R., Wang, A., Janney, C., Fredericksen, Z. S., Cerhan, J. R., Vachon, C. M.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn063</dc:identifier>
<dc:title><![CDATA[Age-specific Trends in Mammographic Density: The Minnesota Breast Cancer Family Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1036</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1027</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1037?rss=1">
<title><![CDATA[Invited Commentary: Assessing Breast Density Change--Lessons for Future Studies]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1037?rss=1</link>
<description><![CDATA[
<p>Breast density is one of the strongest predictors of breast cancer risk, and quantitative measurement is fairly reproducible. However, to study change in breast density, other issues should also be considered. Most studies of breast density have relied on one assessment, yet the mammographic features of the breast that constitute breast density change with age and/or menopause. When measuring breast density change, issues related to assessment are of greater concern. In addition, because age-period and cohort effects are codefined, evaluation of age trends must also consider the possible explanations of period and cohort effects. The prevalence of different factors affecting breast density changed dramatically over the last 50 years. In this issue of the <I>Journal</I> (Am J Epidemiol 2008;167:1027&ndash;1036), Kelemen et al. evaluate how factors known to be related to breast density influence breast density change with age. These authors are to be complimented on their detailed analysis and consideration of many of these issues. They not only describe the averaged effects of age on breast density changes but also consider whether patterns of density change differ for women with different exposure histories.</p>
]]></description>
<dc:creator><![CDATA[Byrne, C.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn062</dc:identifier>
<dc:title><![CDATA[Invited Commentary: Assessing Breast Density Change--Lessons for Future Studies]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1040</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1037</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1041?rss=1">
<title><![CDATA["Culture of Drinking" and Individual Problems with Alcohol Use]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1041?rss=1</link>
<description><![CDATA[
<p>Binge drinking is a substantial and growing health problem. Community norms about drinking and drunkenness may influence individual drinking problems. Using data from the New York Social Environment Study (<I>n</I> = 4,000) conducted in 2005, the authors examined the relation between aspects of the neighborhood drinking culture and individual alcohol use. They applied methods to address social stratification and social selection, both of which are challenges to interpreting neighborhood research. In adjusted models, permissive neighborhood drinking norms were associated with moderate drinking (odds ratio (OR) = 1.28, 95% confidence interval (CI): 1.05, 1.55) but not binge drinking; however, social network and individual drinking norms accounted for this association. By contrast, permissive neighborhood drunkenness norms were associated with more moderate drinking (OR = 1.20, 95% CI: 1.03, 1.39) and binge drinking (OR = 1.92, 95% CI: 1.44, 2.56); the binge drinking association remained after adjustment for social network and individual drunkenness norms (OR = 1.58, 95% CI: 1.20, 2.08). Drunkenness norms were more strongly associated with binge drinking for women than for men (<I>p</I><SUB>interaction</SUB> = 0.006). Propensity distributions and adjustment for drinking history suggested that social stratification and social selection, respectively, were not plausible explanations for the observed results. Analyses that consider social and structural factors that shape harmful drinking may inform efforts targeting the problematic aspects of alcohol consumption.</p>
]]></description>
<dc:creator><![CDATA[Ahern, J., Galea, S., Hubbard, A., Midanik, L., Syme, S. L.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn022</dc:identifier>
<dc:title><![CDATA["Culture of Drinking" and Individual Problems with Alcohol Use]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1049</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1041</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1050?rss=1">
<title><![CDATA[Alcohol Drinking, Cigarette Smoking, and Risk of Colorectal Adenomatous and Hyperplastic Polyps]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1050?rss=1</link>
<description><![CDATA[
<p>The authors evaluated alcohol drinking and cigarette smoking in relation to risk of colorectal polyps in a Nashville, Tennessee, colonoscopy-based case-control study. In 2003&ndash;2005, cases with adenomatous polyps only (<I>n</I> = 639), hyperplastic polyps only (<I>n</I> = 294), and both types of polyps (<I>n</I> = 235) were compared with 1,773 polyp-free controls. Unordered polytomous logistic regression was used to calculate adjusted odds ratios and 95% confidence intervals. Consumption of at least five alcoholic drinks per week was not strongly associated with development of polyps. Odds ratios for all polyp types were increased for dose, duration, and pack-years of cigarette smoking and were stronger for hyperplastic polyps than for adenoma. Compared with never smoking, dose-response relations were particularly strong for current smoking and duration; for &ge;35 years of smoking, odds ratios were 1.9 (95% confidence interval (CI): 1.4, 2.5) for adenomatous polyps only, 5.0 (95% CI: 3.3, 7.3) for hyperplastic polyps only, and 6.9 (95% CI: 4.4, 11.1) for both types of polyps. Compared with current smoking, time since cessation was associated with substantially reduced odds; for &ge;20 years since quitting, odds ratios were 0.4 (95% CI: 0.3, 0.6) for adenoma only, 0.2 (95% CI: 0.1, 0.3) for hyperplastic polyps only, and 0.2 (95% CI: 0.2, 0.4) for both polyp types. These findings support the adverse role of cigarette smoking in colorectal tumorigenesis and suggest that quitting smoking may substantially reduce the risk of colorectal polyps.</p>
]]></description>
<dc:creator><![CDATA[Shrubsole, M. J., Wu, H., Ness, R. M., Shyr, Y., Smalley, W. E., Zheng, W.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm400</dc:identifier>
<dc:title><![CDATA[Alcohol Drinking, Cigarette Smoking, and Risk of Colorectal Adenomatous and Hyperplastic Polyps]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1058</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1050</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1059?rss=1">
<title><![CDATA[Hormonal Risk Factors for Ovarian Cancer in Premenopausal and Postmenopausal Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1059?rss=1</link>
<description><![CDATA[
