Wireless phone use in childhood and adolescence and neuroepithelial brain tumours: Results from the international MOBI-Kids study

In recent decades, the possibility that use of mobile communicating devices, particularly wireless (mobile and cordless) phones, may increase brain tumour risk, has been a concern, particularly given the considerable increase in their use by young people. MOBI-Kids, a 14-country (Australia, Austria, Canada, France, Germany, Greece, India, Israel, Italy, Japan, Korea, the Netherlands, New Zealand, Spain) case-control study, was conducted to evaluate whether wireless phone use (and particularly resulting exposure to radiofrequency (RF) and extremely low frequency (ELF) electromagnetic fields (EMF)) increases risk of brain tumours in young people. Between 2010 and 2015, the study recruited 899 people with brain tumours aged 10 to 24 years old and 1,910 controls (operated for appendicitis) matched to the cases on date of diagnosis, study region and age. Participation rates were 72% for cases and 54% for controls. The mean ages of cases and controls were 16.5 and 16.6 years, respectively; 57% were males. The vast majority of study participants were wireless phones users, even in the youngest age group, and the study included substantial numbers of long-term (over 10 years) users: 22% overall, 51% in the 20-24-year-olds. Most tumours were of the neuroepithelial type (NBT; n = 671), mainly glioma. The odds ratios (OR) of NBT appeared to decrease with increasing time since start of use of wireless phones, cumulative number of calls and cumulative call time, particularly in the 15-19 years old age group. A decreasing trend in ORs was also observed with increasing estimated cumulative RF specific energy and ELF induced current density at the location of the tumour. Further analyses suggest that the large number of ORs below 1 in this study is unlikely to represent an unknown causal preventive effect of mobile phone exposure: they can be at least partially explained by differential recall by proxies and prodromal symptoms affecting phone use before diagnosis of the cases. We cannot rule out, however, residual confounding from sources we did not measure. Overall, our study provides no evidence of a causal association between wireless phone use and brain tumours in young people. However, the sources of bias summarised above prevent us from ruling out a small increased riskFunding for the coordination of the MOBI-Kids study was obtained from the European Community’s Seventh Framework Programme under grant agreements number 226873 and 603794, and from the Spanish Ministry of Science and Innovation (MINECO). In Spain, additional funding was obtained from the Spanish Health Research Fund (FIS) of the National Institute for Health Carlos III, and from the Junta de Andalucía, Consejería de Salud. Proyecto PI-0317-2010. ISGlobal also acknowledges support from the Spanish Ministry of Science, Innovation and Universities through the “Centro de Excelencia Severo Ochoa 2019- 2023” Program (CEX2018-000806-S), support from the Generalitat de Catalunya through the CERCA Program and support from the Secretariat of Universities and Research of the Department of Business and Knowledge of the Generalitat of Catalonia through AGAUR (the Catalan Agency for Management of University and Research Grants) (Project 2017 SGR 1487). Australian participation in MOBI-Kids was supported by the Australian National Health and Medical Research Council with a five-year research grant (grant number: 546130). Austrian participation in MOBI-Kids was partly supported by a grant from the Ministry of Science. In Canada, participation in MOBI-Kids was supported by a university-industry partnership grant from the Canadian Institutes of Health Research (CIHR), reference number 110835, with the Canadian Wireless Telecommunications Association (CWTA) serving as the industrial partner. CWTA provides technical information on wireless telecommunications in Canada and facilitates access to billing records from Canadian network operators, but has no involvement in the design, conduct, analysis, or interpretation of the MOBI-KIDS study. French participation was also supported by the French National Agency for Sanitary Safety of Food, Environment and Labour (ANSES, contract FSRF2008-3), French National Cancer Institute (INCa), Pfizer Foundation and League against cancer. The German study centre received additional funding from the Federal Office for Radiation Protection (BfS) under grant number 3609S30010. In Greece, the study was partially supported by the Hellenic Society for Social Pediatrics and Health Promotion, ELKE (Special Account for Research Grants of the National and Kapodistrian University of Athens) and GGET (General Secretariat for Research and Technology). Mobi-Kids India was supported by Board of Research in Nuclear Sciences (BRNS, sanction no: 2013/38/01-BRNS). Italian participation was partially supported by a Ministry of Health grant (RF-2009-1546284). MOBI-Kids Korea was supported by the ICT R&D program (2017-0-00961 and 2019-0-00102) of MSIT/IITP, Korea. Mobi-Kids Japan was supported by Research on biological electromagnetic environment (Grant Number: 0155-0107) of Ministry of Internal Affairs and Communications Japan. New Zealand participation was supported by the Health Research Council (HRC 12/380) and Cure Kids (grant number 3536). The Netherland’s participation in MOBI-KIDS was partly supported by The Netherlands Organisation for Health Research and Development (ZonMw) within the program Electromagnetic Fields and Health Research under grant number 85800001, and by the ODAS foundation, a private foundation supporting activities in the field of pediatric oncology and visual disabilities. The funding sources had no role in the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the article for publicationDepartamento de Biología Ambiental y Salud Públic

Athletes' exposure to air pollution during World Athletics Relays: A pilot study

Potential adverse consequences of exposure to air pollutants during exercise include decreased lung function, and exacerbation of asthma and exercise-induced bronchoconstriction. These effects are especially relevant for athletes and during international competitions, as they may impact athletic performance. Thus, assessing and mitigating exposure to air pollutants during exercising should be encouraged in sports venues. A comprehensive air quality assessment was carried out during the World Relays Yokohama 2019, in the stadium and the warm-up track. The pilot included on-line and off-line instrumentation for gaseous and particulate pollutants and meteo- rological parameters, and the comparison with local reference data. Air quality perception and exacerbation of symptoms of already-diagnosed diseases (mainly respiratory and cardiovascular) were assessed by athletes by means of questionnaires during training sessions. Median NO2 concentrations inside the stadium (25.6–31.9 μgm−3) were in the range of the Yokohama urban background, evidencing the impact of urban sources (e.g., traffic) on athletes' exposure during training and competition. The assessment of hourly air pollutant trends was identified as a valuable tool to provide guidance to reduce atheletes' exposure, by identifying the periods of Inhalation Track and field Respiratory diseases World Athletics 1. Introduction Evidence supports adverse effects from short-term and long-term inhalation of air pollution to the respiratory and the cardiovascular sys- tems (Brook et al., 2002; Pietropaoli et al., 2004; Gauderman et al., 2007; de Prado Bert et al., 2018). Health impacts have been assessed for gen- eral and high-risk populations, and even for general populations performing physical activities such as walking or cycling while com- muting (de Nazelle et al., 2012; Hofman et al., 2018; Luengo-Oroz and Reis, 2019; Qiu et al., 2019; Quiros et al., 2013; Rivas et al., 2014). How- ever, research is scarce on the effects of ambient air pollution on exercis- ing athletes and their athletic performance, who may have greater than average susceptibility and exposure to air pollutants because of the physiological changes that occur during prolonged exercise (Quin et al., 2019). Specifically, there are 3 reasons why athletes are at higher risk from air pollution (McCafferty, 1981): (1) increased ventilation during exer- cise; (2) a greater fraction of air is inhaled through the mouth during ex- ercise, effectively bypassing the normal nasal filtration mechanisms; and (3) the increased airflow velocity carries pollutants deeper into the respiratory tract. Furthermore, pulmonary diffusion capacity in- creases with exercise (Turcotte et al., 1997; Stokes et al., 1981; Fisher and Cerny, 1982; Flaherty et al., 2013), increasing gaseous pollutant in- take. Nasal mucociliary clearance, impaired in long-distance runners, may also contribute to the higher susceptibility of endurance athletes given that pollutants which are normally cleared from the respiratory system, are instead absorbed (Atkinson, 1987). Even though research is scarce, studies on the relationship between air quality, athletic performance, and respiratory symptoms encourage pursuing further investigations. Lichter et al. (2015) assessed the effects of particulate air pollution on soccer players in German stadiums, re- vealing that performance was reduced under poor air quality condi- tions. Bos et al. (2011) and Quin et al. (2019) observed that the health benefits of active commuting could be negatively influenced by exercis- ing in polluted environments, while Rundell and Caviston (2008) re- ported that the acute inhalation of PM1 at concentrations in the range of many urban environments could impair exercise performance. Carlisle and Sharp (2001) and Cakmak et al. (2011) concluded that O3 was particularly damaging to athletes, with subjects achieving a lower aerobic fitness score on high ozone days. Finally, long-term exposure to outdoor air pollution may trigger intermittent endogenous airway acidification episodes indicative of pollution-related lung inflammation (Ferdinands et al., 2008). These results have particularly relevant impli- cations for top-level athletes participating in international competi- tions: the performance of athletes training in highly polluted environments may be impaired compared to athletes training in cleaner environments and, similarly, athletes used to training in cleaner envi- ronments may be adversely affected when competing in highly polluted locations. Thus, assessing exposure to air pollution in athletics venues becomes a necessity when aiming at understanding environmental drivers of both athletic performance, and athletes' health. In this framework, the aim of this study was to characterize air pol- lutant concentrations in the Yokohama stadium (in the competition and the training area) during the Yokohama 2019 World Relays the day with lowest ambient concentrations. This strategy could be adopted to define training and competition schedules, and would have special added value for athletes with respiratory conditions. Personal exposure to polycyclic aromatic hydrocarbons was quantified through wearable silicone wristbands, and showed highly var- iability across volunteers. The wristbands are a simple approach to assess personal exposure to potentially toxic organic compounds. Further research would be necessary with regard to specific air pollutants that may trigger or exacerbate respiratory conditions typical of the athlete community. The availability of high time-resolved ex- posure data in the stadiums opens up the possibility to calculate doses of specific pollutants for individual ath- letes in future athletics events, to understand the impact of environmental factors on athletic performance

Aspirin but not statins is inversely related to gastric cancer with a duration–risk effect: Results from the Stomach Cancer Pooling Project Consortium

Background: Aspirin and statins have been suggested to have potential chemopreventive effects against gastric cancer (GC), although the results of previous studies have been inconsistent. This study therefore aimed to investigate the association between the use of aspirin and statins and GC. Methods: A pooled analysis of seven case-control studies within the Stomach Cancer Pooling Project, including 3220 cases and 9752 controls, was conducted. Two-stage modeling analyses were used to estimate the association between aspirin and statin use and GC after adjusting for potential confounders. Results: The pooled odds ratio (OR) of GC for aspirin users versus nonusers was 0.72 (95% confidence interval [CI], 0.54–0.95). The protective effect of aspirin appeared stronger in individuals without a GC family history (OR, 0.60; 95% CI, 0.37–0.95), albeit with borderline heterogeneity between those with and without a family history (p =.064). The OR of GC decreased with increasing duration of aspirin use, with an OR of 0.41 (95% CI, 0.18–0.95) for durations of ≥15 years. An inverse, nonsignificant association with the risk of GC was observed for the use of statins alone (OR, 0.79; 95% CI, 0.52–1.18). Conclusions: These findings suggest that aspirin use, particularly long-term use, is associated with a reduced risk of GC, whereas a similar association was not observed with statins, possibly because of the low frequency of use. © 2024 The Author(s). Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society."This study was funded by the Associazione Italiana per la Ricerca sul Cancro (Project 21378 to Carlo La Vecchia) and by the Italian Ministry of Education, University and Research (PNRR per la Missione 4, Componente 2, Investimento1.1.Avviso 104/2022 Finanziato dall'Unione Europea–Next Generation EU Progetto MUR PRIN prot 2022A4WZFC to Stefania Boccia). Nuno Lunet and Samantha Morais are supported by national funds via the Foundation for Science and Technology (FCT) within the scope of Projects UIDB/04750/2020 and LA/P/0064/2020. Samantha Morais also received funding under the scope of Project “NEON-PC—Neuro-oncological complications of prostate cancer: Longitudinal study of cognitive decline” (POCI-01-0145-FEDER-032358; Reference PTDC/SAU-EPI/32358/2017) funded by Fundo Europeu de Desenvolvimento Regional via the Operational Program “Competitiveness and Internationalisation,” national funding from the FCT, and EPIUnit–Junior Research–Prog financing (UIDP/04750/2020). This research was supported in part by the Intramural Research Program of the US National Cancer Institute. The authors thank the European Cancer Prevention Organization for providing support for project meetings. Open access publishing facilitated by Universita degli Studi di Bologna, as part of the Wiley - CRUI-CARE agreement.

Cigarette smoking and gastric cancer in the stomach cancer pooling (StoP) project

Tobacco smoking is a known cause of gastric cancer, but several aspects of the association remain imprecisely quantified. We examined the relation between cigarette smoking and the risk of gastric cancer using a uniquely large dataset of 23 epidemiological studies within the ‘Stomach cancer Pooling (StoP) Project’, including 10 290 cases and 26 145 controls. We estimated summary odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study-specific ORs using random-effects models. Compared with never smokers, the ORs were 1.20 (95% CI: 1.09–1.32) for ever, 1.12 (95% CI: 0.99–1.27) for former, and 1.25 (95% CI: 1.11–1.40) for current cigarette smokers. Among current smokers, the risk increased with number of cigarettes per day to reach an OR of 1.32 (95% CI: 1.10–1.58) for smokers of more than 20 cigarettes per day. The risk increased with duration of smoking, to reach an OR of 1.33 (95% CI: 1.14–1.54) for more than 40 years of smoking and decreased with increasing time since stopping cigarette smoking (P for trend<0.01) and became similar to that of never smokers 10 years after stopping. Risks were somewhat higher for cardia than noncardia gastric cancer. Risks were similar when considering only studies with information on Helicobacter pylori infection and comparing all cases to H. pylori+ controls only. This study provides the most precise estimate of the detrimental effect of cigarette smoking on the risk of gastric cancer on the basis of individual data, including the relationship with dose and duration, and the decrease in risk following stopping smoking

Lifetime exposure to brominated trihalomethanes in drinking water and swimming pool attendance are associated with chronic lymphocytic leukemia: a Multicase-Control Study in Spain (MCC-Spain)

Background: Chronic lymphocytic leukemia (CLL) etiology is poorly understood, and carcinogenic chemicals in drinking and recreational water are candidates. Objective: To evaluate the association between drinking-water exposure to trihalomethanes (THMs) and nitrate as well as lifetime swimming pool attendance and CLL. Methods: During 2010-2013, hospital-based CLL cases and population-based controls were recruited in Spain, providing information on residential histories, type of water consumed and swimming pool attendance. Average THMs and nitrate levels in drinking water were linked to lifetime water consumption. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using mixed models. Results: Final samples for residential tap water analyses and swimming pool attendance analyses were 144 cases/1230 controls and 157 cases/1240 controls, respectively. Mean (SD) values for average lifetime residential brominated THMs and chloroform in tap water (μg/L), and ingested nitrate (mg/day) were 48.1 (35.6), 18.5 (6.7) and 13.7 (9.6) respectively in controls; and 72.9 (40.7), 17.9 (5.4), and 14.1 (8.8) in CLL cases. For each 10 μg/L increase of brominated THMs and chloroform lifetime-average levels, the ORs (95% CI) were 1.22 (1.14, 1.31) and 0.54 (0.34, 0.87), respectively. For each 5 mg/day increase of ingested nitrate, the OR of CLL was 0.91 (0.80, 1.04). The OR of lifetime pool users (vs. non-users) was 2.38 (1.61, 3.52). Upon performing annual frequency of attending pools analysis through categorization, the second and third categories showed an ORs of 2.36 (1.49, 3.72) and 2.40 (1.51, 3.83), respectively, and P-trend of 0.001. Impact statement: This study identifies an association of long-term exposure to THMs in drinking water, at concentrations below the regulatory thresholds and WHO guidelines, and swimming pool attendance, with chronic lymphocytic leukemia (CLL). These unprecedented findings are highly relevant since CLL is an incurable cancer with still unknown etiology and because the widespread exposure to chlorination by-products that remain in drinking and recreational water worldwide. Despite the demonstrated carcinogenicity in animals of several chlorination by-products, little is known about their potential risks on human health. This study makes a significant contribution to the search for environmental factors involved in the etiology of CLL and to the evidence of the health impact of these high prevalent water contaminants.The study was partially funded by the “Accion Transversal del Cancer”, approved on the Spanish Ministry Council on the 11th October 2007, by the Instituto de Salud Carlos III-FEDER (PI08/1770, PI08/0533, PI08/1359, PS09/00773, PS09/01286, PS09/01903, PS09/02078, PS09/01662, PI11/01889, PI11/00226, PI12/01270, PI12/00715, PI14/0613, PI15/00914, PI17CIII/00034), by the Fundación Marqués de Valdecilla (API 10/09), by the Conselleria de Sanitat of the Generalitat Valenciana (AP_061/10), by the European Commission grants FOOD-CT-2006-036224-HIWATE, by the Spanish Association Against Cancer (AECC) Scientific Foundation, by the Catalan Government Agency for Management of University and Research Grants (AGAUR) grants 2017SGR723, 2021SGR01354 and 2014SGR850, by the Fundación Caja de Ahorros de Asturias and by the University of Oviedo. ISGlobal acknowledges support from the Spanish Ministry of Science and Innovation through the “Centro de Excelencia Severo Ochoa 2019-2023” Program (CEX2018-000806-S), and support from the Generalitat de Catalunya through the CERCA Program.S

