Joshua E Muscat

Pennsylvania State University, University Park, Maryland, United States

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Publications (160)735.36 Total impact

  • Epidemiology (Cambridge, Mass.) 11/2014; 25(6):934-935. · 5.51 Impact Factor
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    ABSTRACT: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time-risk relationship are unclear, and there is limited information on the role of antidiabetic medications.
    Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 07/2014;
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    ABSTRACT: Low socioeconomic status has been reported to be associated with head and neck cancer risk. However, previous studies have been too small to examine the associations by cancer subsite, age, sex, global region, and calendar time, and to explain the association in terms of behavioural risk factors. Individual participant data of 23,964 cases with head and neck cancer and 31,954 controls from 31 studies in 27 countries pooled with random effects models. Overall, low education was associated with an increased risk of head and neck cancer (OR = 2·50; 95%CI 2·02- 3·09). Overall one-third of the increased risk was not explained by differences in the distribution of cigarette smoking and alcohol behaviours; and it remained elevated among never users of tobacco and non-drinkers (OR = 1·61; 95%CI 1·13 - 2·31). More of the estimated education effect was not explained by cigarette smoking and alcohol behaviours: in women than in men, in older than younger groups, in the oropharynx than in other sites, in South/Central America than in Europe/North America, and was strongest in countries with greater income inequality. Similar findings were observed for the estimated effect of low vs high household income. The lowest levels of income and educational attainment were associated with more than 2-fold increased risk of head and neck cancer, which is not entirely explained by differences in the distributions of behavioural risk factors for these cancers, and which varies across cancer sites, sexes, countries, and country income inequality levels. © 2014 Wiley Periodicals, Inc.
    International journal of cancer. Journal international du cancer. 07/2014;
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    ABSTRACT: The tobacco-specific nitrosamine NNK is a potent carcinogen found in tobacco smoke and implicated in the development of lung cancer. The major route of NNK metabolism is carbonyl reduction by AKR1C1, AKR1C2, CBR1, and 11β-HSD1 to form NNAL. This study investigated the potential role of variants in this pathway on lung cancer risk by examining 53 tag-SNPs representing the common variations in AKR1C1, AKR1C2, CBR1, and HSD11B1 in 456 lung cancer cases and 807 controls. One SNP in CBR1 (rs2835267) was significantly associated with overall risk of lung cancer, but did not pass multiple testing adjustment (OR: 0.76 95% CI: 0.58-0.99, P = 0.048, FDR P = 0.20). After stratification and multiple testing correction, three SNPs showed significance. One SNP (rs2835267) in CBR1 showed a significant decreased risk for smokers with a high pack-years (OR: 0.3595% CI: 0.17-0.69, P = 0.018) and in SCC (OR: 0.4895% CI: 0.29-0.76, P = 0.018). Another SNP located in CBR1 (rs3787728) also showed a significant decreased risk in SCC (OR: 0.4695% CI: 0.26-0.80, P = 0.024) and small cell carcinoma (only in current smokers) (OR: 0.06895% CI: 0.01-0.42, P = 0.028). The HSD11B1 SNP (rs4844880) showed a significant increased risk for adenocarcinoma within former smokers (OR: 3.9495% CI: 1.68-9.22, P = 0.011). Haplotype analysis found significance with six haplotypes and lung cancer risk. These findings indicate that select variants in genes in the carbonyl reduction pathway of NNK may alter the risk of lung cancer. © 2014 Wiley Periodicals, Inc.
    Molecular Carcinogenesis 06/2014; · 4.27 Impact Factor
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    ABSTRACT: UDP-glucuronosyltransferases (UGTs) play an important role in the phase II metabolism of exogenous and endogenous compounds. As colorectal cancer (CRC) etiology is thought to involve the biotransformation of dietary factors, UGT polymorphisms may affect CRC risk by altering levels of exposure. Genotyping of over 1800 Caucasian subjects was completed to identify the role of genetic variation in nine UGT1A and five UGT2B genes on CRC risk. Unconditional logistic regression and haplotype analyses were conducted to identify associations with CRC risk and potential gene-environment interactions. UGT1A haplotype analysis found that the T-G haplotype in UGT1A10 exon 1 (block 2: rs17864678, rs10929251) decreased cancer risk for the colon [proximal (OR = 0.28, 95% CI = 0.11–0.69) and for the distal colon (OR = 0.32, 95% CI = 0.12–0.91)], and that the C-T-G haplotype in the 3′ region flanking the UGT1A shared exons (block 11: rs7578153, rs10203853, rs6728940) increased CRC risk in males (OR = 2.56, 95% CI = 1.10–5.95). A haplotype in UGT2B15 containing a functional variant (rs4148269, K523T) and an intronic SNP (rs6837575) was found to affect rectal cancer risk overall (OR = 2.57, 95% CI = 1.21–5.04) and in females (OR = 3.08, 95% CI = 1.08–8.74). An interaction was found between high NSAID use and the A-G-T haplotype (block 10: rs6717546, rs1500482, rs7586006) in the UGT1A shared exons that decreased CRC risk. This suggests that UGT genetic variation alters CRC risk differently by anatomical sub-site and gender and that polymorphisms in the UGT1A shared exons may have a regulatory effect on gene expression that allows for the protective effect of NSAIDs on CRC risk.
    Genes Chromosomes and Cancer 06/2014; 53(6):454-66. · 3.55 Impact Factor
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    ABSTRACT: Glutathione (GSH), the most abundant endogenous antioxidant, is a critical regulator of oxidative stress and immune function. While oral GSH has been shown to be bioavailable in laboratory animal models, its efficacy in humans has not been established. Our objective was to determine the long-term effectiveness of oral GSH supplementation on body stores of GSH in healthy adults. A 6-month randomized, double-blinded, placebo-controlled trial of oral GSH (250 or 1,000 mg/day) on GSH levels in blood, erythrocytes, plasma, lymphocytes and exfoliated buccal mucosal cells was conducted in 54 non-smoking adults. Secondary outcomes on a subset of subjects included a battery of immune markers. GSH levels in blood increased after 1, 3 and 6 months versus baseline at both doses. At 6 months, mean GSH levels increased 30-35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells in the high-dose group (P < 0.05). GSH levels increased 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P < 0.05). In most cases, the increases were dose and time dependent, and levels returned to baseline after a 1-month washout period. A reduction in oxidative stress in both GSH dose groups was indicated by decreases in the oxidized to reduced glutathione ratio in whole blood after 6 months. Natural killer cytotoxicity increased >twofold in the high-dose group versus placebo (P < 0.05) at 3 months. These findings show, for the first time, that daily consumption of GSH supplements was effective at increasing body compartment stores of GSH.
    European Journal of Nutrition 05/2014; · 3.13 Impact Factor
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    ABSTRACT: Gastric cancer affects about one million people per year worldwide, being the second leading cause of cancer mortality. The study of its etiology remains therefore a global issue as it may allow the identification of major targets, besides eradication of Helicobacter pylori infection, for primary prevention. It has however received little attention, given its comparatively low incidence in most high-income countries. We introduce a consortium of epidemiological investigations named the 'Stomach cancer Pooling (StoP) Project'. Twenty-two studies agreed to participate, for a total of over 9000 cases and 23 000 controls. Twenty studies have already shared the original data set. Of the patients, 40% are from Asia, 43% from Europe, and 17% from North America; 34% are women and 66% men; the median age is 61 years; 56% are from population-based case-control studies, 41% from hospital-based ones, and 3% from nested case-control studies derived from cohort investigations. Biological samples are available from 12 studies. The aim of the StoP Project is to analyze the role of lifestyle and genetic determinants in the etiology of gastric cancer through pooled analyses of individual-level data. The uniquely large data set will allow us to define and quantify the main effects of each risk factor of interest, including a number of infrequent habits, and to adequately address associations in subgroups of the population, as well as interaction within and between environmental and genetic factors. Further, we will carry out separate analyses according to different histotypes and subsites of gastric cancer, to identify potential different risk patterns and etiological characteristics.
