Particulate matter (PM) emissions were measured in July 2010 from on-road motor vehicles driving through a highway tunnel in the San Francisco Bay area. A soot particle aerosol mass spectrometer ...(SP-AMS) was used to measure the chemical composition of PM emitted by gasoline and diesel vehicles at high time resolution. Organic aerosol (OA) and black carbon (BC) concentrations were measured during various time periods that had different levels of diesel influence, as well as directly in the exhaust plumes of individual heavy-duty (HD) diesel trucks. BC emission factor distributions for HD trucks were more skewed than OA distributions (N = 293), with the highest 10% of trucks accounting for 56 and 42% of total measured BC and OA emissions, respectively. OA mass spectra measured for HD truck exhaust plumes show cycloalkanes are predominate in exhaust OA emissions relative to saturated alkanes (i.e., normal and iso-paraffins), suggesting that lubricating oil rather than fuel is the dominant source of primary organic aerosol (POA) emissions in diesel vehicle exhaust. This finding is supported by the detection of trace elements such as zinc and phosphorus in the exhaust plumes of individual trucks. Trace elements were emitted relative to total OA at levels that are consistent with typical weight fractions of commonly used additives present in lubricating oil. A comparison of measured OA and BC mass spectra across various sampling periods revealed a high degree of similarity in OA and BC emitted by gasoline and diesel engines. This finding indicates a large fraction of OA in gasoline exhaust is lubricant-derived as well. The similarity in OA and BC mass spectra for gasoline and diesel engine exhaust is likely to confound ambient source apportionment efforts to determine contributions to air pollution from these two important sources.
Endometrial cancer (EC) is one of the most common female cancers and there is currently no routine screening strategy for early detection. An altered abundance of circulating microRNAs (miRNAs) and ...other RNA classes have the potential as early cancer biomarkers. We analyzed circulating RNA levels using small RNA sequencing, targeting RNAs in the size range of 17-47 nucleotides, in EC patients with samples collected prior to diagnosis compared to cancer-free controls. The analysis included 316 cases with samples collected 1-11 years prior to EC diagnosis, and 316 matched controls, both from the Janus Serum Bank cohort in Norway. We identified differentially abundant (DA) miRNAs, isomiRs, and small nuclear RNAs between EC cases and controls. The top EC DA miRNAs were miR-155-5p, miR-200b-3p, miR-589-5p, miR-151a-5p, miR-543, miR-485-5p, miR-625-p, and miR-671-3p. miR-200b-3p was previously reported to be among one of the top miRNAs with higher abundance in EC cases. We observed 47, 41, and 32 DA miRNAs for EC interacting with BMI, smoking status, and physical activity, respectively, including two miRNAs (miR-223-3p and miR-29b-3p) interacting with all three factors. The circulating RNAs are altered and show temporal dynamics prior to EC diagnosis. Notably, DA miRNAs for EC had the lowest q-value 4.39-6.66 years before diagnosis. Enrichment analysis of miRNAs showed that signaling pathways Fc epsilon RI, prolactin, toll-like receptor, and VEGF had the strongest associations.
Summary Background Associations between circulating concentrations of oestrogens, progesterone, and androgens with breast cancer and related risk factors in premenopausal women are not well ...understood. We aimed to characterise these associations with a pooled analysis of data from seven studies. Methods Individual participant data for prediagnostic sex hormone and sex hormone-binding globulin (SHBG) concentrations were contributed from seven prospective studies. We restricted analyses to women who were premenopausal and younger than 50 years at blood collection, and to women with breast cancer diagnosed before age 50 years. We estimated odds ratios (ORs) with 95% CIs for breast cancer associated with hormone concentrations by conditional logistic regression in cases and controls matched for age, date of blood collection, and day of cycle, with stratification by study and further adjustment for cycle phase. We examined associations of hormones with risk factors for breast cancer in control women by comparing geometric mean hormone concentrations in categories of these risk factors, adjusted for study, age, phase of menstrual cycle, and body-mass index (BMI). All statistical tests were two-sided. Findings We included data for up to 767 women with breast cancer and 1699 controls in the risk analyses. Breast cancer risk was associated with a doubling in concentrations of oestradiol (OR 1·19, 95% CI 1·06–1·35), calculated free oestradiol (1·17, 1·03–1·33), oestrone (1·27, 1·05–1·54), androstenedione (1·30, 1·10–1·55), dehydroepiandrosterone sulphate (1·17, 1·04–1·32), testosterone (1·18, 1·03–1·35), and calculated free testosterone (1·08, 0·97–1·21). Breast cancer risk was not associated with luteal phase progesterone (doubling in concentration OR 1·00, 95% CI 0·92–1·09), and adjustment for other factors had little effect on any of these ORs. Cross-sectional analyses in control women showed several associations of sex hormones with breast cancer risk factors. Interpretation Circulating oestrogens and androgens are positively associated with the risk for breast cancer in premenopausal women. Funding Cancer Research UK.
Epidemiological studies have reported inconsistent findings for the association between B vitamins and breast cancer (BC) risk. We investigated the relationship between biomarkers of folate and ...vitamin B12 and the risk of BC in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Plasma concentrations of folate and vitamin B12 were determined in 2,491 BC cases individually matched to 2,521 controls among women who provided baseline blood samples. Multivariable logistic regression models were used to estimate odds ratios by quartiles of either plasma B vitamin. Subgroup analyses by menopausal status, hormone receptor status of breast tumors (estrogen receptor ER, progesterone receptor PR and human epidermal growth factor receptor 2 HER2), alcohol intake and MTHFR polymorphisms (677C > T and 1298A > C) were also performed. Plasma levels of folate and vitamin B12 were not significantly associated with the overall risk of BC or by hormone receptor status. A marginally positive association was found between vitamin B12 status and BC risk in women consuming above the median level of alcohol (ORQ4‐Q1 = 1.26; 95% CI 1.00–1.58; Ptrend = 0.05). Vitamin B12 status was also positively associated with BC risk in women with plasma folate levels below the median value (ORQ4‐Q1 = 1.29; 95% CI 1.02–1.62; Ptrend = 0.03). Overall, folate and vitamin B12 status was not clearly associated with BC risk in this prospective cohort study. However, potential interactions between vitamin B12 and alcohol or folate on the risk of BC deserve further investigation.
What's new?
Does B‐vitamin intake play a role in breast cancer (BC) risk? Results have been inconsistent. In this analysis of data from a large, prospective European study, the authors found that, overall, folate and vitamin B12 status were not clearly associated with BC risk. However, the risk did seem to increase somewhat for women who had higher vitamin B12 levels and either low plasma folate or increased alcohol consumption. The authors suggest that this may involve nutrient‐nutrient or gene‐nutrient interactions, such as changes in DNA methylation, which require further investigation.
Microseminoprotein-beta (MSP), a protein secreted by the prostate epithelium, may have a protective role in the development of prostate cancer. The only previous prospective study found a 2% reduced ...prostate cancer risk per unit increase in MSP. This work investigates the association of MSP with prostate cancer risk using observational and Mendelian randomization (MR) methods.
A nested case–control study was conducted with the European Prospective Investigation into Cancer and Nutrition (EPIC) with 1871 cases and 1871 matched controls. Conditional logistic regression analysis was used to investigate the association of pre-diagnostic circulating MSP with risk of incident prostate cancer overall and by tumour subtype. EPIC-derived estimates were combined with published data to calculate an MR estimate using two-sample inverse-variance method.
Plasma MSP concentrations were inversely associated with prostate cancer risk after adjusting for total prostate-specific antigen concentration odds ratio (OR) highest versus lowest fourth of MSP=0.65, 95% confidence interval (CI) 0.51–0.84, Ptrend=0.001. No heterogeneity in this association was observed by tumour stage or histological grade. Plasma MSP concentrations were 66% lower in rs10993994 TT compared with CC homozygotes (per allele difference in MSP: 6.09ng/ml, 95% CI 5.56–6.61, r2=0.42). MR analyses supported a potentially causal protective association of MSP with prostate cancer risk (OR per 1 ng/ml increase in MSP for MR: 0.96, 95% CI 0.95–0.97 versus EPIC observational: 0.98, 95% CI 0.97–0.99). Limitations include lack of complete tumour subtype information and more complete information on the biological function of MSP.
In this large prospective European study and using MR analyses, men with high circulating MSP concentration have a lower risk of prostate cancer. MSP may play a causally protective role in prostate cancer.
IARC periodically convenes such advisory groups to ensure that the agents evaluated in the Monographs are selected on the basis of the latest scientific evidence relevant to carcinogenicity.1 A ...detailed report of the Advisory Group recommendations will be published in due course.2 The Advisory Group assessed the response to a public call for nominations and considered more than 200 candidate agents, including the recommended priority agents remaining from a similar Advisory Group meeting convened in 2019.3 The Advisory Group comprised scientists with expertise across the spectrum of topics relevant to carcinogenicity. In drawing their conclusions, the members appraised, for each nominated agent, the evidence regarding human exposure, cancer in humans, cancer in experimental animals, and carcinogen mechanisms according to precepts described in the Preamble to the IARC Monographs.1 Systematic literature searches were complemented by a text mining and database fusion approach to identify relevant studies, document the relative abundance of literature for the different evidence streams, and map chemical similarity4 in support of decisions on prioritisation for individual agents and groups of agents. Monographs Advisory Group Members A Berrington de González (UK)—Meeting Chair; S A Masten (USA)—Meeting Vice Chair; P Bhatti (Canada); R T Fortner (Norway); S Peters (Netherlands); T Santonen (Finland); M G Yakubovskaya (Russian Federation)—Subgroup Meeting Chairs; R Barouki (France); S B M Barros (Brazil); D Barupal (USA); L E Beane Freeman (USA); G M Calaf (Chile); J Dillner (Sweden); K El Rhazi (Morocco); L Fritschi (Australia); S Fukushima (Japan); L Godderis (Belgium); M Kogevinas (Spain); D W Lachenmeier (Germany); D Mandrioli (Italy); M M Muchengeti (South Africa); R T Niemeier (USA); J J Pappas (Canada); J Pi (China); M P Purdue (USA); E Riboli (UK unable to attend); T Rodríguez (Nicaragua); V Schlünssen (Denmark) Declaration of interests All Monographs Advisory Group members declare no competing interests Invited Specialists None Representatives Y Choi, Division of Cancer Prevention, National Cancer Control Institute (South Korea);B Kim, Division of Cancer Prevention, National Cancer Control Institute (South Korea) Declaration of interests YC and BK declare no competing interests Observers R Bars, Regulatory Science Ltd (France); J Britt, ToxStrategies (USA) Declaration of interests RB is a a salaried employee of Regulatory Science Associates and CropLife International sponsored his travel to and attendance at the Advisory Group meeting. Rationale Agents not previously evaluated by IARC Monographs Disinfection byproducts in water, including haloacetic acids; sleep disruption; hair straightening products; metalworking fluids; obesity*; platinum-based chemotherapies as mechanistic class†; dibutyl phthalate; nitrogen dioxide‡; artificial light at night‡; sugar-sweetened beverage