Long-Term Exposure to Nitrate and Trihalomethanes in Drinking Water and Prostate Cancer: A Multicase–Control Study in Spain (MCC-Spain)

BACKGROUND: Nitrate and trihalomethanes (THMs) in drinking water are widespread and are potential human carcinogens.OBJECTIVE: We evaluated the association between drinking-water exposure to nitrate and THMs and prostate cancer.METHODS: During the period 2008-2013, 697 hospital-based incident prostate cancer cases (97 aggressive tumors) and 927 population-based controls were recruited in Spain, providing information on residential histories and type of water consumed. Average nitrate and THMs levels in drinking water were linked with lifetime water consumption to calculate waterborne ingestion. Odds ratios (OR) and 95% confidence intervals (CI) were esti-mated using mixed models with recruitment area as random effect. Effect modification by tumor grade (Gleason score), age, education, lifestyle, and dietary factors was explored.RESULTS: Mean ( +/- standard deviation) adult lifetime waterborne ingested nitrate (milligrams per day), brominated (Br)-THMs (micrograms per day), and chloroform (micrograms per day) were 11.5 ( +/- 9.0), 20.7 ( +/- 32.4), and 15.1 ( +/- 14.7) in controls. Waterborne ingested nitrate >13.8 vs. = 8. Associations were higher in the youngest and those with lower intakes of fiber, fruit/vegetables, and vitamin C. Waterborne ingested THMs were not associated with prostate cancer. Residential tap water levels of Br-THMs and chloroform showed, respectively, inverse and positive associations with prostate cancer.CONCLUSIONS: Findings suggest long-term waterborne ingested nitrate could be a risk factor of prostate cancer, particularly for aggressive tumors. High intakes of fiber, fruit/vegetables and vitamin C may lower this risk. Association with residential levels but not ingested chloroform/Br-THM may suggest inhalation and dermal routes could be relevant for prostate cancer. https://doi.org/10.1289/EHP1139

Exposure to widespread drinking water chemicals, blood inflammation markers, and colorectal cancer

Background: Trihalomethanes (THMs) and nitrate are widespread chemicals in drinking water associated with colorectal cancer risk but mechanisms are not well understood. Objectives: We explored the association between exposure to THMs and nitrate in drinking water and inflammation markers, and the link with colorectal cancer risk. Methods: A subset of 198 colorectal cancer cases and 205 controls from the multicase-control study MCC-Spain were included. Average concentration of THMs (chloroform, bromodichloromethane, dibromochloromethane, bromoform) and nitrate in tap water at the residence was estimated from age 18 until 2 years before the interview ("long term") and for a recent period (3 years before diagnosis). Serum levels of EGF, eotaxin, G-CSF, IL-17E, IL-1rA, IL-8, IP-10, MDC, MPO, periostin, VEGF, and C-reactive protein (CRP) were measured. We estimated the linear association between inflammation markers and exposure among controls, and the odds ratio of colorectal cancer associated with THM and nitrate exposure, and inflammation markers. A mediation analysis was conducted to identify inflammation markers in the pathway between THM/nitrate exposure and colorectal cancer. Results: Serum concentrations of EGF, IL-8, IL-17E and eotaxin increased with recent residential levels of brominated THMs, chloroforom and/or total THM. No associations were observed for nitrate and for long-term residential THM levels. All residential exposures except chloroform were positively associated with colorectal cancer. Serum concentrations of VEGF and periostin were positively associated with colorectal cancer, while EGF was inversely associated. One protein-exposure combination (periostin-recent ingested brominated THMs) slightly mediated the association with colorectal cancer risk. Discussion: Results suggest that estimated THM exposure is involved in inflammation processes. However, the study design was limited to stablish etiologically relevant associations between the protein levels and colorectal cancer risk. The lack of association between nitrate exposure and inflammation markers suggests other biological mechanisms are involved in the link with colorectal cancer.Acknowledgements: We acknowledge support from the Spanish Ministry of Science and Innovation through the “Centro de Excelencia Severo Ochoa 2019-2023” Program (CEX2018-000806-S), and support from the Generalitat de Catalunya through the CERCA Program. This work was funded by the 7th Framework Programme EXPOSOMICS Project (grant agreement 308610), the Acci´on Transversal del C´ancer del Consejo de Ministros del 11/10/2007, and the Instituto de Salud Carlos III-FEDER (PI08/1770, PI08/0533, PI11/00226) FIS grants

The Association of Nighttime Fasting Duration and Prostate Cancer Risk: Results from the Multicase-Control (MCC) Study in Spain

Nighttime fasting has been inconclusively associated with a reduced risk of cancer. The purpose of this study was to investigate this association in relation to prostate cancer risk. We examined data from 607 prostate cancer cases and 848 population controls who had never worked in night shift work from the Spanish multicase-control (MCC) study, 2008-2013. Through an interview, we collected circadian information on meal timing at mid-age. We estimated odds ratios (OR) and 95% confidence intervals (CI) with unconditional logistic regression. After controlling for time of breakfast, fasting for more than 11 h overnight (the median duration among controls) was associated with a reduced risk of prostate cancer compared to those fasting for 11 h or less (OR = 0.77, 95% 0.54-1.07). Combining a long nighttime fasting and an early breakfast was associated with a lower risk of prostate cancer compared to a short nighttime fasting and a late breakfast (OR = 0.54, 95% CI 0.27-1.04). This study suggests that a prolonged nighttime fasting duration and an early breakfast may be associated with a lower risk of prostate cancer. Findings should be interpreted cautiously and add to growing evidence on the importance of chrononutrition in relation to cancer risk.Funding: Instituto de Salud Carlos III FIS PI11/01889. Anna Palomar-Cros is supported by a MINECO (Ministry of Economy in Spain) fellowship. We acknowledge support from the Spanish State Research Agency and Ministry of Science and Innovation through the “Centro de Excelencia Severo Ochoa 2019–2023” Program (CEX2018-000806-S), and support from the Generalitat de Catalunya through the CERCA Program

Risk model for prostate cancer using environmental and genetic factors in the spanish multi-case-control (MCC) study

Prostate cancer (PCa) is the second most common cancer among men worldwide. Its etiology remains largely unknown compared to other common cancers. We have developed a risk stratification model combining environmental factors with family history and genetic susceptibility. 818 PCa cases and 1,006 healthy controls were compared. Subjects were interviewed on major lifestyle factors and family history. Fifty-six PCa susceptibility SNPs were genotyped. Risk models based on logistic regression were developed to combine environmental factors, family history and a genetic risk score. In the whole model, compared with subjects with low risk (reference category, decile 1), those carrying an intermediate risk (decile 5) had a 265% increase in PCa risk (OR = 3.65, 95% CI 2.26 to 5.91). The genetic risk score had an area under the ROC curve (AUROC) of 0.66 (95% CI 0.63 to 0.68). When adding the environmental score and family history to the genetic risk score, the AUROC increased by 0.05, reaching 0.71 (95% CI 0.69 to 0.74). Genetic susceptibility has a stronger risk value of the prediction that modifiable risk factors. While the added value of each SNP is small, the combination of 56 SNPs adds to the predictive ability of the risk model