<p>Ovarian cancer is most frequently diagnosed in postmenopausal women; however, the strongest risk predictors, pregnancy and oral contraceptive use, occur in most women in their twenties and thirties. Relatively few studies have examined how reproductive risk factors vary between pre- and postmenopausal ovarian cancer. The authors used data from a population-based, case-control study of ovarian cancer (896 cases, 967 controls) conducted in North Carolina from 1999 to 2006. Odds ratios and 95% confidence intervals were calculated by using unconditional logistic regression. Inverse associations with ovarian cancer were observed with duration of oral contraceptive use, later age at last use, and more recent use among premenopausal women; no significant associations were found for postmenopausal women. Analyses limited to oral contraceptive users showed that duration was a more significant predictor of risk than was timing of use. Parity was inversely associated with premenopausal but not postmenopausal ovarian cancer. Later age at pregnancy was associated with reduced risk for both pre- and postmenopausal women. Analyses among parous women showed that pregnancy timing was a stronger risk predictor than number of pregnancies. Findings suggest that associations between ovarian cancer and reproductive characteristics vary by menopausal status. Additional research is needed to further elucidate risk factors for postmenopausal disease.</p>
]]></description>
<dc:creator><![CDATA[Moorman, P. G., Calingaert, B., Palmieri, R. T., Iversen, E. S., Bentley, R. C., Halabi, S., Berchuck, A., Schildkraut, J. M.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn006</dc:identifier>
<dc:title><![CDATA[Hormonal Risk Factors for Ovarian Cancer in Premenopausal and Postmenopausal Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1069</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1059</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1070?rss=1">
<title><![CDATA[Dietary Boron and Hormone Replacement Therapy as Risk Factors for Lung Cancer in Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1070?rss=1</link>
<description><![CDATA[
<p>Hormone replacement therapy (HRT) may reduce lung cancer risk. Dietary boron may have actions similar to those of HRT; however, no previous study has reported the associations between dietary boron intake and lung cancer risk or the joint effects of boron intake and HRT use on lung cancer risk. The authors examined the associations between boron intake and the joint effects of boron intake and HRT on lung cancer risk in women. In an ongoing case-control study in Houston, Texas (July 1995 through April 2005, end date for this analysis), 763 women were diagnosed with lung cancer, and 838 were matched healthy controls with data on both diet and HRT. Multiple logistic regression analyses were conducted to assess the associations between dietary boron and HRT with lung cancer risk. After adjustment for potential confounders, the odds ratios for lung cancer with decreasing quartiles of dietary boron intake were 1.0, 1.39 (95% confidence interval (CI): 1.02, 1.90), 1.64 (95% CI: 1.20, 2.24), and 1.95 (95% CI: 1.42, 2.68) mg/day, respectively, for all women (<I>p</I><SUB>trend</SUB> &lt; 0.0001). In joint-effects analyses, compared with women with high dietary boron intake who used HRT, the odds ratio for lung cancer for low dietary boron intake and no HRT use was 2.07 (95% CI: 1.53, 2.81). Boron intake was inversely associated with lung cancer in women, whereas women who consumed low boron and did not use HRT were at substantial increased odds.</p>
]]></description>
<dc:creator><![CDATA[Mahabir, S., Spitz, M. R., Barrera, S. L., Dong, Y. Q., Eastham, C., Forman, M. R.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn021</dc:identifier>
<dc:title><![CDATA[Dietary Boron and Hormone Replacement Therapy as Risk Factors for Lung Cancer in Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1080</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1070</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1081?rss=1">
<title><![CDATA[Smoking and Lymphoma Risk in the European Prospective Investigation into Cancer and Nutrition]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1081?rss=1</link>
<description><![CDATA[
<p>Lymphomas are one of the few cancers that have been increasing in incidence over the past decades. So far, only a few established risk factors have been identified, including immunosuppression and viral infections. Recent evidence suggests etiologic heterogeneity of different lymphoma subtypes. Smoking may affect risk differently, depending on the lymphoma entity. The European Prospective Investigation into Cancer and Nutrition was used to study the role of smoking in the etiology of lymphomas and individual subtypes within a prospective study. Information on baseline and lifetime tobacco smoking by 478,590 participants was collected between 1992 and 2000. Cox proportional hazards regression was used to calculate multivariate-adjusted hazard ratios and 95% confidence intervals. During 3,567,410 person-years of follow-up, 1,371 lymphoma cases (1,304 non-Hodgkin's lymphomas and 67 Hodgkin's lymphomas) were identified. Relative risk for smokers at recruitment was more than twofold higher for Hodgkin's lymphoma (hazard ratio = 2.14, 95% confidence interval: 1.18, 3.87) but was not elevated for non-Hodgkin's lymphoma (hazard ratio = 1.06, 95% confidence interval: 0.94, 1.19) and individual B-cell non-Hodgkin's lymphoma subtypes. In this prospective study, smoking appeared to increase Hodgkin's lymphoma risk consistently in both genders, whereas B-cell non&ndash;Hodgkin's lymphoma risk was not associated. Future analysis should involve viral biomarkers and genetic susceptibility markers to elucidate potential mechanisms of smoking-induced carcinogenesis, particularly for Hodgkin's lymphoma.</p>
]]></description>
<dc:creator><![CDATA[Nieters, A., Rohrmann, S., Becker, N., Linseisen, J., Ruediger, T., Overvad, K., Tjonneland, A., Olsen, A., Allen, N. E., Travis, R. C., Bingham, S., Khaw, K.-T., Ardanaz, E., Redondo, M. L., Basterrechea, M., Martinez, C., Tormo, M.-J., Rosso, S., Tagliabue, G., Masala, G., Mattiello, A., Tumino, R., Boeing, H., Bergmann, M., Kaaks, R., Trichopoulou, A., Trichopoulos, D., Peeters, P. H., Bueno-de-Mesquita, B., Boffetta, P., Brennan, P., Ferrari, P., Neasham, D., Lund, E., Berglund, G., Manjer, J., Hallmans, G., Johansson, I., Vineis, P., Riboli, E.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn004</dc:identifier>
<dc:title><![CDATA[Smoking and Lymphoma Risk in the European Prospective Investigation into Cancer and Nutrition]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1089</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1081</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1090?rss=1">
<title><![CDATA[Pulmonary Function and the Risk of Functional Limitation in Chronic Obstructive Pulmonary Disease]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1090?rss=1</link>
<description><![CDATA[