consumption‡; GLP-1 analogues‡; Fonofos‡ Relevant human cancer, animal cancer, and mechanistic evidence Fusobacterium nucleatum; human cytomegalovirus; sedentary behaviour; ultraprocessed food consumption; anthracyclines as mechanistic class†; BRAF inhibitors—dabrafenib, encorafenib, vemurafenib; epirubicin; tetracycline; tofacitinib and other Janus kinase inhibitors; perfluorohexanesulfonic acid; cannabis smoking‡; ultrafine particles‡; assisted reproductive techniques‡; chlorpyrifos‡ Relevant human cancer and mechanistic evidence Electronic nicotine delivery systems; estragole; carbadox; alachlor; cyfluthrin; cypermethrin; mancozeb; neonicotinoid insecticides; tebuconazole; vinclozolin; bisphenol A; bisphenol S; bisphenol F; 2,3-butanedione; carbon disulfide; diisononyl phthalate; glycidamide; hexafluoropropylene oxide dimer acid; methanol; ozone; pentabromodiphenyl ethers; triclosan; zearalenone‡ Relevant animal cancer and mechanistic evidence Hepatitis D virus; Salmonella typhi; taconite; terbufos‡ Relevant human cancer evidence Metyltetraprole; proquinazid; butyraldehyde; chlorinated paraffins; tris(chloropropyl)phosphate Relevant animal cancer evidence Methamphetamine; Congo red; cumyl hydroperoxide; 2,4-dihydroxybenzophenone; parabens; electronic waste work‡; polyhexamethyleneguanidine‡ Relevant mechanistic evidence Agents previously evaluated by IARC Monographs§ Hair colouring products (personal use of); coal dust; paracetamol (acetaminophen); textured implants (breast and buttock); carbaryl; ethylenedithiocarbamates; permethrin; pyrethrins and pyrethroids New human cancer, animal cancer, and mechanistic evidence to warrant re-evaluation of the classification Non-ionising radiation (radiofrequency)‡ New human cancer and animal cancer evidence to warrant re-evaluation of the classification Human papillomavirus β; Opisthorchis felineus; indoor combustion of biomass; textile manufacturing industry work; inorganic lead compounds; daunorubicin; doxorubicin; methotrexate; atrazine and other triazine pesticides; acetaldehyde; acrylamide; Merkel cell polyomavirus‡; clomiphene citrate‡; progestogen-only contraceptives‡; chlordecone‡ New human cancer and mechanistic evidence to warrant re-evaluation of the classification Multiwalled carbon nanotubes; butyl benzyl phthalate; 5-nitro-o-toluidine; 4-nitrotoluene; p-phenylenediamine New animal cancer and mechanistic evidence to warrant re-evaluation of the classification Metallic nickel; very hot beverages and food¶; carbon tetrachloride‡; tetrachloroethylene‡ New human cancer evidence to warrant re-evaluation of the classification Piperonyl butoxide New animal cancer evidence to warrant re-evaluation of the classification Schistosoma japonicum; Schistosoma mansoni; patulin; safrole; anaesthetics, volatile—isoflurane, sevoflurane, and desflurane; malathion; bromate compounds; 3,3′-dimethoxybenzidine; 3,3′-dimethylbenzidine; isoprene; fluoranthene‡ New mechanistic evidence to warrant re-evaluation of the classification Helicobacter pylori‡; aflatoxins‡; outdoor air pollution‡; tobacco smoking and second-hand smoke‡; silica dust‡; asbestos‡; hormone replacement therapy‡; radon and its decay products‡; ethylene oxide‡; formaldehyde† Group 1 carcinogen with evidence for new cancer sites (see section 3 of the Preamble to the IARC Monographs1) Table 1 Agents recommended for evaluation by the IARC Monographs with high priority Previous evaluation status Toxoplasma gondii; black cohosh extracts; outdoor combustion of biomass; tattoos and permanent make up; anatase-type nano-TiO2; neonatal phototherapy; anti-thymocyte globulin; bifenthrin; biphenyl; pendimethalin; α-pinene; sulfolane Agents not previously evaluated by the IARC Monographs Fumonisin B1; pyrrolizidine alkaloids; ingested nitrate; selenium and selenium compounds; xylenes Agents previously evaluated by the IARC Monographs* Table 2 Agents recommended for evaluation by the IARC Monographs with medium priority Rationale