    European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 02/2014; · 2.21 Impact Factor
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    ABSTRACT: The time to first cigarette (TTFC) of the day is an indicator of nicotine intake in adults and adolescents. However, the relation between TTFC and biological markers of nicotine addiction and health risk in youths has not been well described. The current study examined whether an earlier TTFC predicts higher levels of a tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridal)-1 (NNAL), in regular and intermittent adolescent smokers and if this relation is mediated by nicotine intake (measured by cotinine) or cigarettes per day (CPD). A cross-sectional analysis of a nationally representative subsample of adolescents. A general community sample from the 2007-2008 and 2009-2010 National Health and Nutrition and Examination Survey. 215 adolescents in the United States between the ages of 12 and 19 who reported smoking at least once in the 5 days prior to data collection. The primary outcome measure was urinary levels of NNAL. In both regular and intermittent smokers, earlier TTFC was dose-dependently associated with higher levels of NNAL (p's < 0.03 in both cases). TTFC had an indirect effect on NNAL, mediated by nicotine intake (cotinine) in both regular (β = -.08, SE = .03, 95% CI [-.15, -.04]), and intermittent (β = -.02, SE = .01, 95% CI [-.05, -.002]) smokers. CPD was not found to be an important mediator of the relation between TTFC and NNAL. Time between waking and the first cigarette of the day is correlated in daily and non-daily adolescent smokers with overall nicotine and therefore carcinogen intake.
    Addiction 02/2014; · 4.58 Impact Factor
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    ABSTRACT: The incidence of oropharyngeal and oral tongue cancers has increased over the last 20 years which parallels increased use of marijuana among individuals born after 1950. A pooled analysis was conducted comprising individual-level data from nine case-control studies from the United States and Latin America in the INHANCE consortium. Self-reported information on marijuana smoking, demographic, and behavioral factors was obtained from 1,921 oropharyngeal cases, 356 oral tongue cases, and 7,639 controls. Compared with never marijuana smokers, ever marijuana smokers had an elevated risk of oropharyngeal [adjusted OR (aOR), 1.24; 95% confidence interval (CI): 1.06-1.47] and a reduced risk of oral tongue cancer (aOR, 0.47; 95% CI, 0.29, 0.75). The risk of oropharyngeal cancer remained elevated among never tobacco and alcohol users. The risk of oral tongue cancer was reduced among never users of tobacco and alcohol. Sensitivity analysis adjusting for potential confounding by HPV exposure attenuated the association of marijuana use with oropharyngeal cancer (aOR, 0.99; 95% CI, 0.71-1.25), but had no effect on the oral tongue cancer association. These results suggest that the association of marijuana use with head and neck carcinoma may differ by tumor site. The associations of marijuana use with oropharyngeal and oral tongue cancer are consistent with both possible pro- and anticarcinogenic effects of cannabinoids. Additional work is needed to rule out various sources of bias, including residual confounding by HPV infection and misclassification of marijuana exposure. Cancer Epidemiol Biomarkers Prev; 1-12. ©2013 AACR.
    Cancer Epidemiology Biomarkers &amp Prevention 12/2013; · 4.56 Impact Factor
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    ABSTRACT: A microarray (LungCaGxE), based on Illumina BeadChip technology, was developed for high-resolution genotyping of genes that are candidates for involvement in environmentally driven aspects of lung cancer oncogenesis and/or tumor growth. The iterative array design process illustrates techniques for managing large panels of candidate genes and optimizing marker selection, aided by a new bioinformatics pipeline component, Tagger Batch Assistant. The LungCaGxE platform targets 298 genes and the proximal genetic regions in which they are located, using ∼13,000 DNA single nucleotide polymorphisms (SNPs), which include haplotype linkage markers with a minimum allele frequency of 1% and additional specifically targeted SNPs, for which published reports have indicated functional consequences or associations with lung cancer or other smoking-related diseases. The overall assay conversion rate was 98.9%; 99.0% of markers with a minimum Illumina design score of 0.6 successfully generated allele calls using genomic DNA from a study population of 1873 lung-cancer patients and controls.
    Journal of biomolecular techniques: JBT 12/2013; 24(4):198-217.
