Search

Background: A healthy diet, as defined by the US Dietary Guidelines for Americans (DGA), has been associated with lower morbidity and mortality from major chronic diseases in studies conducted in predominantly non-Hispanic white individuals. It is unknown whether this association can be extrapolated to African-Americans and low-income populations. Methods and Findings: We examined the associations of adherence to the DGA with total and cause-specific mortality in the Southern Community Cohort Study, a prospective study that recruited 84,735 American adults, aged 40–79 y, from 12 southeastern US states during 2002–2009, mostly through community health centers that serve low-income populations. The present analysis included 50,434 African-Americans, 24,054 white individuals, and 3,084 individuals of other racial/ethnic groups, among whom 42,759 participants had an annual household income less than US$15,000. Usual dietary intakes were assessed using a validated food frequency questionnaire at baseline. Adherence to the DGA was measured by the Healthy Eating Index (HEI), 2010 and 2005 editions (HEI-2010 and HEI-2005, respectively). During a mean follow-up of 6.2 y, 6,906 deaths were identified, including 2,244 from cardiovascular disease, 1,794 from cancer, and 2,550 from other diseases. A higher HEI-2010 score was associated with lower risks of disease death, with adjusted hazard ratios (HRs) of 0.80 (95% CI, 0.73–0.86) for all-disease mortality, 0.81 (95% CI, 0.70–0.94) for cardiovascular disease mortality, 0.81 (95% CI, 0.69–0.95) for cancer mortality, and 0.77 (95% CI, 0.67–0.88) for other disease mortality, when comparing the highest quintile with the lowest (all p-values for trend < 0.05). Similar inverse associations between HEI-2010 score and mortality were observed regardless of sex, race, and income (all p-values for interaction > 0.50). Several component scores in the HEI-2010, including whole grains, dairy, seafood and plant proteins, and ratio of unsaturated to saturated fatty acids, showed significant inverse associations with total mortality. HEI-2005 score was also associated with lower disease mortality, with a HR of 0.86 (95% CI, 0.79–0.93) when comparing extreme quintiles. Given the observational study design, however, residual confounding cannot be completely ruled out. In addition, future studies are needed to evaluate the generalizability of these findings to African-Americans of other socioeconomic status. Conclusions: Our results showed, to our knowledge for the first time, that adherence to the DGA was associated with lower total and cause-specific mortality in a low-income population, including a large proportion of African-Americans, living in the southeastern US. [ABSTRACT FROM AUTHOR]

Prior studies of risk factors associated with external causes of death have been limited in the number of covariates investigated and external causes examined. Herein, associations between numerous demographic, lifestyle, and health-related factors and the major causes of external mortality, such as suicide, homicide, and accident, were assessed prospectively among 73,422 black and white participants in the Southern Community Cohort Study (SCCS). Hazard ratios (HR) and 95% confidence intervals (CI) were calculated in multivariate regression analyses using the Cox proportional hazards model. Men compared with women (HR = 2.32; 95% CI: 1.87–2.89), current smokers (HR = 1.74; 95% CI: 1.40–2.17), and unemployed/never employed participants at the time of enrollment (HR = 1.67; 95% CI 1.38–2.02) had increased risk of dying from all external causes, with similarly elevated HRs for suicide, homicide, and accidental death among both blacks and whites. Blacks compared with whites had lower risk of accidental death (HR = 0.46; 95% CI: 0.38–0.57) and suicide (HR = 0.55; 95% CI: 0.31–0.99). Blacks and whites in the SCCS had comparable risks of homicide death (HR = 1.05; 95% CI: 0.63–1.76); however, whites in the SCCS had unusually high homicide rates compared with all whites who were resident in the 12 SCCS states, while black SCCS participants had homicide rates similar to those of all blacks residing in the SCCS states. Depression was the strongest risk factor for suicide, while being married was protective against death from homicide in both races. Being overweight/obese at enrollment was associated with reduced risks in all external causes of death, and the number of comorbid conditions was a risk factor for iatrogenic deaths. Most risk factors identified in earlier studies of external causes of death were confirmed in the SCCS cohort, in spite of the low SES of SCCS participants. Results from other epidemiologic cohorts are needed to confirm the novel findings identified in this study. [ABSTRACT FROM AUTHOR]