Chronic circadian dysfunction; diabetes; insomnia; reduction of sex hormones with human aging; violation of tissue renewal or regeneration with human aging; alefacept No evidence of exposure, or not an exogenous exposure Dysbiotic microbiota; poor oral hygiene; nitrate-reducing bacteria in tobacco; SARS-CoV-2; cleaning products; long working hours; social isolation and loneliness; phosphorescent paints; laboratory work and occupation as a chemist; occupation as a pesticide applicator; semiconductor industry work; acrylonitrile-butadiene-styrene particles emitted by three-dimensional printers; engineered stone fabrication; microplastics and nanoplastics; aluminium; rare earth elements; intense pulsed light; artificially sweetened beverage consumption; dietary salt intake; indole-3-carbinol; isoflavones; sucralose; gadolinium-based contrast agents; gene or cell therapy or vectors; glucocorticoids; glutathione; reversible acetylcholinesterase inhibitors; allyl alcohol; ametryn; atraric acid; boscalid; o-benzyl-p-chlorophenol; cinidon ethyl; p-cresol; 1,2-cyclohexanedicarboxylic acid, diisononyl ester; 2,4-dichlorophenol; 2,4-dimethylphenol; ethyl anthranilate; S-ethyl-N,N-dipropylthiocarbamate; furmecyclox; hexythiazox; 2-hydroxy-4-methoxybenzophenone; menthyl anthranilate; methyl anthranilate; palmitic acid; phosmet; red dye number 3 (erythrosine); styrene-acrylonitrile (SAN) trimer; 2,4,6-tribromophenol
Findings on the association between alcohol consumption and bladder cancer are inconsistent. We investigated that association in the European Prospective Investigation into Cancer and Nutrition ...cohort. We included 476,160 individuals mostly aged 35–70 years, enrolled in ten countries and followed for 13.9 years on average. Hazard ratios (HR) for developing urothelial cell carcinoma (UCC; 1,802 incident cases) were calculated using Cox proportional hazards models. Alcohol consumption at baseline and over the life course was analyzed, as well as different types of beverages (beer, wine, spirits). Baseline alcohol intake was associated with a statistically nonsignificant increased risk of UCC (HR 1.03; 95% confidence interval (CI) 1.00–1.06 for each additional 12 g/day). HR in smokers was 1.04 (95% CI 1.01–1.07). Men reporting high baseline intakes of alcohol (>96 g/day) had an increased risk of UCC (HR 1.57; 95% CI 1.03–2.40) compared to those reporting moderate intakes (<6 g/day), but no dose–response relationship emerged. In men, an increased risk of aggressive forms of UCC was observed even at lower doses (>6 to 24 g/day). Average lifelong alcohol intake was not associated with the risk of UCC, however intakes of spirits > 24 g/day were associated with an increased risk of UCC in men (1.38; 95% CI 1.01–1.91) and smokers (1.39; 95% CI 1.01–1.92), compared to moderate intakes. We found no association between alcohol and UCC in women and never smokers. In conclusion, we observed some associations between alcohol and UCC in men and in smokers, possibly because of residual confounding by tobacco smoking.
What's new?
Findings from the EPIC cohort do not suggest a clear detrimental effect of alcohol on bladder cancer risk. However, we found some association between alcohol and risk of the most aggressive forms of bladder cancer in men and in smokers. Among the different beverages, high intakes of spirits were associated with an increased risk of bladder cancer in men and in smokers, while beer and wine were not. Further studies confirming these results are warranted.
Evidence suggests that the hormonal milieu of pregnancy is an important determinant of subsequent cancer and other chronic diseases in both the mother and the offspring. Many of the existing ...maternity and birth cohorts include specimens drawn only once during pregnancy. How well a single blood specimen collected during a pregnancy characterizes exposure to these hormones throughout gestation, and also in subsequent pregnancies, is not well understood.