<p>The authors' objective was to analyze the impact of respiratory impairment on the risk of physical functional limitations among adults with chronic obstructive pulmonary disease (COPD). They hypothesized that greater pulmonary function decrement would result in a broad array of physical functional limitations involving organ systems remote from the lung, a key step in the pathway leading to overall disability. The authors used baseline data from the Function, Living, Outcomes, and Work (FLOW) study, a prospective cohort study of adults with COPD recruited from northern California in 2005&ndash;2007. They studied the impact of pulmonary function impairment on the risk of functional limitations using validated measures: lower extremity function (Short Physical Performance Battery), submaximal exercise performance (6-Minute Walk Test), standing balance (Functional Reach Test), skeletal muscle strength (manual muscle testing with dynamometry), and self-reported functional limitation (standardized item battery). Multiple variable analysis was used to control for confounding by age, sex, race, height, educational attainment, and cigarette smoking. Greater pulmonary function impairment, as evidenced by lower forced expiratory volume in 1 second (FEV<SUB>1</SUB>), was associated with poorer Short Physical Performance Battery scores and less distance walked during the 6-Minute Walk Test. Lower forced expiratory volume in 1 second was also associated with weaker muscle strength and with a greater risk of self-reported functional limitation (<I>p</I> &lt; 0.05). In conclusion, pulmonary function impairment is associated with multiple manifestations of physical functional limitation among COPD patients. Longitudinal follow-up can delineate the impact of these functional limitations on the prospective risk of disability, guiding preventive strategies that could attenuate the disablement process.</p>
]]></description>
<dc:creator><![CDATA[Eisner, M. D., Iribarren, C., Yelin, E. H., Sidney, S., Katz, P. P., Ackerson, L., Lathon, P., Tolstykh, I., Omachi, T., Byl, N., Blanc, P. D.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn025</dc:identifier>
<dc:title><![CDATA[Pulmonary Function and the Risk of Functional Limitation in Chronic Obstructive Pulmonary Disease]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1101</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1090</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1102?rss=1">
<title><![CDATA[Gang Exposure and Pregnancy Incidence among Female Adolescents in San Francisco: Evidence for the Need to Integrate Reproductive Health with Violence Prevention Efforts]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1102?rss=1</link>
<description><![CDATA[
<p>Among a cohort of 237 sexually active females aged 14&ndash;19 years recruited from community venues in a predominantly Latino neighborhood in San Francisco, California, the authors examined the relation between gang exposure and pregnancy incidence over 2 years of follow-up between 2001 and 2004. Using discrete-time survival analysis, they investigated whether gang membership by individuals and partners was associated with pregnancy incidence and determined whether partnership characteristics, contraceptive behaviors, and pregnancy intentions mediated the relation between gang membership and pregnancy. Pregnancy incidence was determined by urine-based testing and self-report. Latinas represented 77% of participants, with one in five born outside the United States. One quarter (27.4%) became pregnant over follow-up. Participants' gang membership had no significant effect on pregnancy incidence (hazard ratio = 1.25, 95% confidence interval: 0.54, 3.45); however, having partners who were in gangs was associated with pregnancy (hazard ratio = 1.90, 95% confidence interval: 1.09, 3.32). The male partner's perceived pregnancy intentions and having a partner in detention each mediated the effect of partner's gang membership on pregnancy risk. Increased pregnancy incidence among young women with gang-involved partners highlights the importance of integrating reproductive health prevention into programs for gang-involved youth. In addition, high pregnancy rates indicate a heightened risk for sexually transmitted infections.</p>
]]></description>
<dc:creator><![CDATA[Minnis, A. M., Moore, J. G., Doherty, I. A., Rodas, C., Auerswald, C., Shiboski, S., Padian, N. S.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn011</dc:identifier>
<dc:title><![CDATA[Gang Exposure and Pregnancy Incidence among Female Adolescents in San Francisco: Evidence for the Need to Integrate Reproductive Health with Violence Prevention Efforts]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1109</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1102</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1110?rss=1">
<title><![CDATA[The Association between Obesity and the Prevalence of Low Back Pain in Young Adults: The Cardiovascular Risk in Young Finns Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1110?rss=1</link>
<description><![CDATA[
<p>Both low back pain (LBP) and obesity are common public health problems, yet their relation remains controversial. The aim of this study was to investigate the associations between weight-related factors and the prevalence of LBP in young adults in Finland. Participants in the ongoing Cardiovascular Risk in Young Finns Study aged 24&ndash;39 years were included (<I>N</I> = 2,575). In 2001, 31.2% of men and 39.5% of women reported LBP with recovery within a month or recurrent or continuous pain during the preceding 12 months. For women only, those with higher body mass index, waist circumference, hip circumference, waist-to-hip ratio, serum leptin level, and C-reactive protein level showed an increased prevalence of LBP. With all weight-related factors in the model, only waist circumference was related to LBP in women. For women, the odds ratios of LBP were 1.2 (95% confidence interval: 0.8, 1.8) for a waist circumference of 80&ndash;87.9 cm and 1.8 (95% confidence interval: 1.0, 3.2) for a waist circumference of &ge;88 cm compared with a waist circumference of &lt;80 cm. This association was independent of C-reactive protein, leptin, and adiponectin levels. The authors' findings in a relatively young population suggest that abdominal obesity may increase the risk of LBP in women.</p>
]]></description>
<dc:creator><![CDATA[Shiri, R., Solovieva, S., Husgafvel-Pursiainen, K., Taimela, S., Saarikoski, L. A., Huupponen, R., Viikari, J., Raitakari, O. T., Viikari-Juntura, E.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn007</dc:identifier>
<dc:title><![CDATA[The Association between Obesity and the Prevalence of Low Back Pain in Young Adults: The Cardiovascular Risk in Young Finns Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1119</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1110</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1120?rss=1">
<title><![CDATA[Evidence from Nonrandomized Studies: A Case Study on the Estimation of Causal Effects]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1120?rss=1</link>
<description><![CDATA[
<p>Although randomized controlled trials are regarded as the gold standard for comparison of treatments, evidence from observational studies is still relevant. To cope with the problem of possible confounding in these studies, investigators need methods for analyzing their results which adjust for confounders and lead to unbiased estimation of the treatment effect. In this paper, the authors describe the main principles of three statistical methods for doing this. The first method is the classical approach of a multiple regression model including the effects of treatment and covariates. This considers the relation between prognostic factors and the outcome variable as a relevant criterion for adjustment. The second method is based on the propensity score, focusing on the relation between prognostic factors and treatment assignment. The third method is an ecologic approach using a grouped treatment variable, which may aid in avoiding confounding by indication. These approaches are applied to a partially randomized trial conducted in 720 German breast cancer patients between 1984 and 1997. The study had a comprehensive cohort study design that included recruitment of patients who had consented to participation but not to randomization because of a preference for one of the treatments. This design offers a unique opportunity to contrast results from the nonrandomized portion of a study with those for a randomized subcohort as a reference.</p>