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    ABSTRACT: Several epidemiological studies have shown a positive association between adult height and cancer incidence. The only study conducted among women on mouth and pharynx cancer risk, however, reported an inverse association. This study aims to investigate the association between height and the risk of head and neck cancer (HNC) within a large international consortium of HNC. We analyzed pooled individual-level data from 24 case-control studies participating in the International Head and Neck Cancer Epidemiology Consortium. Odds ratios (ORs) and 95 % confidence intervals (CIs) were estimated separately for men and women for associations between height and HNC risk. Educational level, tobacco smoking, and alcohol consumption were included in all regression models. Stratified analyses by HNC subsites were performed. This project included 17,666 cases and 28,198 controls. We found an inverse association between height and HNC (adjusted OR per 10 cm height = 0.91, 95 % CI 0.86-0.95 for men; adjusted OR = 0.86, 95 % CI 0.79-0.93 for women). In men, the estimated OR did vary by educational level, smoking status, geographic area, and control source. No differences by subsites were detected. Adult height is inversely associated with HNC risk. As height can be considered a marker of childhood illness and low energy intake, the inverse association is consistent with prior studies showing that HNC occur more frequently among deprived individuals. Further studies designed to elucidate the mechanism of such association would be warranted.
    European Journal of Epidemiology 11/2013; · 5.12 Impact Factor
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    ABSTRACT: Previous research has shown that greater intakes of dietary folate are associated with reduced risk for colorectal cancer (CRC) and that single nucleotide polymorphisms (SNPs) in genes involved in folate-mediated one-carbon metabolism (FOCM) also may be involved in altering CRC risk. The objective of this study was to evaluate the role of folate intake (and intakes of related dietary components such as methionine), 35 SNPs in three FOCM pathway genes (MTHFD1, MTHFR, and TYMS), and their interactions on CRC risk in a population-based case-control study in Pennsylvania (686 cases, 740 controls). Diet and supplement use was assessed for the year before diagnosis or interview for cases and controls, respectively, with a modified Diet History Questionnaire from the National Cancer Institute. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using unconditional logistic regression. Using a dominant model for the variant allele, several SNPs were significantly associated with CRC including MTHFD1 rs8003379 (OR = 1.65; 95% CI = 1.00-2.73) and rs17824591 (OR = 1.98; 95% CI = 1.14-3.41) and the TYMS rs2853533 SNP (OR = 1.38; 95% CI = 1.05-1.80). Using a nondominant model, the AA genotype for MTHFR rs1476413 exhibited a marginally significant (OR = 1.56; 95% CI = 1.00-2.44) association with CRC. Two TYMS SNPs (rs16948305 and rs495139) exhibited significant (P = 0.024 and P = 0.040, respectively) gene-diet interactions with folate intake. One MTHFD1 (P = 0.019) and one MTHFR (P = 0.042) SNP exhibited gene-diet interactions with methionine intake. These findings suggest that allelic variants in genes involved in FOCM interact with dietary factors including folate and methionine to modify risk for CRC. © 2013 Wiley Periodicals, Inc.
    Genes Chromosomes and Cancer 07/2013; · 3.55 Impact Factor
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    ABSTRACT: Cigar and pipe smoking are considered risk factors for head and neck cancers, but the magnitude of effect estimates for these products has been imprecisely estimated. By using pooled data from the International Head and Neck Cancer Epidemiology (INHANCE) Consortium (comprising 13,935 cases and 18,691 controls in 19 studies from 1981 to 2007), we applied hierarchical logistic regression to more precisely estimate odds ratios and 95% confidence intervals for cigarette, cigar, and pipe smoking separately, compared with reference groups of those who had never smoked each single product. Odds ratios for cigar and pipe smoking were stratified by ever cigarette smoking. We also considered effect estimates of smoking a single product exclusively versus never having smoked any product (reference group). Among never cigarette smokers, the odds ratio for ever cigar smoking was 2.54 (95% confidence interval (CI): 1.93, 3.34), and the odds ratio for ever pipe smoking was 2.08 (95% CI: 1.55, 2.81). These odds ratios increased with increasing frequency and duration of smoking (Ptrend ≤ 0.0001). Odds ratios for cigar and pipe smoking were not elevated among ever cigarette smokers. Head and neck cancer risk was elevated for those who reported exclusive cigar smoking (odds ratio = 3.49, 95% CI: 2.58, 4.73) or exclusive pipe smoking (odds ratio = 3.71, 95% CI: 2.59, 5.33). These results suggest that cigar and pipe smoking are independently associated with increased risk of head and neck cancers.
    American journal of epidemiology 06/2013; · 5.59 Impact Factor
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    ABSTRACT: This study examined the relationship between the time to the first cigarette (TTFC) of the morning with quit status among adolescent smokers at the completion of a school-based smoking cessation program. Among those who did not quit, the relationship of TTFC with changes in cigarettes/day (CPD) was also examined. A total of 1,167 adolescent smokers (1,024 nonquitters and 143 quitters) from 4 states participating in efficacy and effectiveness studies of the Not-On-Tobacco (N-O-T) cessation program were assessed prior to entry into the program and again 3 months later, at the end of treatment. Linear and logistic regression analyses determined the influence of treatment condition, age, gender, motivation to quit, confidence in quitting ability, baseline CPD, and TTFC on quit status and end-of-treatment CPD. Adolescents with a TTFC of >30min of waking were twice as likely to quit at end of treatment. Additionally, among those who did not quit at end of treatment (n = 700 for TTFC ≤30min and n = 324 for TTFC for >30min), those with a TTFC within 30min of waking smoked a greater number of CPD. The relationships of TTFC with both of these outcomes remained when controlling for all other predictor variables. Identifying adolescent smokers who smoke their first cigarette of the day within the first 30min of waking prior to a quit attempt may help to classify those individuals as having a greater risk for cessation failure. Thus, TTFC may be a behavioral indicator of nicotine dependence in adolescents.
    Nicotine & Tobacco Research 06/2013; · 2.48 Impact Factor
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    ABSTRACT: BACKGROUND: Genetic polymorphisms in combination with the Western-style diet, physical inactivity, smoking, excessive alcohol consumption, and obesity have been hypothesized to affect colorectal cancer (CRC) risk. Metabolizers of environmental carcinogenic and endogenous compounds affecting CRC risk include the phase II detoxification UDP-glucuronosyltransferase (UGT) enzymes UGT2B17 and UGT2B28, which are 2 of the most commonly deleted genes in the genome. METHODS: To study the effect of UGT2B17 and UGT2B28 copy number variation (CNV) on CRC risk, 665 Caucasian CRC cases and 621 Caucasian controls were genotyped who had completed extensive demographics and lifestyle questionnaires. RESULTS: A significant association between the UGT2B17 deletion genotype (0/0) and decreased CRC risk was found when the entire population was analyzed (P = .044). Stratification by sex yielded a decreased risk (P = .020) in men with the UGT2B17 deletion (0/0), but no association was observed in women (P = .724). A significant association between UGT2B17 (0/0) and decreased risk for rectal (P = .0065) but not colon cancer was found. No significant association was found between UGT2B28 CNV and CRC risk. CONCLUSIONS: The UGT2B17 deletion genotype (0/0) was associated with a decreased CRC risk in a Caucasian population. After sex stratification, the association was observed in men but not in women, which is consistent with previous findings that men have higher UGT2B17 expression and activity than women. Because UGT2B17 metabolizes certain nonsteroidal anti-inflammatory drugs and flavonoids with antioxidative properties, individuals with a gene deletion may have higher levels of these protective dietary components. Cancer 2013;000:000-000. © 2013 American Cancer Society.
    Cancer 04/2013; · 5.20 Impact Factor
  • Steven A Branstetter, Joshua E Muscat
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    ABSTRACT: BACKGROUND: The time to first cigarette (TTFC) is a good indicator of several dimensions of nicotine dependence. An early TTFC is also associated with increased lung and oral cancer risk. Our objective was to determine the relationship between TTFC and exposure to tobacco smoke carcinogens.METHODS: We conducted a cross-sectional analysis of a nationally representative subsample of smoking adults that had urinary samples analyzed for tobacco biomarkers. The study included 1,945 participants from the 2007-2008 and 2009-2010 National Health and Nutrition and Examination Survey. The main outcome measure was creatinine-adjusted urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) levels.RESULTS: The cigarette-per-day adjusted levels of NNAL were twice as high in participants who smoked within 5 minutes after waking than in participants who refrained from smoking for at least 1 hour (0.58 vs. 0.28 ng/mL, P < 0.001). In multivariate linear models, a shorter TTFC was significantly associated with increasing NNAL levels, after adjusting for cigarettes smoked per day (or cotinine), secondhand smoke exposure, age, sex, race/ethnicity, and other potential confounders.CONCLUSIONS: These data show that in a nationally representative sample, there is a dose-dependent relationship between earlier smoking in the day and higher biologic exposure to a tobacco smoke carcinogen.Impact: Our study provides further evidence that highlights the relationship between TTFC, nicotine dependence, and cancer risk. Cancer Epidemiol Biomarkers Prev; 22(4); 1-8. ©2013 AACR.
    Cancer Epidemiology Biomarkers &amp Prevention 03/2013; · 4.56 Impact Factor
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    ABSTRACT: We evaluated the role of dietary iron, heme iron, and supplemental iron on colorectal cancer (CRC) risk in a population-based case-control study in Pennsylvania, including 1005 incident cases and 1062 controls. Diet was assessed through a modified food frequency questionnaire that included supplement use and a meat-specific module. Cases reported intakes for the year before diagnosis, whereas controls reported intakes for the year before interview. Heme iron intake was calculated using a new heme database developed by the US National Cancer Institute. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. After multivariate adjustment, there were no significant associations between heme iron or total iron intake and CRC incidence. Dietary iron intake was inversely associated with CRC among women (OR Q5 vs. Q1=0.45; 95% CI=0.22-0.92), but not among men. Supplemental iron intake of more than 18 mg/day versus none was positively associated with CRC incidence (OR=2.31; 95% CI=1.48-3.59; P-trend<0.001), an effect that was observed in both men (OR=2.56; 95% CI=1.30-5.05) and women (OR=2.46; 95% CI=1.34-4.52). These findings suggest that consumption of more than 18 mg/day of supplemental iron may increase risk for CRC.
    European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 03/2013; · 2.21 Impact Factor
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    ABSTRACT: Since meat may be involved in the etiology of colorectal cancer, associations between meat-related compounds were examined to elucidate underlying mechanisms in a population-based case-control study. Participants (989 cases/1,033 healthy controls) completed a food frequency questionnaire with a meat-specific module. Multivariable logistic regression was used to examine associations between meat variables and colorectal cancer; polytomous logistic regression was used for subsite-specific analyses. The following significant positive associations were observed for meat-related compounds: 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) and colorectal, distal colon, and rectal tumors; 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and colorectal and colon cancer tumors; nitrites/nitrates and proximal colon cancer; 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and rectal cancer; and benzo[a]pyrene and rectal cancer (P-trends < 0.05). For analyses by meat type, cooking method, and doneness preference, positive associations between red processed meat and proximal colon cancer and pan-fried red meat and colorectal cancer were found (P-trends < 0.05). Inverse associations were observed between unprocessed poultry and colorectal, colon, proximal colon, and rectal tumors; grilled/barbequed poultry and proximal colon cancer; and well-done/charred poultry and colorectal, colon, and proximal colon tumors (P-trends < 0.05). HCAs, PAHs, nitrites, and nitrates may be involved in colorectal cancer etiology. Further examination into the unexpected inverse associations between poultry and colorectal cancer is warranted.