Purpose: The primary objective of this study is to examine the race-specific associations between statin use and overall mortality, as well as cardiovascular and cancer mortality, among blacks and whites in the Southeastern United States (US). Little is known about these associations in blacks. Patients and methods: The Southern Community Cohort Study is an ongoing, prospective cohort study, which enrolled from 2002 through 2009 nearly 86,000 participants aged 40-79 years. We used Cox regression models to estimate race-specific hazard ratios (HRs) and 95% confidence intervals (CI) for overall and cause-specific mortality associated with statin use based on self-reported hypercholesterolemia and treatment at cohort entry. Mean age at cohort entry was 51.4 years in blacks (n=48,825) and 53.5 years in whites (n=18,560). Sixty-one percent of participants were women. Whites were more likely to have self-reported hypercholesterolemia (40% versus 27%, P,0.001), and to report being treated with either statins (52% versus 47%, P,0.001) or combination lipid therapy (9% versus 4%, P,0.001) compared with blacks, regardless of sex. During follow-up (median: 5.6 years) 5,199 participants died. Compared with untreated hypercholesterolemic individuals, statin use was associated with reduced all-cause mortality (adjusted HR [aHR] 0.86; 95% CI 0.77-0.95) and cardiovascular disease mortality overall (aHR 0.75; 95% CI 0.64-0.89) and among whites (aHR 0.67; 95% CI 0.50-0.90), blacks (aHR, 0.80; 95% CI 0.65-0.98), men (aHR 0.70; 95% CI 0.55-0.90), and women (aHR 0.79; 95% CI 0.63-0.99) (P.0.05 for race and sex interaction). Statin use was not associated with cancer mortality overall or in subgroup analyses. Conclusion: Regardless of race or sex, self-reported statin use was linked to reduced all-cause and cardiovascular disease mortality. However, factors contributing to the modestly lower statin use and markedly lower prevalence of self-reported hypercholesterolemia among blacks remain to be determined. [ABSTRACT FROM AUTHOR]

Purpose: The primary objective of this study is to examine the race-specific associations between statin use and overall mortality, as well as cardiovascular and cancer mortality, among blacks and whites in the Southeastern United States (US). Little is known about these associations in blacks. Patients and methods: The Southern Community Cohort Study is an ongoing, prospective cohort study, which enrolled from 2002 through 2009 nearly 86,000 participants aged 40-79 years. We used Cox regression models to estimate race-specific hazard ratios (HRs) and 95% confidence intervals (CI) for overall and cause-specific mortality associated with statin use based on self-reported hypercholesterolemia and treatment at cohort entry. Mean age at cohort entry was 51.4 years in blacks (n=48,825) and 53.5 years in whites (n=18,560). Sixty-one percent of participants were women. Whites were more likely to have self-reported hypercholesterolemia (40% versus 27%, P,0.001), and to report being treated with either statins (52% versus 47%, P,0.001) or combination lipid therapy (9% versus 4%, P,0.001) compared with blacks, regardless of sex. During follow-up (median: 5.6 years) 5,199 participants died. Compared with untreated hypercholesterolemic individuals, statin use was associated with reduced all-cause mortality (adjusted HR [aHR] 0.86; 95% CI 0.77-0.95) and cardiovascular disease mortality overall (aHR 0.75; 95% CI 0.64-0.89) and among whites (aHR 0.67; 95% CI 0.50-0.90), blacks (aHR, 0.80; 95% CI 0.65-0.98), men (aHR 0.70; 95% CI 0.55-0.90), and women (aHR 0.79; 95% CI 0.63-0.99) (P.0.05 for race and sex interaction). Statin use was not associated with cancer mortality overall or in subgroup analyses. Conclusion: Regardless of race or sex, self-reported statin use was linked to reduced all-cause and cardiovascular disease mortality. However, factors contributing to the modestly lower statin use and markedly lower prevalence of self-reported hypercholesterolemia among blacks remain to be determined. [ABSTRACT FROM AUTHOR]

Background Trichloroethylene (TCE) is a widely used chlorinated solvent with demonstrated carcinogenicity in animal assays. Some epidemiologic studies have reported increased risk of cancer of the kidney, cervix, liver and biliary passages, non-Hodgkin lymphoma, and esophageal adenocarcinoma. Methods We established a pooled cohort, including 5553 workers with individual documented exposure to TCE in Finland, Sweden, and Denmark. Study participants were monitored for the urinary TCE metabolite trichloroacetic acid from 1947 to 1989 and followed for cancer. Standardized incidence ratios (SIRs) were calculated based on cancer incidence rates in the three national populations. Cox proportionate hazard analyses were used for internal comparisons.Tests of statistical significance are two-sided. Results Overall, 997 cases of cancer (n = 683 in men; n = 314 in women) were identified during 154 778 person-years of follow-up. We observed statistically significant elevated standardized incidence ratios for primary liver cancer (1.93; 95% confidence interval [Cl] = 1.19 to 2.95) and cervical cancer (2.31; 95% Cl = 1.32 to 3.75).The standardized incidence ratio for kidney cancer was 1.01 (95% Cl = 0.70 to 1.42) based on 32 cases; we did not observe a statistically significant increased risk of non-Hodgkin's lymphoma (SIR = 1.26; 95% Cl = 0.89 to 1.73) or esophageal adenocarcinoma (SIR = 1.84; 95% Cl = 0.65 to 4.65).Tobacco- and alcohol-associated cancers were not statistically significantly increased. Conclusions Our results suggest TCE exposure is possibly associated with an increased risk for liver cancer. The relationship between TCE exposure and risks of cancers of low incidence and those with confounding by lifestyle and other factors not known in our cohort require further study. [ABSTRACT FROM AUTHOR]

Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are used in a variety of consumer products and have been detected worldwide in human blood. Recent studies mainly of highly exposed populations have indicated that PFOA and PFOS may affect serum cholesterol levels, but the magnitude of the effect may be inconsistent across exposure levels. The aim of the present cross-sectional study was to investigate the association between plasma PFOA and PFOS and total cholesterol in a general, middle-aged Danish population. The study population comprised 753 individuals (663 men and 90 women), 50–65 years of age, nested within a Danish cohort of 57,053 participants. Blood samples were taken from all cohort members at enrolment (1993–1997) and stored in a biobank at -150°C. Plasma levels of PFOA and PFOS and serum levels of total cholesterol were measured. The associations between plasma PFOA and PFOS levels and total cholesterol levels were analysed by generalized linear models, both crude and adjusted for potential confounders. We observed statistically significant positive associations between both perfluorinated compounds and total cholesterol, e.g. a 4.4 [95% CI  =  1.1–7.8] higher concentration of total cholesterol (mg/dL) per interquartile range of PFOA plasma level. Sex and prevalent diabetes appeared to modify the association between PFOA and PFOS, respectively, and cholesterol. In conclusion, this study indicated positive associations between plasma PFOA and PFOS levels and total cholesterol in a middle-aged Danish population, although whether the observed pattern of results reflects a causal association is unclear. [ABSTRACT FROM AUTHOR]

We evaluated whether black race is associated with higher incidence of End Stage Renal Disease (ESRD) among a cohort of blacks and whites of similar, generally low socioeconomic status, and whether risk factor patterns differ among blacks and whites and explain the poorly understood racial disparity in ESRD. Incident diagnoses of ESRD among 79,943 black and white participants in the Southern Community Cohort Study (SCCS) were ascertained by linkage with the United States Renal Data System (USRDS) from 2002 through 2009. Person-years of follow up were calculated from date of entry into the SCCS until date of ESRD diagnosis, date of death, or September 1, 2009, whichever occurred first. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) for incident ESRD among black and white participants in relation to baseline characteristics. After 329,003 person-years of follow-up, 687 incident cases of ESRD were identified in the cohort. The age-adjusted ESRD incidence rate was 273 (per 100,000) among blacks, 3.5-fold higher than the rate of 78 among whites. Risk factors for ESRD included male sex (HR = 1.6; 95% CI 1.4-1.9), low income (HR = 1.5; 95% CI 1.2-1.8 for income below vs. above $15,000), smoking (HR = 1.2; 95% CI 1.02-1.4) and histories of diabetes (HRs increasing to 9.4 (95% CI 7.4-11.9) among those with ≥20 years diabetes duration) and hypertension (HR = 2.9; 95% CI 2.3- 3.7). Patterns and magnitudes of association were virtually identical among blacks and whites. After adjustment for these risk factors, blacks continued to have a higher risk for ESRD (HR = 2.4; 95% CI = 1.9-3.0) relative to whites. The black-white disparity in risk of ESRD was attenuated but not eliminated after control for known risk factors in a closely socioeconomically matched cohort. Further research characterizing biomedical factors, including CKD progression, in ESRD occurrence in these two racial groups is needed. [ABSTRACT FROM AUTHOR]

In recent pooled analyses among whites and Asians, mortality was shown to rise markedly with increasing body mass index (BMI; weight (kg)/height (m)2), but much less is known about this association among blacks. This study prospectively examined all-cause mortality in relation to BMI among 22,014 black males, 9,343 white males, 30,810 black females, and 14,447 white females, aged 40–79 years, from the Southern Community Cohort Study, an epidemiologic cohort of largely low-income participants in 12 southeastern US states. Participants enrolled in the cohort from 2002 to 2009 and were followed up to 8.9 years. Hazard ratios and 95% confidence intervals for mortality were obtained from sex- and race-stratified Cox proportional hazards models in association with BMI at cohort entry, adjusting for age, education, income, cigarette smoking, and alcohol consumption. Elevated BMI was associated with increased mortality among whites (hazard ratios for BMI >40 vs. 20–24.9 = 1.37 (95% confidence interval (CI): 1.02, 1.84) and 1.47 (95% CI: 1.15, 1.89) for white males and white females, respectively) but not significantly among blacks (hazard ratios = 1.13 (95% CI: 0.89, 1.43) and 0.87 (95% CI: 0.72, 1.04) for black males and black females, respectively). In this large cohort, obesity in mid-to-late adulthood among blacks was not associated with the same excess mortality risk seen among whites. [ABSTRACT FROM PUBLISHER]

Background. The number of women suitable for breast conserving treatment as well as immediate reconstruction after breast cancer has been increasing, and studies of complications hereafter are needed. Material and methods. The cohort was identified in the prospective database of the Danish Registry for Plastic Surgery of the Breast during the period 1999 to 2006; 167 women with 189 immediate breast reconstructions (40 one-stage and 149 two-stage procedures) after breast cancer without a history of radiation therapy. The women were followed for complications until November 2009. Cumulative incidence risks were computed for infection, hematoma, seroma, severe capsular contracture (modified Baker III and IV), extrusion of the implant, implant rupture, asymmetry/displacement of the implant, any complication, and reoperation. In addition, we compared the postoperative course of immediate two-stage procedures with delayed two-stage procedures. Results. The overall eight-year risk estimates for the immediate procedures were 76.4% for any complication, 5.3% for severe capsular contracture, 29.5% for displacement/asymmetry of the implant and 40.6% for reoperation. Significantly higher risk for reoperation was observed after immediate one-stage than after two-stage procedures. For immediate two-stage procedures acute complications such as infection, seroma and hematoma were higher in the expansion period than after the second planned surgery. Higher risks for acute complications were observed after immediate than after delayed two-stage procedures. Conclusion. Immediate breast implant reconstruction was found to have substantial risks of complications in non-radiated women, which should be considered in the guidance of breast cancer patients before choosing reconstructive procedure. [ABSTRACT FROM AUTHOR]

The association of silicone breast implants with connective tissue diseases (CTDs), including systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis, and fibromyalgia, as well as a hypothesized new 'atypical' disease, which does not meet established diagnostic criteria for any known CTD, has been extensively studied. We have reviewed the epidemiologic literature regarding an association between cosmetic breast implants and CTDs, with particular emphasis on results drawn from the most recent investigations, many of which are large cohort studies with long-term follow-up, as well as on those studies that address some of the misinformation and historically widespread claims regarding an association between breast implants and CTDs. These claims have been unequivocally refuted by the remarkably consistent evidence from published studies, as well as numerous independent meta-analyses and critical reviews, which have demonstrated that cosmetic breast implants are not associated with a subsequent increased occurrence of individual CTDs or all CTDs combined, including fibromyalgia. Moreover, there is no credible evidence for the conjectured excess of 'atypical' CTD among women with cosmetic breast implants, or of a rheumatic symptom profile unique to these women. No increased risk of CTDs is evident in women with extracapsular ruptures in two studies, which evaluated risk by implant rupture status, and no consistent association has been observed between silicone breast implants and a variety of serologic markers or autoantibodies. Thus, any claims that remain regarding an association between cosmetic breast implants and CTDs are not supported by the scientific literature but rather are a residual byproduct of the unprecedented large-scale product liability litigation in the USA. [ABSTRACT FROM AUTHOR]

Background Menthol cigarettes, preferred by African American smokers, have been conjectured to be harder to quit and to contribute to the excess lung cancer burden among black men in the Unites States. However, data showing an association between smoking menthol cigarettes and increased lung cancer risk compared with smoking nonmenthol cigarettes are limited. The Food and Drug Administration is currently considering whether to ban the sale of menthol cigarettes in the United States. Methods We conducted a prospective study among 85 806 racially diverse adults enrolled in the Southern Community Cohort Study during March 2002 to September 2009 according to cigarette smoking status, with smokers classified by preference for menthol vs nonmenthol cigarettes. Among 12 373 smokers who responded to a follow-up questionnaire, we compared rates of quitting between menthol and nonmenthol smokers. In a nested case–control analysis of 440 incident lung cancer case patients and 2213 matched control subjects, using logistic regression modeling we computed odds ratios (ORs) and accompanying 95% confidence intervals (CIs) of lung cancer incidence, and applied Cox proportional hazards modeling to estimate hazard ratios (HRs) of lung cancer mortality, according to menthol preference. Results Among both blacks and whites, menthol smokers reported smoking fewer cigarettes per day; an average of 1.6 (95% CI = 1.3 to 2.0) fewer for blacks and 1.8 (95% CI = 1.3 to 2.3) fewer for whites, compared with nonmenthol smokers. During an average of 4.3 years of follow-up, 21% of participants smoking at baseline had quit, with menthol and nonmenthol smokers having equal odds of quitting (OR = 1.02, 95% CI = 0.89 to 1.16). A lower lung cancer incidence was noted in menthol vs nonmenthol smokers (for smokers of <10, 10–19, and ≥20 cigarettes per day, compared with never smokers, OR = 5.0 vs 10.3, 8.7 vs 12.9, and 12.2 vs 21.1, respectively). These trends were mirrored for lung cancer mortality. In multivariable analyses adjusted for pack-years of smoking, menthol cigarettes were associated with a lower lung cancer incidence (OR = 0.65, 95% CI = 0.47 to 0.90) and mortality (hazard ratio of mortality = 0.69, 95% CI = 0.49 to 0.95) than nonmenthol cigarettes. Conclusions The findings suggest that menthol cigarettes are no more, and perhaps less, harmful than nonmenthol cigarettes. [ABSTRACT FROM PUBLISHER]

The article presents the results of a study on the risk of patients with diabetes mellitus for cancer in the pancreas. The odd ratio of patients diagnosed with diabetes in the previous two years was more pronounced than those with diabetes diagnosed more than two years ago. The association of pancreatitis with pancreatic cancer in diabetics diagnosed within two years is mentioned. The risk for pancreatic cancer is said to be heightened in patients diagnosed up to 10 years.

Incidence rates for renal cell cancer, which accounts for 85% of kidney cancers, have been rising more rapidly among blacks than whites, almost entirely accounted for by an excess of localized disease. This excess dates back to the 1970s, despite less access among blacks to imaging procedures in the past. In contrast, mortality rates for this cancer have been virtually identical among blacks and whites since the early 1990s, despite the fact that nephrectomy rates, regardless of stage, are lower among blacks than among whites. These observations suggest that renal cell cancer may be a less aggressive tumor in blacks. We have reviewed the epidemiology of renal cell cancer, with emphasis on factors which may potentially play a role in the observed differences in incidence and mortality patterns of renal cell cancer among blacks and whites. To date, the factors most consistently, albeit modestly, associated with increased renal cell cancer risk in epidemiologic studies among whites - obesity, hypertension, cigarette smoking - likely account for less than half of these cancers, and there is virtually no epidemiologic evidence in the literature pertaining to their association with renal cell cancer among blacks. There is a long overdue need for detailed etiologic cohort and case-control studies of renal cell cancer among blacks, as they now represent the population at highest risk in the United States. In particular, investigation of the influence on renal cell cancer development of hypertension and chronic kidney disease, both of which occur substantially more frequently among blacks, is warranted, as well as investigations into the biology and natural history of this cancer among blacks. [ABSTRACT FROM AUTHOR]

Objective Perfluorooctanoate (PFOA) has been associated with impaired lactation in mice. We examined whether maternal perfluorooctanesulfonate (PFOS) and PFOA concentrations correlated with duration of breastfeeding among women. Methods We randomly selected 1400 pregnant women from the Danish national birth cohort (1996-2002) and measured PFOS and PFOA concentrations in early pregnancy by using high performance liquid chromatography/tandem mass spectrometry. Self-reported data on the duration of any and exclusive breastfeeding were collected twice during telephone interviews around 6 and 18 months after the birth of the child. Results The duration of breastfeeding decreased with increasing concentrations of pregnancy PFOS and PFOA among multiparous women, for whom the adjusted odds ratios (OR) for weaning before 6 months of age were 1.20 (95% CI 1.06-1.37) per 10 ng/ml increase in PFOS concentrations and 1.23 (95% CI 1.13-1.33) per 1 ng/ml increase in PFOA concentrations. No consistent association was found for primiparous women. Conclusions These findings suggest that PFOA and PFOS may reduce the ability to lactate, but could equally reflect reverse causation since no association was seen in primiparous women. [ABSTRACT FROM AUTHOR]