We used serial serum samples from 71 pregnant women (25 primiparous, 25 multiparous, and 21 with two consecutive pregnancies) with natural, complication-free pregnancies and a healthy offspring at term who participated in a population-based screening trial for congenital infections in Finland between January 1st, 1988 and June 30, 1989 and provided a blood sample in each trimester.
Hormone levels were more strongly correlated between consecutive trimesters of a pregnancy than between the 1st and 3rd trimester (e.g., estradiol, rT1 vs. T2 = 0.51 and rT2 vs. T3 = 0.60, p < 0.01; rT1 vs. T3 = 0.32, p < 0.05). Concentrations of sRANKL remained stable throughout gestation, whereas estradiol, estrone, progesterone, testosterone, prolactin, and osteoprotegerin increased throughout pregnancy. First trimester hormone concentrations explained less of the variation in the third trimester on their own than second trimester hormone levels (e.g. estradiol R(2) T1 = 16 % and R(2) T2 = 42 %). Addition of maternal (e.g., smoking) and/or child characteristics (e.g., sex) improved the accuracy of the 3rd trimester estimates for some of the hormones.
One hormone measurement in early pregnancy, in conjunction with maternal and fetal characteristics, permits estimation of 3rd trimester hormone concentrations. Therefore, single hormone measurements available from maternity cohorts are suitable to quantify hormone exposure during pregnancy. To our knowledge, we provide the first data on correlations between hormone concentrations both across trimesters of a single pregnancy, as well as between two subsequent pregnancies.
Abstract
Epidemiologic, clinical, molecular and translational research findings support an interrelationship between Chlamydia trachomatis, pelvic inflammatory disease (PID), and epithelial ovarian ...cancer (EOC). Overall, the link between C. trachomatis, PID, and EOC seems to be relatively weak, although nondifferential misclassification bias may have attenuated the results. The predominant tubal origin of EOC and the role of chronic inflammation in tumorigenesis suggest that the association is biologically plausible. Thus, C. trachomatis and PID may represent potential risk factors or risk markers for EOC. However, many steps in this chain of events are still poorly understood and need to be addressed in future studies. Research gaps include time of exposure in relation to the long-term consequences and lag time to EOC. Data of differential risk for EOC between chlamydial and nonchlamydial PID is also needed. Another major research gap has been the absence of high-performance biomarkers for C. trachomatis, PID, and EOC, as well as EOC precursors. Biomarkers for C. trachomatis and PID leading to increased risk of EOC should be developed. If the association is confirmed, C. trachomatis and PID prevention efforts may play a role in reducing the burden of EOC.
The Mullerian ducts are the embryological precursors of the female reproductive tract, including the uterus; anti-Mullerian hormone (AMH) has a key role in the regulation of foetal sexual ...differentiation. Anti-Mullerian hormone inhibits endometrial tumour growth in experimental models by stimulating apoptosis and cell cycle arrest. To date, there are no prospective epidemiologic data on circulating AMH and endometrial cancer risk.
We investigated this association among women premenopausal at blood collection in a multicohort study including participants from eight studies located in the United States, Europe, and China. We identified 329 endometrial cancer cases and 339 matched controls. Anti-Mullerian hormone concentrations in blood were quantified using an enzyme-linked immunosorbent assay. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) across tertiles and for a doubling of AMH concentrations (OR
). Subgroup analyses were performed by ages at blood donation and diagnosis, oral contraceptive use, and tumour characteristics.
Anti-Mullerian hormone was not associated with the risk of endometrial cancer overall (OR
: 1.07 (0.99-1.17)), or with any of the examined subgroups.
Although experimental models implicate AMH in endometrial cancer growth inhibition, our findings do not support a role for circulating AMH in the aetiology of endometrial cancer.
PDF