    Nutrition and Cancer 02/2013; 65(2):202-26. · 2.70 Impact Factor
  • Joshua E Muscat
    Nicotine & Tobacco Research 10/2012; 14(10):1246-7. · 2.48 Impact Factor
  • Steven A Branstetter, Joshua E Muscat
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    ABSTRACT: INTRODUCTION: Nicotine dependence and uptake among adolescents remains challenging to characterize and measure. Among adults, a shorter time to the first cigarette after waking up in the morning (TTFC) has become increasingly recognized as an indicator of nicotine dependence because of its association with biological measures of nicotine exposure, smoking relapse, and failed cessation attempts. However, the relation between TTFC and these measures has not been studied among adolescents. This study explored the association between TTFC and cotinine among adolescent smokers. METHODS: The study utilized 2007-2008 and 2009-2010 National Health and Nutrition Examination Survey (NHANES) data from 220 regular adolescent smokers between the ages of 12 and 19 who provided blood samples for cotinine evaluation. Regression modeling was conducted to determine whether TTFC predicts cotinine levels, a marker of nicotine uptake. RESULTS: The time to first cigarette was significantly correlated with several smoking behaviors including number of cigarettes per day, time since last cigarette, and having a family member who smokes at home. Mean cotinine levels were more than 200ng/ml in youths who smoked within 5min after waking, compared with less than 34ng/ml in youths who waited for more than 1hr. In multiple regression models, a shorter time to first cigarette predicted higher cotinine levels after controlling for number of cigarettes per day and other factors. The TTFC was a predictor of cotinine for both male and female smokers.Conclusion:The TTFC is a strong indicator of nicotine dependence in adolescents and could be an important component in screening for high-risk smoking and the development of tailored adolescent smoking intervention programs.
    Nicotine & Tobacco Research 09/2012; · 2.48 Impact Factor

Publication Stats

4k Citations
735.36 Total Impact Points

Institutions

  • 2008–2014
    • Pennsylvania State University
      • • Department of Biobehavioral Health
      • • Department of Nutritional Sciences
      • • Department of Public Health Sciences
      University Park, Maryland, United States
    • Mario Negri Institute for Pharmacological Research
      Milano, Lombardy, Italy
  • 2005–2014
    • Penn State Hershey Medical Center and Penn State College of Medicine
      • • Public Health Sciences
      • • Pharmacology
      • • Department of Health Evaluation Sciences
      Hershey, Pennsylvania, United States
    • Boston University
      • Department of Epidemiology
      Boston, MA, United States
  • 2013
    • University of North Carolina at Chapel Hill
      North Carolina, United States
  • 2011–2013
    • Catholic University of the Sacred Heart
      • Institute of Hygiene
      Milano, Lombardy, Italy
    • Universitätsmedizin Göttingen
      • Department of Genetic Epidemiology
      Göttingen, Lower Saxony, Germany
    • Columbia University
      • Department of Epidemiology
      New York City, New York, United States
  • 2009–2013
    • National Institutes of Health
      • Division of Cancer Epidemiology and Genetics
      Maryland, United States
  • 2012
    • Karmanos Cancer Institute
      Detroit, Michigan, United States
    • Imperial College London
      Londinium, England, United Kingdom
    • Philadelphia College of Osteopathic Medicine
      Philadelphia, Pennsylvania, United States
  • 2010–2011
    • International Agency for Research on Cancer
      Lyons, Rhône-Alpes, France
    • PinnacleHealth Harrisburg Hospital in Harrisburg
      Harrisburg, Pennsylvania, United States
    • Albert Einstein College of Medicine
      New York City, New York, United States
  • 2009–2011
    • National Cancer Institute (USA)
      • Division of Cancer Epidemiology and Genetics
      Bethesda, MD, United States
  • 2008–2009
    • University of South Carolina
      • Department of Family and Preventive Medicine
      Columbia, SC, United States
  • 2007
    • University of Wisconsin - Stevens Point
      Stevens Point, Wisconsin, United States
    • New York University
      • Medicine
      New York City, NY, United States
  • 2003
    • University of South Florida
      Tampa, Florida, United States
  • 2001
    • German Cancer Research Center
      Heidelburg, Baden-Württemberg, Germany
  • 1997–2000
    • Temple University
      • • Department of Pathology and Laboratory Medicine
      • • Department of Medicine
      Philadelphia, PA, United States
  • 1998
    • Emory University
      Atlanta, Georgia, United States
    • Analysis Group
      Boston, Massachusetts, United States
  • 1995
    • Massachusetts General Hospital
      • Department of Radiation Oncology
      Boston, MA, United States
  • 1989
    • Memorial Sloan-Kettering Cancer Center
      New York City, New York, United States
  • 1987
    • The Ottawa Hospital
      Ottawa, Ontario, Canada