]]></description>
<dc:creator><![CDATA[Schmoor, C., Caputo, A., Schumacher, M.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn010</dc:identifier>
<dc:title><![CDATA[Evidence from Nonrandomized Studies: A Case Study on the Estimation of Causal Effects]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1129</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1120</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1130?rss=1">
<title><![CDATA[Detecting Trends in Noisy Data Series: Application to Biomarker Series]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1130?rss=1</link>
<description><![CDATA[
<p>It is common to define a change in health status or in a disease state on the basis of a sustained rise (or decline) in a biomarker over time. However, such observations are often subject to important variability unrelated to the underlying biologic process. The authors propose a method to evaluate rules that define an event on the basis of consecutive increases (or decreases) in the observations, given the presence of random variation. They examine how well these rules correctly identify a truly rising biomarker trajectory and, conversely, how often they can recognize a truly stable series or a slowly rising series. The method relies on simulation of realistic, sophisticated data sets that accurately reflect the systematic and random variations observed in marker series. These flexible, empirically based simulations enable estimation of the sensitivity and specificity of rules of consecutive rises as a function of the underlying trend, amount of random variation, and schedule of measurements (frequency and duration of follow-up). The authors illustrate the approach with postradiotherapy series of prostate-specific antigen, where three consecutive rises in prostate-specific antigen indicate treatment failure; the data are described by using a Bayesian hierarchical changepoint model. The method is particularly flexible and could be applied to evaluate other rules that purport to accurately detect upturns (downturns) in other noisy data series, including other medical data or other application areas.</p>
]]></description>
<dc:creator><![CDATA[Bellera, C. A., Hanley, J. A., Joseph, L., Albertsen, P. C.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn003</dc:identifier>
<dc:title><![CDATA[Detecting Trends in Noisy Data Series: Application to Biomarker Series]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1139</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1130</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1140?rss=1">
<title><![CDATA[RE: "A PROSPECTIVE STUDY OF THE EFFECTIVENESS OF THE NEW ZEALAND MENINGOCOCCAL B VACCINE"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1140?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lennon, D., Stewart, J., Crengle, S.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn051</dc:identifier>
<dc:title><![CDATA[RE: "A PROSPECTIVE STUDY OF THE EFFECTIVENESS OF THE NEW ZEALAND MENINGOCOCCAL B VACCINE"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1141</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1140</prism:startingPage>
<prism:section>LETTER</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1141?rss=1">
<title><![CDATA[THE AUTHORS REPLY]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1141?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kelly, C., Arnold, R., Galloway, Y., O'Hallahan, J.]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn050</dc:identifier>
<dc:title><![CDATA[THE AUTHORS REPLY]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1142</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1141</prism:startingPage>
<prism:section>LETTER</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/9/1142?rss=1">
<title><![CDATA[RE: "INVITED COMMENTARY: VARIABLE SELECTION VERSUS SHRINKAGE IN THE CONTROL OF MULTIPLE CONFOUNDERS"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/9/1142?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-04-25</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn088</dc:identifier>
<dc:title><![CDATA[RE: "INVITED COMMENTARY: VARIABLE SELECTION VERSUS SHRINKAGE IN THE CONTROL OF MULTIPLE CONFOUNDERS"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1142</prism:endingPage>
<prism:publicationDate>2008-05-01</prism:publicationDate>
<prism:startingPage>1142</prism:startingPage>
<prism:section>CORRECTION</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/889?rss=1">
<title><![CDATA[An Overview of Methods for Monitoring Social Disparities in Cancer with an Example Using Trends in Lung Cancer Incidence by Area-Socioeconomic Position and Race-Ethnicity, 1992-2004]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/889?rss=1</link>
<description><![CDATA[
<p>The authors provide an overview of methods for summarizing social disparities in health using the example of lung cancer. They apply four measures of relative disparity and three measures of absolute disparity to trends in US lung cancer incidence by area-socioeconomic position and race-ethnicity from 1992 to 2004. Among females, measures of absolute and relative disparity suggested that area-socioeconomic and race-ethnic disparities increased over these 12 years but differed widely with respect to the magnitude of the change. Among males, the authors found substantial disagreement among summary measures of relative disparity with respect to the magnitude and the direction of change in disparities. Among area-socioeconomic groups, the index of disparity increased by 47% and the relative concentration index decreased by 116%, while for race-ethnicity the index of disparity increased by 36% and the Theil index increased by 13%. The choice of a summary measure of disparity may affect the interpretation of changes in health disparities. Important issues to consider are the reference point from which differences are measured, whether to measure disparity on the absolute or relative scale, and whether to weight disparity measures by population size. A suite of indicators is needed to provide a clear picture of health disparity change.</p>
]]></description>
<dc:creator><![CDATA[Harper, S., Lynch, J., Meersman, S. C., Breen, N., Davis, W. W., Reichman, M. E.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn016</dc:identifier>
<dc:title><![CDATA[An Overview of Methods for Monitoring Social Disparities in Cancer with an Example Using Trends in Lung Cancer Incidence by Area-Socioeconomic Position and Race-Ethnicity, 1992-2004]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>899</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>889</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/900?rss=1">
<title><![CDATA[Invited Commentary: Measuring Social Disparities in Health--What Was the Question Again?]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/900?rss=1</link>
<description><![CDATA[
<p>Monitoring social disparities in health is not a straightforward project. Defining what constitutes a disparity is challenging, and multiple measures have been proposed to track changes in disparity over time. In this issue, Harper et al. (Am J Epidemiol 2008;167:889&ndash;899) present seven health disparity measures and apply them to US lung cancer incidence rates (1992&ndash;2004). They find that different summary measures provide different answers to the question "Has disparity increased or decreased?" Their findings leave us uncertain how to use and interpret these measures to track changes in social disparities in health. In this invited commentary, the author proposes that increased attention to the scale at which disparities are measured, the interpretations attached to the various measures used, and the way in which these measures are assembled on the basis of conceptual models would benefit the field. Specifically, attention to these three areas would increase the capacity to communicate research findings to the public and policy-making consumers of disparity-related research.</p>
]]></description>
<dc:creator><![CDATA[Messer, L. C.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn019</dc:identifier>
<dc:title><![CDATA[Invited Commentary: Measuring Social Disparities in Health--What Was the Question Again?]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>904</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>900</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/905?rss=1">
<title><![CDATA[Harper et al. Respond to "Measuring Social Disparities in Health"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/905?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Harper, S., Lynch, J., Meersman, S. C., Breen, N., Davis, W. W., Reichman, M. E.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn015</dc:identifier>
<dc:title><![CDATA[Harper et al. Respond to "Measuring Social Disparities in Health"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>907</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>905</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/908?rss=1">
<title><![CDATA[Overcoming Ecologic Bias using the Two-Phase Study Design]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/908?rss=1</link>
<description><![CDATA[
<p>Ecologic (aggregate) data are widely available and widely utilized in epidemiologic studies. However, ecologic bias, which arises because aggregate data cannot characterize within-group variability in exposure and confounder variables, can only be removed by supplementing ecologic data with individual-level data. Here the authors describe the two-phase study design as a framework for achieving this objective. In phase 1, outcomes are stratified by any combination of area, confounders, and error-prone (or discretized) versions of exposures of interest. Phase 2 data, sampled within each phase 1 stratum, provide accurate measures of exposure and possibly of additional confounders. The phase 1 aggregate-level data provide a high level of statistical power and a cross-classification by which individuals may be efficiently sampled in phase 2. The phase 2 individual-level data then provide a control for ecologic bias by characterizing the within-area variability in exposures and confounders. In this paper, the authors illustrate the two-phase study design by estimating the association between infant mortality and birth weight in several regions of North Carolina for 2000&ndash;2004, controlling for gender and race. This example shows that the two-phase design removes ecologic bias and produces gains in efficiency over the use of case-control data alone. The authors discuss the advantages and disadvantages of the approach.</p>
]]></description>
<dc:creator><![CDATA[Wakefield, J., Haneuse, S. J.-P. A.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm386</dc:identifier>
<dc:title><![CDATA[Overcoming Ecologic Bias using the Two-Phase Study Design]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>916</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>908</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/917?rss=1">
<title><![CDATA[Associations of the Local Food Environment with Diet Quality--A Comparison of Assessments based on Surveys and Geographic Information Systems: The Multi-Ethnic Study of Atherosclerosis]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/917?rss=1</link>
<description><![CDATA[
<p>There is growing interest in understanding how food environments affect diet, but characterizing the food environment is challenging. The authors investigated the relation between global diet measures (an empirically derived "fats and processed meats" (FPM) dietary pattern and the Alternate Healthy Eating Index (AHEI)) and three complementary measures of the local food environment: 1) supermarket density, 2) participant-reported assessments, and 3) aggregated survey responses of independent informants. Data were derived from the baseline examination (2000&ndash;2002) of the Multi-Ethnic Study of Atherosclerosis, a US study of adults aged 45&ndash;84 years. A healthy diet was defined as scoring in the top or bottom quintile of AHEI or FPM, respectively. The probability of having a healthy diet was modeled by each environment measure using binomial regression. Participants with no supermarkets near their homes were 25&ndash;46% less likely to have a healthy diet than those with the most stores, after adjustment for age, sex, race/ethnicity, and socioeconomic indicators: The relative probability of a healthy diet for the lowest store density category versus the highest was 0.75 (95% confidence interval: 0.59, 0.95) for the AHEI and 0.54 (95% confidence interval: 0.42, 0.70) for FPM. Similarly, participants living in areas with the worst-ranked food environments (by participants or informants) were 22&ndash;35% less likely to have a healthy diet than those in the best-ranked food environments. Efforts to improve diet may benefit from combining individual and environmental approaches.</p>
]]></description>
<dc:creator><![CDATA[Moore, L. V., Diez Roux, A. V., Nettleton, J. A., Jacobs, D. R.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm394</dc:identifier>
<dc:title><![CDATA[Associations of the Local Food Environment with Diet Quality--A Comparison of Assessments based on Surveys and Geographic Information Systems: The Multi-Ethnic Study of Atherosclerosis]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>924</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>917</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/925?rss=1">
<title><![CDATA[Dietary Patterns, Supplement Use, and the Risk of Symptomatic Benign Prostatic Hyperplasia: Results from the Prostate Cancer Prevention Trial]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/925?rss=1</link>
<description><![CDATA[
<p>This study examined dietary risk factors for incident benign prostatic hyperplasia (BPH) in 4,770 Prostate Cancer Prevention Trial (1994&ndash;2003) placebo-arm participants who were free of BPH at baseline. BPH was assessed over 7 years and was defined as medical or surgical treatment or repeated elevation (&gt;14) on the International Prostate Symptom Score questionnaire. Diet, alcohol, and supplement use were assessed by use of a food frequency questionnaire. There were 876 incident BPH cases (33.6/1,000 person-years). The hazard ratios for the contrasts of the highest to lowest quintiles increased 31% for total fat and 27% for polyunsaturated fat and decreased 15% for protein (all <I>p</I><SUB>trend</SUB> &lt; 0.05). The risk was significantly lower in high consumers of alcoholic beverages (0 vs. &ge;2/day: hazard ratio (HR) = 0.67) and vegetables (&lt;1 vs. &ge;4/day: HR = 0.68) and higher in daily (vs. &lt;1/week) consumers of red meat (HR = 1.38). There were no associations of supplemental antioxidants with risk, and there was weak evidence for associations of lycopene, zinc, and supplemental vitamin D with reduced risk. A diet low in fat and red meat and high in protein and vegetables, as well as regular alcohol consumption, may reduce the risk of symptomatic BPH.</p>
]]></description>
<dc:creator><![CDATA[Kristal, A. R., Arnold, K. B., Schenk, J. M., Neuhouser, M. L., Goodman, P., Penson, D. F., Thompson, I. M.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm389</dc:identifier>
<dc:title><![CDATA[Dietary Patterns, Supplement Use, and the Risk of Symptomatic Benign Prostatic Hyperplasia: Results from the Prostate Cancer Prevention Trial]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>934</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>925</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/935?rss=1">
<title><![CDATA[Dietary Intake Related to Prevalent Functional Limitations in Midlife Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/935?rss=1</link>
<description><![CDATA[
<p>Physical functioning measures are considered integrated markers of the aging process. This prospective investigation examined relations between dietary intake of women at midlife in 1996&ndash;1997 and prevalence of physical functioning limitations 4 years later, defined by the Medical Outcomes Study Short-Form 36. The sample included 2,160 multiethnic women, aged 42&ndash;52 years, from six geographic areas participating in the Study of Women's Health Across the Nation (SWAN). Associations between measures of diet quality and number of fruit and vegetable servings and prevalent physical functional limitations (no, moderate, or substantial limitations) were tested by logistic regression. The prevalence of moderate and substantial functional limitations was 31% and 10%, respectively. Women in the highest quartile of cholesterol intake had 40% greater odds (odds ratio = 1.4, 95% confidence interval: 1.1, 1.8) of being more limited versus those in the lowest quartile. Women in the highest quartile of fat and saturated fat intakes were 50% and 60% more likely to be more limited, with respective odds ratios of 1.5 and 1.6 (95% confidence intervals: 1.2, 2.0 and 1.2, 2.1) versus those in the lowest quartiles. Lower fruit, vegetable, and fiber intakes were related to reporting greater functional limitations. Modifying dietary practices could be important in minimizing physical limitations.</p>
]]></description>
<dc:creator><![CDATA[Tomey, K. M., Sowers, M. R., Crandall, C., Johnston, J., Jannausch, M., Yosef, M.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm397</dc:identifier>
<dc:title><![CDATA[Dietary Intake Related to Prevalent Functional Limitations in Midlife Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>943</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>935</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/944?rss=1">
<title><![CDATA[Association between Neighborhood Active Living Potential and Walking]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/944?rss=1</link>
<description><![CDATA[
<p>This paper examines the association between neighborhood active living potential and walking among middle-aged and older adults. A sample of 2,614 (61.1% women) persons aged 45 years or older and living in one of 112 census tracts in Montreal, Canada, were recruited between February and May of 2005 to participate in a 20-minute telephone survey. Data were linked to observational data on neighborhood active living potential in the 112 census tracts and analyzed through multilevel modeling. Greater density of destinations in the census tract was associated with greater likelihoods of walking for any reason at least 5 days per week for at least 30 minutes (odds ratio = 1.53, 95% confidence interval: 1.21, 1.94). Associations were attenuated but remained statistically significant after controlling for socioeconomic, health, lifestyle, and other physical activity characteristics. Sensitivity analyses showed that associations were robust across smaller and larger volumes of walking. No associations were found between dimensions of neighborhood active living potential and walking for recreational reasons. The authors conclude that a larger number and variety of neighborhood destinations in one's residential environment are associated with more walking and possibly more utilitarian walking among middle-aged or older adults.</p>
]]></description>
<dc:creator><![CDATA[Gauvin, L., Riva, M., Barnett, T., Richard, L., Craig, C. L., Spivock, M., Laforest, S., Laberge, S., Fournel, M.-C., Gagnon, H., Gagne, S.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm391</dc:identifier>
<dc:title><![CDATA[Association between Neighborhood Active Living Potential and Walking]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>953</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>944</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/954?rss=1">
<title><![CDATA[Folate, Vitamin B6, Vitamin B12, and Methionine Intakes and Risk of Stroke Subtypes in Male Smokers]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/954?rss=1</link>
<description><![CDATA[
<p>The associations of dietary folate, vitamin B<SUB>6</SUB>, vitamin B<SUB>12</SUB>, and methionine intakes with risk of stroke subtypes were examined among 26,556 male Finnish smokers, aged 50&ndash;69 years, enrolled in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Dietary intake was assessed at baseline by using a validated food frequency questionnaire. During a mean follow-up of 13.6 years, from 1985 through 2004, 2,702 cerebral infarctions, 383 intracerebral hemorrhages, and 196 subarachnoid hemorrhages were identified from national registers. In analyses adjusting for age and cardiovascular risk factors, a high folate intake was associated with a statistically significant lower risk of cerebral infarction but not intracerebral or subarachnoid hemorrhages. The multivariate relative risk of cerebral infarction was 0.80 (95% confidence interval: 0.70, 0.91; <I>p</I><SUB>trend</SUB> = 0.001) for men in the highest versus lowest quintile of folate intake. Vitamin B<SUB>6</SUB>, vitamin B<SUB>12</SUB>, and methionine intakes were not significantly associated with any subtype of stroke. These findings in men suggest that a high dietary folate intake may reduce the risk of cerebral infarction.</p>
]]></description>
<dc:creator><![CDATA[Larsson, S. C., Mannisto, S., Virtanen, M. J., Kontto, J., Albanes, D., Virtamo, J.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm395</dc:identifier>
<dc:title><![CDATA[Folate, Vitamin B6, Vitamin B12, and Methionine Intakes and Risk of Stroke Subtypes in Male Smokers]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>961</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>954</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/962?rss=1">
<title><![CDATA[Prevalence of and Risk Factors for Subclinical Cardiovascular Disease in Selected US Hispanic Ethnic Groups: The Multi-Ethnic Study of Atherosclerosis]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/962?rss=1</link>
<description><![CDATA[
