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ABSTRACT: BACKGROUND: : A recent attempt to estimate the false positive rate for cancer epidemiology studies is based on agents in IARC category 3 (agent not classifiable as to its carcinogenicity to humans) in the IARC Monographs Programme. METHODS: The estimation method is critiqued regarding biases caused by its reliance on the IARC classification criteria for assessing carcinogenic potential. RESULTS: The privileged position given to epidemiologic studies by the IARC criteria ensures that the percentage of positive epidemiologic studies for an agent will depend strongly on the IARC category to which the agent is assigned. Because IARC category 3 is composed of agents with the lowest assessed carcinogenic potential to which the estimation approach in question could be applied, a very low estimated false positive rate was, by necessity, the outcome of this approach. CONCLUSIONS: Tendentious estimation approaches like that employed will perforce produce spuriously low and misleading false positive rates. Impact: The recently reported estimates of the false positive rate in cancer epidemiology are seriously biased and contribute nothing substantive to the literature on the very real problems related to false positive findings in epidemiology.
Cancer Epidemiology Biomarkers & Prevention 11/2012; · 4.12 Impact Factor
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European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 10/2012; · 2.21 Impact Factor
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ABSTRACT: OBJECTIVE:: To evaluate cancer incidence overall and renal cancer in particular among workers at the Valley Forge satellite manufacturing complex in Pennsylvania. A previous mortality study observed a slightly elevated risk estimate for brain cancer. METHODS:: A cohort of 27,586 workers, employed between 1962 and 2008 and alive in 1990 when cancer follow-up began, was investigated. Standardized incidence ratios (SIRs) were calculated. RESULTS:: A total of 4303 incident cancers were diagnosed. The SIRs were significantly reduced for all cancers (0.88; 95% confidence interval [CI], 0.85 to 0.90) and several site-specific cancers. The renal cancer SIR was 1.00 (95% CI, 0.84 to 1.19) and the brain cancer SIR was 1.17 (95% CI, 0.90 to 1.49). CONCLUSIONS:: This cancer incidence study of satellite manufacturing workers found no convincing evidence of increased cancer risk overall, or for renal or brain cancer in particular.
Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 08/2012; · 1.88 Impact Factor
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ABSTRACT: Conjectured associations between dietary acrylamide intake and cancer have been evaluated in more than 15 epidemiologic studies examining almost every major cancer site. We have critically reviewed the epidemiologic studies of estimated dietary acrylamide exposure and cancer. As substantially greater acrylamide exposure occurs through tobacco smoke than dietary exposure, we present the results separately for never smokers or adjusted statistically for smoking status, where possible. After an extensive examination of the published literature, we found no consistent or credible evidence that dietary acrylamide increases the risk of any type of cancer in humans, either overall or among nonsmokers. In particular, the collective evidence suggests that a high level of dietary acrylamide intake is not a risk factor for breast, endometrial, or ovarian cancers, which have generated particular interest because of a conjectured hormonal mechanism of acrylamide. Moreover, the absence of a positive association between smoking and ovarian and endometrial cancers suggests that any association of these cancers with the much lower, more sporadic dietary acrylamide intake is unlikely. In conclusion, epidemiologic studies of dietary acrylamide intake have failed to demonstrate an increased risk of cancer. In fact, the sporadically and slightly increased and decreased risk ratios reported in more than two dozen papers examined in this review strongly suggest the pattern one would expect to find for a true null association over the course of a series of trials. Therefore, continued epidemiologic investigation of acrylamide and cancer risk appears to be a misguided research priority.
European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 04/2012; 21(4):375-86. · 2.21 Impact Factor
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New England Journal of Medicine 03/2012; 366(13):1259-60; author reply 1260. · 53.30 Impact Factor
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ABSTRACT: 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.
PLoS ONE 01/2012; 7(10):e48407. · 4.09 Impact Factor
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ABSTRACT: Extended cancer follow-up among 77,943 aircraft workers.
Comprehensive exposure information enabled detailed classification of trichloroethylene (TCE), perchloroethylene (PCE), mixed solvents, and chromates exposure among these workers.
Exposure to TCE, PCE, mixed solvents or chromates was not associated with increased cancer risk overall or for most cancer sites. Elevated rates compared with the general population were seen for non-Hodgkin lymphoma for PCE exposure, and colon and testicular cancers and multiple myeloma for mixed solvents exposure. Internal cohort analyses, however, showed no significant trends of increasing risk for these cancers with increasing years of exposure to TCE, PCE or mixed solvents.
This large, long-term cohort study with comprehensive exposure assessment found no consistent evidence of increased cancer risk overall or by site among aircraft workers, including those with long-term exposure to TCE, PCE, and mixed solvents.
Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 08/2011; 53(9):992-1007. · 1.88 Impact Factor
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CancerSpectrum Knowledge Environment 08/2011; 103(16):1211-3. · 14.07 Impact Factor
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ABSTRACT: To compare temporal trends in the incidence and mortality of renal cell cancer among blacks and whites for clues to etiologic differences. We examined trends in age-adjusted and age-specific Surveillance Epidemiology and End Results incidence and US mortality rates for renal cancer for 1973 through 2007, as well as nephrectomy rates from surgery codes for kidney cancer for 2000 through 2007. For nearly four decades, incidence rates for renal cell cancer have been rising more rapidly among blacks than whites, leading to a shift in excess from among whites to among blacks, almost entirely accounted for by an excess of localized disease. The incidence patterns are puzzling, as localized renal cell cancer is primarily detected incidentally by imaging, to which blacks have historically had less access. In contrast to the incidence patterns, there has been an unexpected convergence of renal cancer mortality rates, which have been virtually identical among blacks and whites since the early 1990 s. Nephrectomy rates, regardless of stage, were lower among blacks than among whites, despite almost identical cause-specific survival rates in both races. The identical mortality patterns, combined with higher and more rapidly increasing incidence and lower rates of nephrectomies among blacks, suggest that renal cell cancer may tend to be a less aggressive tumor in blacks. This hypothesis is supported by the favorable stage distribution among blacks and their higher survival for distant and unstaged cancer. Further research into the enigmatic descriptive epidemiology and the biology and natural history of renal cell cancer may shed light on the etiology of this malignancy and its more frequent occurrence among black Americans.
European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 07/2011; 20(4):331-3. · 2.21 Impact Factor
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ABSTRACT: 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.
BMC Cancer 01/2011; 11:133. · 3.01 Impact Factor
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ABSTRACT: To evaluate potential cancer risks in the US semiconductor wafer fabrication industry.
A cohort of 100,081 semiconductor workers employed between 1968 and 2002 was studied. Standardized mortality ratios and relative risks (RRs) were estimated.
Standardized mortality ratios were similar and significantly low among fabrication and nonfabrication workers for all causes (0.54 and 0.54) and all cancers (0.74 and 0.72). Internal comparisons also showed similar overall cancer risks among fabrication workers (RR = 0.98), including process equipment operators and process equipment service technicians (OP/EST) employed in cleanrooms (RR = 0.97), compared with nonfabrication workers. Nonsignificantly elevated RRs were observed for a few cancer sites among OP/EST workers, but the numbers of deaths were small and there were no trends of increasing risk with duration of employment.
Work in the US semiconductor industry, including semiconductor wafer fabrication in cleanrooms, was not associated with increased cancer mortality overall or mortality from any specific form of cancer. However, due to the young average age of this cohort and its associated relatively low numbers of deaths, regular mortality updates of this semiconductor worker cohort are warranted.
Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 11/2010; 52(11):1082-97. · 1.88 Impact Factor
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ABSTRACT: To review the epidemiological literature relevant to evaluating the risk of adverse effects on thyroid function associated with environmental perchlorate exposure.
All studies investigating possible adverse effects of environmental perchlorate exposure on thyroid function in adults or in pregnant women and their newborns were critically evaluated.
There is no credible or consistent evidence from any of the numerous studies using a variety of designs that environmental exposure to perchlorate has any adverse effect on thyroid function, whether measured as changes in thyroid hormone levels or, among newborns, as the diagnosis of primary congenital hypothyroidism. The absence of adverse effects of environmental perchlorate on the thyroid likely reflects the very low perchlorate exposure levels worldwide, compared with much higher levels of exposure to nitrate and thiocyanate, goitrogens that inhibit thyroid function by the identical mechanism of action proposed for perchlorate. Adjusted for potency, perchlorate accounts for <1% of the inhibition of iodide uptake in the thyroid resulting from environmental exposure to nitrate and thiocyanate. Occupational studies of workers with substantially higher perchlorate exposure than the general population indicate that even extended exposure to high perchlorate levels does not adversely affect thyroid function.
There is no epidemiologic evidence that environmental or occupational exposure to perchlorate adversely affects thyroid function in the United States. Even if all perchlorate could be removed from the environment, >99% of the inhibition of iodide uptake in the thyroid resulting from exposure to environmental goitrogens would remain.
Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 06/2010; 52(6):653-60. · 1.88 Impact Factor
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ABSTRACT: In the past, concerns about lymphoma among women with breast implants have been raised by anecdotal observations. A recent report of a case-control study from The Netherlands reported an association of breast implants with anaplastic large T-cell lymphoma, but limitations inherent in the study design and the restriction of the association to saline implants preclude any causal evaluation.
To determine whether lymphoma risk is in fact elevated in women with breast implants, the authors have reviewed the evidence from five long-term follow-up studies comprising over 43,000 women with cosmetic breast implants followed for up to 37 years, which reported results specifically regarding the incidence of non-Hodgkin's lymphoma, among other cancers.
Overall, there were 48 observed incident cases of non-Hodgkin's lymphoma compared with 53.9 cases expected, yielding a summary standardized incidence ratio of 0.89 (95 percent confidence interval, 0.67 to 1.18). None of the epidemiologic cohort studies reported a primary lymphoma originating in the breast.
To date, there is no credible evidence of an increase of non-Hodgkin's lymphoma regardless of site or specifically originating in the breast among women with cosmetic breast implants.
