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2.
Environ Res ; 167: 673-683, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30196934

RESUMO

Epidemiology studies (case-control, cohort, time trend and case studies) published since the International Agency for Research on Cancer (IARC) 2011 categorization of radiofrequency radiation (RFR) from mobile phones and other wireless devices as a possible human carcinogen (Group 2B) are reviewed and summarized. Glioma is an important human cancer found to be associated with RFR in 9 case-control studies conducted in Sweden and France, as well as in some other countries. Increasing glioma incidence trends have been reported in the UK and other countries. Non-malignant endpoints linked include acoustic neuroma (vestibular Schwannoma) and meningioma. Because they allow more detailed consideration of exposure, case-control studies can be superior to cohort studies or other methods in evaluating potential risks for brain cancer. When considered with recent animal experimental evidence, the recent epidemiological studies strengthen and support the conclusion that RFR should be categorized as carcinogenic to humans (IARC Group 1). Opportunistic epidemiological studies are proposed that can be carried out through cross-sectional analyses of high, medium, and low mobile phone users with respect to hearing, vision, memory, reaction time, and other indicators that can easily be assessed through standardized computer-based tests. As exposure data are not uniformly available, billing records should be used whenever available to corroborate reported exposures.


Assuntos
Neoplasias Encefálicas , Telefone Celular , Glioma , Animais , Neoplasias Encefálicas/epidemiologia , Telefone Celular/estatística & dados numéricos , Estudos Transversais , Campos Eletromagnéticos , França , Glioma/epidemiologia , Humanos , Suécia
3.
Environ Sci Pollut Res Int ; 24(15): 13666-13673, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28397118

RESUMO

Although cell phones have been used worldwide, some adverse and toxic effects were reported for this communication technology apparatus. To analyze in vivo effects of exposure to radiofrequency-electromagnetic field (RF-EMF) on protein expression in rat testicular proteome, 20 Sprague-Dawley rats were exposed to 900 MHz RF-EMF for 0, 1, 2, or 4 h/day for 30 consecutive days. Protein content of rat testes was separated by high-resolution two-dimensional electrophoresis using immobilized pH gradient (pI 4-7, 7 cm) and 12% acrylamide and identified by MALDI-TOF/TOF-MS. Two protein spots were found differentially overexpressed (P < 0.05) in intensity and volume with induction factors 1.7 times greater after RF-EMF exposure. After 4 h of daily exposure for 30 consecutive days, ATP synthase beta subunit (ASBS) and hypoxia up-regulated protein 1 precursor (HYOU1) were found to be significantly up-regulated. These proteins affect signaling pathways in rat testes and spermatogenesis and play a critical role in protein folding and secretion in the endoplasmic reticulum. Our results indicate that exposure to RF-EMF produces increases in testicular proteins in adults that are related to carcinogenic risk and reproductive damage. In light of the widespread practice of men carrying phones in their pockets near their gonads, where exposures can exceed as-tested guidelines, further study of these effects should be a high priority.


Assuntos
Campos Eletromagnéticos , Proteômica , Testículo/efeitos da radiação , Animais , Telefone Celular , Humanos , Masculino , Ondas de Rádio , Ratos , Ratos Sprague-Dawley , Testículo/metabolismo
4.
Int J Oncol ; 46(5): 1865-71, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25738972

RESUMO

Quickly changing technologies and intensive uses of radiofrequency electromagnetic field (RF-EMF)­emitting phones pose a challenge to public health. Mobile phone users and uses and exposures to other wireless transmitting devices (WTDs) have increased in the past few years. We consider that CERENAT, a French national study, provides an important addition to the literature evaluating the use of mobile phones and risk of brain tumors. The CERENAT finding of increased risk of glioma is consistent with studies that evaluated use of mobile phones for a decade or longer and corroborate those that have shown a risk of meningioma from mobile phone use. In CERENAT, exposure to RF­EMF from digitally enhanced cordless telephones (DECTs), used by over half the population of France during the period of this study, was not evaluated. If exposures to DECT phones could have been taken into account, the risks of glioma from mobile phone use in CERENAT are likely to be higher than published. We conclude that radiofrequency fields should be classified as a Group 2A ̔probable̓ human carcinogen under the criteria used by the International Agency for Research on Cancer (Lyon, France). Additional data should be gathered on exposures to mobile and cordless phones, other WTDs, mobile phone base stations and Wi­Fi routers to evaluate their impact on public health. We advise that the as low as reasonable achievable (ALARA) principle be adopted for uses of this technology, while a major cross­disciplinary effort is generated to train researchers in bioelectromagnetics and provide monitoring of potential health impacts of RF­EMF.


Assuntos
Neoplasias Encefálicas/etiologia , Carcinógenos/classificação , Telefone Celular , Campos Eletromagnéticos/efeitos adversos , Glioma/etiologia , Neoplasias Encefálicas/epidemiologia , França/epidemiologia , Glioma/epidemiologia , Humanos , Fatores de Risco
5.
Pathophysiology ; 20(2): 123-9, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23664410

RESUMO

With 5.9 billion reported users, mobile phones constitute a new, ubiquitous and rapidly growing exposure worldwide. Mobile phones are two-way microwave radios that also emit low levels of electromagnetic radiation. Inconsistent results have been published on potential risks of brain tumors tied with mobile phone use as a result of important methodological differences in study design and statistical power. Some studies have examined mobile phone users for periods of time that are too short to detect an increased risk of brain cancer, while others have misclassified exposures by placing those with exposures to microwave radiation from cordless phones in the control group, or failing to attribute such exposures in the cases. In 2011, the World Health Organization, International Agency for Research on Cancer (IARC) advised that electromagnetic radiation from mobile phone and other wireless devices constitutes a "possible human carcinogen," 2B. Recent analyses not considered in the IARC review that take into account these methodological shortcomings from a number of authors find that brain tumor risk is significantly elevated for those who have used mobile phones for at least a decade. Studies carried out in Sweden indicate that those who begin using either cordless or mobile phones regularly before age 20 have greater than a fourfold increased risk of ipsilateral glioma. