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  • 1
    Keywords: CELLS ; BLOOD ; CELL ; PATHWAY ; PATHWAYS ; EXPOSURE ; WORKERS ; DNA ; MARKER ; AIR ; BIOMARKERS ; FREQUENCY ; FREQUENCIES ; METABOLITES ; ACID ; ACIDS ; NO ; CHROMOSOMAL-ABERRATIONS ; DNA-REPAIR ; REPAIR ; RATES ; ABERRATIONS ; MARKERS ; COMET ASSAY ; DAMAGE ; genotoxicity ; LYMPHOCYTES ; PARAMETERS ; Jun ; CANCER-PATIENTS ; ADDUCTS ; INDIVIDUALS ; PERIPHERAL-BLOOD ; METABOLITE ; SISTER-CHROMATID EXCHANGES ; micronuclei ; OCCUPATIONAL-EXPOSURE ; EXCRETION ; lamination ; STYRENE ; CULTURED HUMAN-LYMPHOCYTES ; DNA repair rates ; MERCAPTURIC ACIDS ; styrene exposure ; urinary metabolites
    Abstract: The effect of occupational exposure to styrene on frequencies of chromosomal aberrations and binucleated cells with micronuclei and on single-strand break levels in peripheral blood lymphocytes was studied in 86 reinforced plastic workers and 42 control individuals (including 16 maintenance workers with intermittent, low-dose exposure). In these individuals, the irradiation-specific DNA repair rates and the repair rates of 8-oxoguanines were investigated. We assessed the exposure by, measuring the concentrations of styrene in air and in blood and of mandelic acid, phenylglyoxylic acid, 4-vinyl phenol conjugates and regioisomeric phenyl hydroxyethyl mercapturic acids in urine. All these parameters correlated with one another. No clear relationship was found between the styrene exposure and the frequencies of chromosomal aberrations. Binucleated cells with micronuclei were moderately related to the parameters of styrene exposure. We found a negative correlation between all exposure parameters and single-strand breaks. The positive correlation between exposure parameters and DNA repair rates suggests that particular DNA repair pathways may be induced by styrene exposure
    Type of Publication: Journal article published
    PubMed ID: 15175174
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  • 2
    Keywords: PROGRAM ; PUBLIC-HEALTH ; POLICY ; ADHERENCE ; PRINCIPLES UNDERLYING SCIENCE ; EPIDEMIOLOGIC ENTERPRISE ; CANCER-EPIDEMIOLOGY ; PLEA ; FALSE ; RECIPE
    Abstract: BACKGROUND: Recently, the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also for the approach used to perform these evaluations. Some critics have claimed that failures of IARC Working Groups to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans. OBJECTIVES: The authors of this Commentary are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We examined criticisms of the IARC classification process to determine the validity of these concerns. Here, we present the results of that examination, review the history of IARC evaluations, and describe how the IARC evaluations are performed. DISCUSSION: We concluded that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various disciplines and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed. CONCLUSIONS: The IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.
    Type of Publication: Journal article published
    PubMed ID: 25712798
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  • 3
    Abstract: BACKGROUND: Various occupations have been associated with an elevated risk of non-Hodgkin lymphoma (NHL), but results have been inconsistent across studies. OBJECTIVES: We investigated occupational risk of NHL and of four common NHL subtypes with particular focus on occupations of a priori interest. METHODS: We conducted a pooled analysis of 10,046 cases and 12,025 controls from 10 NHL studies participating in the InterLymph Consortium. We harmonized the occupational coding using the 1968 International Standard Classification of Occupations (ISCO-1968) and grouped occupations previously associated with NHL into 25 a priori groups. Odds ratios (ORs) adjusted for center, age, and sex were determined for NHL overall and for the following four subtypes: diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), and peripheral T-cell lymphoma (PTCL). RESULTS: We confirmed previously reported positive associations between NHL and farming occupations [field crop/vegetable farm workers OR = 1.26; 95% confidence interval (CI): 1.05, 1.51; general farm workers OR = 1.19; 95% CI: 1.03, 1.37]; we also confirmed associations of NHL with specific occupations such as women's hairdressers (OR = 1.34; 95% CI: 1.02, 1.74), charworkers/cleaners (OR = 1.17; 95% CI: 1.01, 1.36), spray-painters (OR = 2.07; 95% CI: 1.30, 3.29), electrical wiremen (OR = 1.24; 95% CI: 1.00, 1.54), and carpenters (OR = 1.42; 95% CI: 1.04, 1.93). We observed subtype-specific associations for DLBCL and CLL/SLL in women's hairdressers and for DLBCL and PTCL in textile workers. CONCLUSIONS: Our pooled analysis of 10 international studies adds to evidence suggesting that farming, hairdressing, and textile industry-related exposures may contribute to NHL risk. Associations with women's hairdresser and textile occupations may be specific for certain NHL subtypes. CITATION: 't Mannetje A, De Roos AJ, Boffetta P, Vermeulen R, Benke G, Fritschi L, Brennan P, Foretova L, Maynadie M, Becker N, Nieters A, Staines A, Campagna M, Chiu B, Clavel J, de Sanjose S, Hartge P, Holly EA, Bracci P, Linet MS, Monnereau A, Orsi L, Purdue MP, Rothman N, Lan Q, Kane E, Seniori Costantini A, Miligi L, Spinelli JJ, Zheng T, Cocco P, Kricker A. 2016. Occupation and risk of non-Hodgkin lymphoma and its subtypes: a pooled analysis from the InterLymph Consortium. Environ Health Perspect 124:396-405; http://dx.doi.org/10.1289/ehp.1409294.
    Type of Publication: Journal article published
    PubMed ID: 26340796
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  • 4
    Keywords: ENVIRONMENT ; CANCER ; AGENTS ; evaluation ; human ; INFORMATION ; VOLUME ; EPIDEMIOLOGY ; occupation ; RISK ; RISKS ; SITE ; SITES ; CARCINOGENESIS ; FORM ; TARGET ; HEALTH ; etiology ; cancer risk ; US ; CARCINOGENS ; CANCER RISKS ; INDIVIDUALS ; ORGANIZATION ; AGENT ; review ; INDUSTRY ; HUMAN CANCER ; CARCINOGEN ; ENVIRONMENTS
    Abstract: The occupational environment has been a most fruitful one for investigating the etiology of human cancer. Many recognized human carcinogens are occupational carcinogens. There is a large volume of epidemiologic and experimental data concerning cancer risks in different work environments. It is important to synthesize this information for both scientific and public health purposes. Various organizations and individuals have published lists of occupational carcinogens. However, such lists have been limited by unclear criteria for which recognized carcinogens should be considered occupational carcinogens, and by inconsistent and incomplete information on the occupations and industries in which the carcinogenic substances may be found and on their target sites of cancer. Based largely on the evaluations published by the International Agency for Research on Cancer, and augmented with additional information, the present article represents an attempt to summarize, in tabular form, current knowledge on occupational carcinogens, the occupations and industries in which they are found, and their target organs. We have considered 28 agents as definite occupational carcinogens, 27 agents as probable occupational carcinogens, and 113 agents as possible occupational carcinogens. These tables should be useful for regulatory or preventive purposes and for scientific purposes in research priority setting and in understanding carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 15531427
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  • 5
    Keywords: BLOOD ; human ; GENERATION ; POPULATION ; GENE ; EFFICIENCY ; METABOLISM ; INDEX ; REDUCTION ; GENETIC POLYMORPHISMS ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; METABOLITES ; HEALTH ; DIFFERENCE ; GLUTATHIONE ; PLASMA ; AGE ; WOMEN ; MEN ; mass spectrometry ; SWEDEN ; MASS-SPECTROMETRY ; US ; genetic polymorphism ; INDIVIDUALS ; LIQUID-CHROMATOGRAPHY ; BODY ; METHYLATION ; SKIN-CANCER ; URINE ; glutathione-S-transferase ; METABOLITE ; MASS INDEX ; MASSES ; BODIES ; RE ; arsenic ; DRINKING-WATER ; CAPACITY ; METHYLTRANSFERASE ; WEIGHT ; METHYLENETETRAHYDROFOLATE REDUCTASE ; MTHFR ; methods ; MASS ; OVERWEIGHT ; USA ; HUMAN-CELLS ; METHYLTRANSFERASES ; female ; Male ; WHOLE-BLOOD ; PUBLIC-HEALTH ; steroids ; BODY-MASS ; BODY-MASS-INDEX ; sex ; body mass ; AS3MT ; BLADDER-CANCER RISK ; GSTO1 ; HUMAN URINE ; METHYLATION CAPABILITY ; MMA(V) REDUCTASE ; MONOMETHYLARSONOUS ACID MMA(III) ; WEST-BENGAL
    Abstract: BACKGROUND: There is a wide variation in susceptibility to health effects of arsenic, which, in part, may be due to differences in arsenic metabolism. Arsenic is metabolized by reduction and methylation reactions, catalyzed by reductases and methyltransferases. OBJECTIVES: Our goal in this study was to elucidate the influence of various demographic and genetic factors on the metabolism of arsenic. METHODS: We studied 415 individuals from Hungary, Romania, and Slovakia by measuring arsenic metabolites in urine using liquid chromatography with hydride generation and inductively coupled plasma mass spectrometry (HPLC-HG-ICPMS). We performed genotyping of arsenic (+III) methyltransferase (AS3M7), glutathione S-transferase omega 1 (GSTO1), and