We previously investigated bladder cancer risk in a cohort of dyestuff workers who were heavily exposed to aromatic amines from 1922 through 1972. We updated the follow-up by 14 years (through 2003) for 590 exposed workers to include more than 30 years of follow-up since last exposure to aromatic amines. Expected numbers of deaths from bladder cancer and other causes were computed by use of national mortality rates from 1951 to 1980 and regional mortality rates subsequently. There were 394 deaths, compared with 262.7 expected (standardized mortality ratio = 1.50, 95% confidence interval = 1.36 to 1.66). Overall, 56 deaths from bladder cancer were observed, compared with 3.4 expected (standardized mortality ratio = 16.5, 95% confidence interval = 12.4 to 21.4). The standardized mortality ratio for bladder cancer increased with younger age at first exposure and increasing duration of exposure. Although the standardized mortality ratio for bladder cancer steadily decreased with time since exposure stopped, the absolute risk remained approximately constant at 3.5 deaths per 1000 man-years up to 29 years after exposure stopped. Excess risk was apparent 30 years or more after last exposure. [ABSTRACT FROM PUBLISHER]

The purpose of this study was to estimate black/white differences in cotinine levels for current smokers of both sexes, and to explore the potential contribution of mentholated cigarettes to these differences. Sera from 255 current smokers sampled from Southern Community Cohort Study participants (65 black men, 65 black women, 63 white men, 62 white women) were analyzed for cotinine, and linear regression was used to model the effect of race on cotinine level, adjusting for the number of cigarettes smoked within the last 24 hours, use of menthol vs. non-menthol cigarettes, exposure to environmental tobacco smoke, and age. Black smokers smoked fewer cigarettes than white smokers, yet had crude mean cotinine levels nearly as high or higher than white smokers. After multivariate adjustment, cotinine levels were an average of 50 ng/ml higher among black than white women (p=0.008) and non-significantly 12 ng/ml higher among black than white men (p=0.52). We observed no increase in cotinine levels associated with menthol cigarette use. We conclude that differences in cotinine levels among smokers suggest racial variation in exposure to and/or metabolism of tobacco smoke constituents, but our findings do not support a role for menthol preference in this disparity. [ABSTRACT FROM AUTHOR]

Perfluorooctanoate and perfluorooctanesulfonate are used in many industrial products and have been widely detected in human blood. Both chemicals are associated with tumor development in animal studies, but data on carcinogenic potential in humans are sparse. We investigated the association between plasma levels of perfluorooctanoate and perfluorooctanesulfonate and cancer risk within a prospective Danish cohort of participants with no previous cancer diagnosis at enrollment. From enrollment, between December 1, 1993, and May 31, 1997, and through July 1, 2006, we identified 713 participants with prostate cancer, 332 with bladder cancer, 128 with pancreatic cancer, and 67 with liver cancer in the entire cohort and we selected a comparison subcohort of 772. Plasma concentrations of perfluorooctanoate and perfluorooctanesulfonate were measured in each participant by use of high-pressure liquid chromatography coupled to tandem mass spectrometry. We found no clear differences in incidence rate ratios for these cancers in relation to plasma concentrations of perfluorooctanoate or perfluorooctanesulfonate. A 30%-40% increase in risk estimates for prostate cancer was observed for the three upper quartiles of perfluorooctanesulfonate concentration compared with the lowest quartile (eg, for the lowest vs the fourth quartile, incidence rate ratio = 1.38, 95% confidence interval = 0.99 to 1.93). Plasma concentrations of perfluorooctanoate and perfluorooctanesulfonate in the general Danish population appear not to be associated with risk of prostate, bladder, pancreatic, or liver cancer. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article on the commentary in cancer epidemiology's false-positive results by Boffetta and colleagues.

No increased risks of specific types of cancer following breast implantation have been consistently reported, but data on risk beyond 15 years are limited. We have pooled the results of 2 nationwide cohort studies of 3,486 Swedish and 2,736 Danish women who underwent cosmetic breast implantation between 1965 and 1993. Cancer incidence through 2002 was ascertained through nationwide cancer registries. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were calculated to compare cancer incidence among women with implants with women in the general population. Mean duration of follow up was 16.6 years (range 0.1-37.8 years). Over 50% of women were followed for 15 years or more after breast implantation and 13.3% for at least 25 years. There was a reduced incidence of breast cancer (SIR = 0.73; 95% CI 0.58-0.90), whereas lung cancer was above expectation (SIR = 1.64; 95% CI 1.10-2.36). The increased risk of lung cancer is expected due to the high prevalence of smoking among the women with implants in our study. With respect to other site-specific cancers, no significantly increased or decreased SIR was observed. This study, which includes women followed for almost 4 decades, represents the longest follow up of women with cosmetic breast implants to date. The results provide no evidence of an association between breast implants and any type of cancer. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

The article provides an overview of a population-based historical cohort study which investigates the impact of cholecystitis on patients with cancer in Denmark between 1995 and 2003. Researchers examined that 230 cases of cholecystitis were identified in the cancer cohort during 130,185 person-years. They found that the relative risk (RR) for cholecystitis among patients was 1.38%. Overall, they observed that RR for cholecystitis was doubled during the first 6 months after cancer diagnosis.