<p>In this study, the authors determined the prevalence and extent of cardiovascular disease (CVD) risk factors and subclinical CVD in four US Hispanic subgroups, as well as associations between the CVD risk factors and subclinical CVD in these groups. Participants were 1,437 Hispanic men and women enrolled in the Multi-Ethnic Study of Atherosclerosis in 2000&ndash;2002. Fifty-six percent were Mexican-American, 12% were Dominican-American, 14% were Puerto Rican-American, and 18% were Other Hispanic-American. All participants underwent clinical examinations for coronary artery calcium, thoracic aortic calcium, carotid intimal-medial thickness, ankle-brachial index, left ventricular mass, and left ventricular size. Mexican Americans had the highest levels of coronary artery calcium, thoracic aortic calcium, and carotid intimal-medial thickness, while Puerto Rican Americans had the highest prevalence of an ankle-brachial index less than 1.0 and levels of left ventricular mass. The magnitudes of the associations between coronary artery calcium and age, sex, and body mass index were similar across all Hispanic subgroups. However, there were differences in the magnitude and significance of the associations between coronary artery calcium and hypertension, hypercholesterolemia, and cigarette smoking among the different Hispanic subgroups. This finding was also present for the other subclinical CVD measures. These results suggest a differential relationship between risk factors and either prevalence or extent of subclinical disease by Hispanic subgroup.</p>
]]></description>
<dc:creator><![CDATA[Allison, M. A., Budoff, M. J., Wong, N. D., Blumenthal, R. S., Schreiner, P. J., Criqui, M. H.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm402</dc:identifier>
<dc:title><![CDATA[Prevalence of and Risk Factors for Subclinical Cardiovascular Disease in Selected US Hispanic Ethnic Groups: The Multi-Ethnic Study of Atherosclerosis]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>969</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>962</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/970?rss=1">
<title><![CDATA[Cigarette Smoking and Cancer: Intensity Patterns in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study in Finnish Men]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/970?rss=1</link>
<description><![CDATA[
<p>Relative risks for lung and bladder cancers by smoking intensity level off at more than 15&ndash;20 cigarettes per day. A three-parameter excess relative risk model in pack-years and intensity quantified this leveling (Lubin et al., <I>Am J Epidemiol</I> 2007;166:479&ndash;89). Above 15&ndash;20 cigarettes per day was an "inverse exposure rate" effect whereby, for equal pack-years, the excess relative risk/pack-year decreased with increasing intensity; that is, smoking at a lower intensity for a longer duration was more deleterious than smoking at a higher intensity for a shorter duration. After adjustment for pack-years, intensity effects were quantitatively homogeneous across multiple case-control studies of lung, bladder, oral cavity, pancreas, and esophagus cancers. The authors extended those analyses to examine intensity patterns for incident bladder, esophagus, kidney, larynx, liver, lung, oropharynx, and pancreas cancers by using data from a single prospective cohort in Finland, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, with follow-up from enrollment, which occurred between 1985 and 1988, through April 2004. At more than 10 cigarettes per day, they found an inverse exposure rate pattern for each cancer site. After adjustment for pack-years, intensity effects were quantitatively homogeneous across the diverse cancer sites and homogeneous with intensity effects from the prior analysis of multiple studies. Consistency of intensity patterns suggested a general phenomenon and may provide clues to the molecular basis of smoking-related cancer risk.</p>
]]></description>
<dc:creator><![CDATA[Lubin, J. H., Virtamo, J., Weinstein, S. J., Albanes, D.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm392</dc:identifier>
<dc:title><![CDATA[Cigarette Smoking and Cancer: Intensity Patterns in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study in Finnish Men]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>975</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>970</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/976?rss=1">
<title><![CDATA[Occupational Exposure to Pesticides and Risk of Adult Brain Tumors]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/976?rss=1</link>
<description><![CDATA[
<p>The authors examined incident glioma and meningioma risk associated with occupational exposure to insecticides and herbicides in a hospital-based, case-control study of brain cancer. Cases were 462 glioma and 195 meningioma patients diagnosed between 1994 and 1998 in three US hospitals. Controls were 765 patients admitted to the same hospitals for nonmalignant conditions. Occupational histories were collected during personal interviews. Exposure to pesticides was estimated by use of a questionnaire, combined with pesticide measurement data abstracted from published sources. Using logistic regression models, the authors found no association between insecticide and herbicide exposures and risk for glioma and meningioma. There was no association between glioma and exposure to insecticides or herbicides, in men or women. Women who reported ever using herbicides had a significantly increased risk for meningioma compared with women who never used herbicides (odds ratio = 2.4, 95% confidence interval: 1.4, 4.3), and there were significant trends of increasing risk with increasing years of herbicide exposure (<I>p</I> = 0.01) and increasing cumulative exposure (<I>p</I> = 0.01). There was no association between meningioma and herbicide or insecticide exposure among men. These findings highlight the need to go beyond job title to elucidate potential carcinogenic exposures within different occupations.</p>
]]></description>
<dc:creator><![CDATA[Samanic, C. M., De Roos, A. J., Stewart, P. A., Rajaraman, P., Waters, M. A., Inskip, P. D.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm401</dc:identifier>
<dc:title><![CDATA[Occupational Exposure to Pesticides and Risk of Adult Brain Tumors]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>985</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>976</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/986?rss=1">
<title><![CDATA[Effect Modification by Community Characteristics on the Short-term Effects of Ozone Exposure and Mortality in 98 US Communities]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/986?rss=1</link>
<description><![CDATA[
<p>Previous research provided evidence of an association between short-term exposure to ozone and mortality risk and of heterogeneity in the risk across communities. The authors investigated whether this heterogeneity can be explained by community-specific characteristics: race, income, education, urbanization, transportation use, particulate matter and ozone levels, number of ozone monitors, weather, and use of air conditioning. Their study included data on 98 US urban communities for 1987 to 2000 from the National Morbidity, Mortality, and Air Pollution Study; US Census; and American Housing Survey. On average across the communities, a 10-ppb increase in the previous week's ozone level was associated with a 0.52% (95% posterior interval: 0.28, 0.77) increase in mortality. The authors found that community-level characteristics modify the relation between ozone and mortality. Higher effect estimates were associated with higher unemployment, fraction of the Black/African-American population, and public transportation use and with lower temperatures or prevalence of central air conditioning. These differences may relate to underlying health status, differences in exposure, or other factors. Results show that some segments of the population may face higher health burdens of ozone pollution.</p>