Plastic and reconstructive surgery 04/2009; 123(3):790-3. · 2.74 Impact Factor
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ABSTRACT: A previous county mortality study of populations living near two nuclear materials processing and fabrication facilities in Westmoreland and Armstrong counties in Pennsylvania (1950-1995) was extended through 2004. Noncancer mortality (1996-2004) and cancer incidence (1990-2004) were also evaluated. Among the Westmoreland and Armstrong populations, 10,547 cancer deaths occurred during the period 1996 through 2004 and the relative risk (RR) based on comparisons with six demographically similar counties in western Pennsylvania was 0.97, that is, almost exactly as expected, and no different from our previously published analyses covering the years 1950-1995. The results based on cancer incidence data were very similar to those based on cancer mortality data. Over the years 1990 though 2004, 39,350 incident cancers were reported among residents of Armstrong and Westmoreland counties and the RR based on the six demographically similar counties was 0.99, that is, almost exactly as expected. The number of deaths from nonmalignant conditions was 36,565 and very close to the number expected (RR 1.01). Overall, no increases in cancer or nonmalignant diseases could be attributed to living in counties with nuclear materials processing and fabrication facilities.
Health physics 03/2009; 96(2):128-37. · 0.92 Impact Factor
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International Journal of Epidemiology 02/2009; 38(3):678-9. · 6.41 Impact Factor
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ABSTRACT: 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.
Disease markers 01/2009; 27(5):187-92. · 1.64 Impact Factor
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ABSTRACT: Incidence rates of renal cell cancer, which accounts for 85% of kidney cancers, have been rising in the United States and in most European countries for several decades. Family history is associated with a two- to four-fold increase in risk, but the major forms of inherited predisposition together account for less than 4% of renal cell cancers. Cigarette smoking, obesity, and hypertension are the most consistently established risk factors. Analgesics have not been convincingly linked with renal cell cancer risk. A reduced risk of renal cell cancer among statin users has been hypothesized but has not been adequately studied. A possible protective effect of fruit and vegetable consumption is the only moderately consistently reported dietary finding, and, with the exception of a positive association with parity, evidence for a role of hormonal or reproductive factors in the etiology of renal cell cancer in humans is limited. A recent hypothesis that moderate levels of alcohol consumption may be protective for renal cell cancer is not strongly supported by epidemiologic results, which are inconsistent with respect to the categories of alcohol consumption and the amount of alcohol intake reportedly associated with decreased risk. For occupational factors, the weight of the evidence does not provide consistent support for the hypotheses that renal cell cancer may be caused by asbestos, gasoline, or trichloroethylene exposure. The established determinants of renal cell cancer, cigarette smoking, obesity, and hypertension, account for less than half of these cancers. Novel epidemiologic approaches, including evaluation of gene-environment interactions and epigenetic mechanisms of inherited and acquired increased risk, are needed to explain the increasing incidence of renal cell cancer.
Clinical Epidemiology 01/2009; 1:33-43.
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ABSTRACT: 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.
International Journal of Cancer 12/2008; 124(2):490-3. · 5.44 Impact Factor
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ABSTRACT: To the authors' knowledge, little information is available regarding the incidence of cholecystitis among patients with cancer.
The authors conducted a population-based historical cohort study of 51,228 patients with incident cancer, identified in medical databases of western Denmark between 1995 and 2003. A general population comparison cohort of 512,280 persons was assembled using the Danish Civil Registration System. The occurrence of cholecystitis in the 2 groups was determined by linkage to the regional Hospital Discharge Registry.
In all, 230 incident diagnoses of cholecystitis were identified in the cancer cohort during 130,185 person-years (median follow-up time: 1.6 years), corresponding to an incidence rate of 1.8 of 1000 person-years. After adjustment for confounders, the relative risk (RR) for cholecystitis among cancer patients compared with the general population cohort was 1.38 (95% confidence interval [95% CI], 1.20-1.58). Overall, the RR for cholecystitis was doubled during the first 6 months after cancer diagnosis (RR = 1.95; 95% CI, 1.50-2.54), after which the RR declined but remained greater than 1 throughout the rest of the follow-up period (RR = 1.23; 95% CI, 1.05-1.45). Cancer patients between the ages of 51 and 70 years had the highest risk increase for cholecystitis compared with other age groups. During the first 6 months after a cancer diagnosis, pancreatic cancers (12 cholecystitis events; RR = 9.44 [95% CI, 5.18-17.18]) and colorectal cancers (10 cholecystitis events; RR = 4.98 [95% CI, 2.65-9.34]) were found to be associated with the greatest cholecystitis risk increase compared with other tumor types. After 6 months, most cancers were associated with a relatively small increased risk, although there was an RR of 4.72 (95% CI, 1.99-11.21) based on 5 cholecystitis events among thyroid cancer patients.
The results of the current study indicate that cholecystitis occurs more frequently among cancer patients than in the general population, particularly within the first 6 months after a cancer diagnosis. Clinicians who treat cancer patients should remain vigilant about this type of infection.
Cancer 11/2008; 113(12):3410-9. · 4.77 Impact Factor
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ABSTRACT: 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.
CancerSpectrum Knowledge Environment 08/2008; 100(14):988-95. · 14.07 Impact Factor