BACKGROUND: Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) are fluorinated organic compounds present in the general population at low concentrations. Animal studies have shown that they may affect neuromuscular development at high concentrations. OBJECTIVES: We investigated the association between plasma levels of PFOS and PFOA in pregnant women and motor and mental developmental milestones of their children. METHODS: We randomly selected 1,400 pairs of pregnant women and their children from the Danish National Birth Cohort. PFOS and PFOA were measured in maternal blood samples taken in early pregnancy. Apgar score was abstracted from the National Hospital Discharge Register in Denmark. Developmental milestones were reported by mothers using highly structured questionnaires when the children were around 6 months and 18 months of age. RESULTS: Mothers who had higher levels of PFOA and PFOS gave birth to children who had similar Apgar scores and reached virtually all of the development milestones at the same time as children born to mothers with lower exposure levels. Children who were born to mothers with higher PFOS levels were slightly more likely to start sitting without support at a later age. CONCLUSION: We found no convincing associations between developmental milestones in early childhood and levels of PFOA or PFOS as measured in maternal plasma early in pregnancy. [ABSTRACT FROM AUTHOR]

False-positive results are inherent in the scientific process of testing hypotheses concerning the determinants of cancer and other human illnesses. Although much of what is known about the etiology of human cancers has arisen from well-conducted epidemiological studies, epidemiology has been increasingly criticized for producing findings that are often sensationalized in the media and fail to be upheld in subsequent studies. Herein we describe examples from cancer epidemiology of likely false-positive findings and discuss conditions under which such results may occur. We suggest general guidelines or principles, including the endorsement of editorial policies requiring the prominent listing of study caveats, which may help reduce the reporting of misleading results. Increased epistemological humility regarding findings in epidemiology would go a long way to diminishing the detrimental effects of false-positive results on the allocation of limited research resources, on the advancement of knowledge of the causes and prevention of cancer, and on the scientific reputation of epidemiology and would help to prevent oversimplified interpretations of results by the media and the public. [ABSTRACT FROM AUTHOR]

False-positive results are inherent in the scientific process of testing hypotheses concerning the determinants of cancer and other human illnesses. Although much of what is known about the etiology of human cancers has arisen from well-conducted epidemiological studies, epidemiology has been increasingly criticized for producing findings that are often sensationalized in the media and fail to be upheld in subsequent studies. Herein we describe examples from cancer epidemiology of likely false-positive findings and discuss conditions under which such results may occur. We suggest general guidelines or principles, including the endorsement of editorial policies requiring the prominent listing of study caveats, which may help reduce the reporting of misleading results. Increased epistemological humility regarding findings in epidemiology would go a long way to diminishing the detrimental effects of false-positive results on the allocation of limited research resources, on the advancement of knowledge of the causes and prevention of cancer, and on the scientific reputation of epidemiology and would help to prevent oversimplified interpretations of results by the media and the public. [ABSTRACT FROM AUTHOR]

Objectives. We investigated whether racial disparities in the prevalence of type 2 diabetes exist beyond what may be attributable to differences in socioeconomic status (SES) and other modifiable risk factors. Methods. We analyzed data from 34331 African American and 9491 White adults aged 40 to 79 years recruited into the ongoing Southern Community Cohort Study. Participants were enrolled at community health centers and had similar socioeconomic circumstances and risk factor profiles. We used logistic regression to estimate the association between race and prevalence of self-reported diabetes after taking into account age, SES, health insurance coverage, body mass index, physical activity, and hypertension. Results. Multivariate analyses accounting for several diabetes risk factors did not provide strong support for higher diabetes prevalence rates among African Americans than among Whites (men: odds ratio [OR] = 1.07; 95% confidence interval [CI] = 0.95, 1.20); women: OR = 1.13, 95% CI = 1.04, 1.22). Conclusions. Our findings suggest that major differences in diabetes prevalence between African Americans and Whites may simply reflect differences in established risk factors for the disease, such as SES, that typically vary according to race. (Am J Public Health. 2007;97:2260-2267. doi:10.2105/AJPH.2006.094482) [ABSTRACT FROM AUTHOR]

BACKGROUND: Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) are man-made, persistent organic pollutants widely spread throughout the environment and human populations. They have been found to interfere with fetal growth in some animal models, but whether a similar effect is seen in humans is uncertain. OBJECTIVES: We investigated the association between plasma levels of PFOS and PFOA in pregnant women and their infants' birth weight and length of gestation. METHODS: We randomly selected 1,400 women and their infants from the Danish National Birth Cohort among those who completed all four computer-assisted telephone interviews, provided the first blood samples between gestational weeks 4 and 14, and who gave birth to a single live-born child without congenital malformation. PFOS and PFOA were measured by high performance liquid chromatography-tandem mass spectrometer. RESULTS: PFOS and PFOA levels in maternal plasma were on average 35.3 and 5.6 ng/mL, respectively. Only PFOA levels were inversely associated with birth weight (adjusted β = -10.63 g; 95% confidence interval, -20.79 to -0.47 g). Neither maternal PFOS nor PFOA levels were consistently associated with the risk for preterm birth or low birth weight. We observed no adverse effects for maternal PFOS or PFOA levels on small for gestational age. CONCLUSION: Our nationwide cohort data suggest an inverse association between maternal plasma PFOA levels and birth weight. Because of widespread exposure to these chemicals, our findings may be of potential public health concern. [ABSTRACT FROM AUTHOR]

Background: The widespread use of cellular telephones has heightened concerns about possible adverse health effects. The objective of this study was to investigate cancer risk among Danish cellular telephone users who were followed for up to 21 years. Methods: This study is an extended follow-up of a large nationwide cohort of 420 095 persons whose first cellular telephone subscription was between 1982 and 1995 and who were followed through 2002 for cancer incidence. Standardized incidence ratios (SIRs) were calculated by dividing the number of observed cancer cases in the cohort by the number expected in the Danish population. Results: A total of 14249 cancers were observed (SIR = 0.95; 95% confidence interval [CI] = 0.93 to 0.97) for men and women combined. Cellular telephone use was not associated with increased risk for brain tumors (SIR = 0.97), acoustic neuromas (SIR = 0.73), salivary gland tumors (SIR 0.77), eye tumors (SIR = 0.96), or leukemias (SIR 1.00). Among long-term subscribers of 10 years or more, cellular telephone use was not associated with increased risk for brain tumors (SIR = 0.66, 95% CI = 0.44 to 0.95), and there was no trend with time since first subscription. The risk for smoking-related cancers was decreased among men (SIR = 0.88, 95% CI = 0.86 to 0.91) but increased among women (SIR = 1.11, 95% CI = 1.02 to 1.21). Additional data on income and smoking prevalence, primarily among men, indicated that cellular telephone users who started subscriptions in the mid-1980s appeared to have a higher income and to smoke less than the general population. Conclusions: We found no evidence for an association between tumor risk and cellular telephone use among either short-term or long-term users. Moreover, the narrow confidence intervals provide evidence that any large association of risk of cancer and cellular telephone use can be excluded. [ABSTRACT FROM AUTHOR]

What is already known about this subject • There is some evidence that the risk of cutaneous reactions is lower in patients taking newer cyclooxygenase (COX)-2 selective inhibitors than in users of other nonsteroidal anti-inflammatory drugs (NSAIDs). • However, the data are inconclusive and formal epidemiological evidence is lacking. What this study adds • This population-based case–control study found no elevated risk for angio-oedema amongst users of newer COX-2 selective inhibitors, whilst users of other NSAIDS were shown to have an increased risk. • Our data support the hypothesis that newer COX-2 selective inhibitors are safe in relation to angio-oedema. • However, given other current health concerns related to these drugs, their use should continue to be carefully monitored. Aim To examine the risk of angio-oedema among users of the newer cyclooxygenase (COX)-2 selective inhibitors celecoxib and rofecoxib and other non-aspirin nonsteroidal anti-inflammatory drugs (NSAIDs) in a population-based case–control study. Methods Cases of angio-oedema were identified from hospital discharge registries from three Danish counties between 1 January 2000 and 31 December 2003 ( n = 377) and 10 matched population controls per case were selected from the Civil Registration System ( n = 3747). Data on newer COX-2 selective inhibitor and other NSAID use (current and former) were obtained from prescription databases. Data on potential confounding factors were also collected. Conditional logistic regression was used to compute relative risks for angio-oedema according to drug exposure. Results The crude relative risks for the newer COX-2 selective inhibitors were higher than those for other NSAIDs. After adjustment for confounding, the relative risk for current use of newer COX-2 selective inhibitors was 0.96 [95% confidence interval (CI) 0.46, 2.03], whereas the risk for other NSAIDs was 1.77 (95% CI 1.23, 2.58). Conclusion Our data support the hypothesis that newer COX-2 selective inhibitors are safe in relation to angio-oedema. However, given other current health concerns related to these drugs, their use should continue to be carefully monitored. [ABSTRACT FROM AUTHOR]