]]></description>
<dc:creator><![CDATA[Bell, M. L., Dominici, F.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm396</dc:identifier>
<dc:title><![CDATA[Effect Modification by Community Characteristics on the Short-term Effects of Ozone Exposure and Mortality in 98 US Communities]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>997</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>986</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/998?rss=1">
<title><![CDATA[Risk Factors for Chronic Obstructive Pulmonary Disease Mortality in Chinese Adults]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/998?rss=1</link>
<description><![CDATA[
<p>Chronic obstructive pulmonary disease mortality and risk factors were studied in a nationally representative sample of 169,871 Chinese men and women aged 40 years or older. Baseline data were collected in 1991 by using a standard protocol, and a follow-up evaluation was conducted in 1999&ndash;2000, with a response rate of 93.4%. Age-standardized mortality (per 100,000 person-years) was 179.9 for men and 141.3 for women. After adjustment for important covariables, the respective relative risks of chronic obstructive pulmonary disease&ndash;related mortality for baseline risk factors in men and women were 2.80 (95% confidence interval (CI): 2.64, 2.98) and 2.71 (95% CI: 2.53, 2.89) for each 10-year increase in age, 0.84 (95% CI: 0.74, 0.95) and 1.44 (95% CI: 1.07, 1.95) for alcohol consumption, 1.18 (95% CI: 1.04, 1.35) and 1.77 (95% CI: 1.45, 2.15) for &ge;20 pack-years of smoking, 2.37 (95% CI: 1.91, 2.94) and 2.47 (95% CI: 1.66, 3.67) for non-high-school graduation, 1.57 (95% CI: 1.38, 1.79) and 1.35 (95% CI: 1.17, 1.56) for physical inactivity, 2.66 (95% CI: 2.34, 3.02) and 2.60 (95% CI: 2.25, 3.00) for underweight, 1.39 (95% CI: 1.23, 1.57) and 1.73 (95% CI: 1.50, 2.00) for living in northern China, and 2.14 (95% CI: 1.86, 2.46) and 1.79 (95% CI: 1.55, 2.07) for living in rural China. This study indicated that cigarette smoking, low educational level, physical inactivity, and underweight are important modifiable risk factors for chronic obstructive pulmonary disease&ndash;related mortality in China.</p>
]]></description>
<dc:creator><![CDATA[Reilly, K. H., Gu, D., Duan, X., Wu, X., Chen, C.-S., Huang, J., Kelly, T. N., Chen, J., Liu, X., Yu, L., Bazzano, L. A., He, J.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm393</dc:identifier>
<dc:title><![CDATA[Risk Factors for Chronic Obstructive Pulmonary Disease Mortality in Chinese Adults]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1004</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>998</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/1005?rss=1">
<title><![CDATA[Weight Cycling and Risk of Forearm Fractures: A 28-Year Follow-up of Men in the Oslo Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/1005?rss=1</link>
<description><![CDATA[
<p>Weight cycling may lead to fractures in non-weight-bearing bone. The authors investigated the association between self-reported episodes of weight loss and forearm fracture in a cohort of elderly Norwegian men (<I>n</I> = 4,601; mean age = 71.6 years). Men initially examined in 1972&ndash;1973 as part of the population-based Oslo Study were reexamined in 2000. Weight and height were measured both times; histories of weight cycling (amount and frequency) and fracture and information on covariates were elicited by questionnaire. Irrespective of amount of weight loss, 35&ndash;43% of men reporting four or more weight loss episodes at ages 25&ndash;50 years had experienced a forearm fracture, as compared with 17&ndash;18% of men without weight loss episodes. For weight loss episodes that had occurred after age 50 years, associations were weaker. In an analysis limited to men whose last fracture had occurred after the weight loss episodes, the adjusted odds ratio for forearm fracture was 2.91 (95% confidence interval: 1.10, 7.64) for four or more weight loss episodes versus none. These findings suggest that weight cycling may predict forearm fracture in elderly men and indicate that the potentially harmful effects of weight cycling are related to the number of episodes occurring at ages 25&ndash;50 years.</p>
]]></description>
<dc:creator><![CDATA[Sogaard, A. J., Meyer, H. E., Tonstad, S., Haheim, L. L., Holme, I.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwm384</dc:identifier>
<dc:title><![CDATA[Weight Cycling and Risk of Forearm Fractures: A 28-Year Follow-up of Men in the Oslo Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1013</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>1005</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/1014?rss=1">
<title><![CDATA[Infectious Disease Epidemiology: Theory and Practice, Second Edition: By Kenrad E. Nelson and Carolyn F. Masters Williams]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/1014?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Padian, N.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn045</dc:identifier>
<dc:title><![CDATA[Infectious Disease Epidemiology: Theory and Practice, Second Edition: By Kenrad E. Nelson and Carolyn F. Masters Williams]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1015</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>1014</prism:startingPage>
<prism:section>REVIEW-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/1016?rss=1">
<title><![CDATA[FOUR AUTHORS REPLY]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/1016?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Margolis, K. L., Luo, J., Ye, W., Adami, H.-O., for the Women's Health Initiative Investigators]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn039</dc:identifier>
<dc:title><![CDATA[FOUR AUTHORS REPLY]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1016</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>1016</prism:startingPage>
<prism:section>LETTER</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/8/1016-a?rss=1">
<title><![CDATA[RE: "BODY SIZE, WEIGHT CYCLING, AND RISK OF RENAL CELL CARCINOMA AMONG POSTMENOPAUSAL WOMEN: THE WOMEN'S HEALTH INITIATIVE (UNITED STATES)"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/8/1016-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sharifi, N., Farrar, W. L.]]></dc:creator>
<dc:date>2008-04-11</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn040</dc:identifier>
<dc:title><![CDATA[RE: "BODY SIZE, WEIGHT CYCLING, AND RISK OF RENAL CELL CARCINOMA AMONG POSTMENOPAUSAL WOMEN: THE WOMEN'S HEALTH INITIATIVE (UNITED STATES)"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1016</prism:endingPage>
<prism:publicationDate>2008-04-15</prism:publicationDate>
<prism:startingPage>1016</prism:startingPage>
<prism:section>LETTER</prism:section>
</item>

</rdf:RDF>