methylenetetrahydrofolate reductase (MTHFR). RESULTS: The results show that the M287T (T -〉 C) polymorphism in the AS3MT gene, the A222V (C -〉 T) polymorphism in the MTHFR gene, body mass index, and sex are major factors that influence arsenic metabolism in this population, with a median of 8.0 mu g/L arsenic in urine. Females 〈 60 years of age had, in general, higher methylation efficiency than males, indicating an influence of sex steroids. That might also explain the observed better methylation in overweight or obese women, compared with normal weight men. The influence of the M287T (T -〉 C) polymorphism in the AS3MT gene on the methylation capacity was much more pronounced in men than in women. CONCLUSIONS: The factors investigated explained almost 20% of the variation seen in the metabolism of arsenic among men and only around 4% of the variation among women. The rest of the variation is probably explained by other methyltransferases backing up the methylation of arsenic
    Type of Publication: Journal article published
    PubMed ID: 17637926
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  • 6
    Keywords: proliferation ; CELL ; SYSTEM ; POPULATION ; PROTEIN ; MARKER ; ASSOCIATION ; TRIAL ; HEALTH ; HUMANS ; ASSAY ; WOMEN ; MARKERS ; POPULATIONS ; C-REACTIVE PROTEIN ; OUTCOMES ; questionnaires ; inflammation ; CYTOTOXICITY ; exercise ; SERUM ; air pollution ; INTERLEUKIN-6 ; IMMUNE-SYSTEM ; methods ; ASSAYS ; OVERWEIGHT ; USA ; female ; cross-sectional studies ; Middle Aged ; outcome ; immune system ; postmenopause ; CONFIDENCE ; MEDIATOR ; C-REACTIVE-PROTEIN ; Serum Amyloid A Protein/analysis ; Air Pollutants/*toxicity ; C-Reactive Protein/analysis ; Cell Proliferation/drug effects ; Geographic Information Systems ; Immunity,Cellular/*drug effects ; Inflammation/*chemically induced ; Interleukin-6/analysis ; Interviews as Topic ; Killer Cells,Natural/drug effects ; Linear Models ; T-Lymphocytes/drug effects ; Vehicle Emissions/*toxicity ; Washington
    Abstract: BACKGROUND: Traffic-related air pollution has been associated with adverse health outcomes, and the immune system may be a biologic mediator of health effects. OBJECTIVES: We analyzed associations between living near major roads and immune status as measured by five immune assays. We hypothesized that living near a freeway, arterial, or truck route would be associated with increased inflammation and decreased immune function. METHODS: We used a geographic information system (GIS) to determine residential proximity to major roads among 115 postmenopausal, overweight women in the greater Seattle, Washington (USA), area whose immunity was assessed at the baseline visit of an exercise intervention trial. We evaluated three inflammatory markers (C-reactive protein, serum amyloid A, and interleukin-6) and two functional assays of cellular immunity [natural killer (NK) cell cytotoxicity and T-lymphocyte proliferation]. RESULTS: Women living within 150 m of arterial roads had 21% lower NK cytotoxicity compared with women who lived farther from an arterial [mean cytotoxicity, 19.5%; 95% confidence interval (CI), 15.6-23.5%; vs. mean cytotoxicity, 24.8%; 95% CI, 22.0-27.5%], after adjustment for both individual-level and census tract-level demographic characteristics. This association was limited to women who reported exercising near traffic. Fewer women lived near freeways and truck routes. Markers of inflammation and lymphocyte proliferation did not consistently differ according to proximity to major roads. CONCLUSIONS: If the observed association between residential proximity to traffic and decreased NK cytotoxicity is confirmed in other populations, our results may have implications for local land use policy.
    Type of Publication: Journal article published
    PubMed ID: 19337511
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  • 7
    Keywords: CELLS ; EXPRESSION ; LUNG-CANCER ; CIGARETTE-SMOKING ; MYOCARDIAL-INFARCTION ; ALL-CAUSE MORTALITY ; CESSATION ; CARDIOVASCULAR RISK ; PROTEINASE-ACTIVATED RECEPTOR-4 ; DIFFERENTIAL DNA METHYLATION
    Abstract: Background: Recent genome-wide DNA methylation studies have found a pronounced difference in methylation of the F2RL3 gene (also known as PAR-4) in blood DNA according to smoking exposure. Knowledge on the variation of F2RL3 methylation by various degrees of smoking exposure is still very sparse. Objectives: We aimed to assess dose-response relationships of current and lifetime active smoking exposure with F2RL3 methylation. Methods: In a large population-based study, we quantified blood DNA methylation at F2RL3 for 3,588 participants using matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Associations of smoking exposure with methylation intensity were examined by multiple linear regression, controlling for potential confounding factors and paying particular attention to dose-response patterns with respect to current and lifetime smoking exposure as well as time since cessation of smoking. Results: F2RL3 methylation intensity showed a strong association with smoking status (p 〈 0.0001), which persisted after controlling for potential confounding factors. Clear inverse dose-response relationships with F2RL3 methylation intensity were seen for both current intensity and lifetime pack-years of smoking. Among former smokers, F2RL3 methylation intensity increased gradually from levels close to those of current smokers for recent quitters to levels close to never smokers for long-term (〉 20 years) quitters. Conclusions: F2RL3 methylation is a promising biomarker for both current and long-term past tobacco exposure, and its predictive value for smoking-related diseases warrants further exploration.
    Type of Publication: Journal article published
    PubMed ID: 24273234
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  • 8
    Keywords: CELLS ; HEALTH ; POLYCYCLIC AROMATIC-HYDROCARBONS ; DIET ; OUTCOMES ; VITAMIN-C ; PREGNANCY ; pooled analysis ; PRENATAL EXPOSURE ; FETAL-GROWTH
    Abstract: BACKGROUND: Tobacco-smoke, airborne, and dietary exposures to polycyclic aromatic hydrocarbons (PAHs) have been associated with reduced prenatal growth. Evidence from biomarker-based studies of low-exposed populations is limited. Bulky DNA adducts in cord blood reflect the prenatal effective dose to several genotoxic agents including PAHs. OBJECTIVES: We estimated the association between bulky DNA adduct levels and birth weight in a multicenter study and examined modification of this association by maternal intake of fruits and vegetables during pregnancy. METHODS: Pregnant women from Denmark, England, Greece, Norway, and Spain were recruited in 2006-2010. Adduct levels were measured by the 32P-postlabeling technique in white blood cells from 229 mothers and 612 newborns. Maternal diet was examined through questionnaires. RESULTS: Adduct levels in maternal and cord blood samples were similar and positively correlated (median, 12.1 vs. 11.4 adducts in 108 nucleotides; Spearman rank correlation coefficient = 0.66, p 〈 0.001). Cord blood adduct levels were negatively associated with birth weight, with an estimated difference in mean birth weight of -129 g (95% CI: -233, -25 g) for infants in the highest versus lowest tertile of adducts. The negative association with birth weight was limited to births in Norway, Denmark, and England, the countries with the lowest adduct levels, and was more pronounced in births to mothers with low intake of fruits and vegetables (-248 g; 95% CI: -405, -92 g) compared with those with high intake (-58 g; 95% CI: -206, 90 g). CONCLUSIONS: Maternal exposure to genotoxic agents that induce the formation of bulky DNA adducts may affect intrauterine growth. Maternal fruit and vegetable consumption may be protective.
    Type of Publication: Journal article published
    PubMed ID: 23906905
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  • 9
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    Abstract: BACKGROUND: Testicular germ cell tumors (TGCT) were suggested to have a prenatal environmentally related origin. The potential endocrine disrupting properties of certain solvents may interfere with the male genital development in utero. OBJECTIVES: We aimed to assess the association between maternal and paternal occupational exposures to organic solvents during the prenatal period and TGCT risk in their offspring. METHODS: This registry-based case control study included TGCT cases aged 14-49 y (n=8,112) diagnosed from 1978 to 2012 in Finland, Norway, and Sweden. Controls (n=26,264) were randomly selected from the central population registries and were individually matched to cases on year and country of birth. Occupational histories of parents prior to the child's birth were extracted from the national censuses. Job codes were converted into solvent exposure using the Nordic job-Nordic Occupational Cancer Study Job-Exposure Matrix. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). RESULTS: Overall, no association was found between prenatal maternal exposure to solvents and TGCT risk. In subset analyses using only mothers for whom occupational information was available in the year of or in the year prior to the child's birth, there was an association with maternal exposure to aromatic hydrocarbon solvents (ARHC) (OR=1.53; CI: 1.08, 2.17), driven by exposure to toluene (OR=1.67; CI: 1.02, 2.73). No association was seen for any paternal occupational exposure to solvents with the exception of exposure to perchloroethylene in Finland (OR=2.42; CI: 1.32, 4.41). CONCLUSIONS: This study suggests a modest increase in TGCT risk associated with maternal prenatal exposure to ARHC. https://doi.org/10.1289/EHP864.
    Type of Publication: Journal article published
    PubMed ID: 28893722
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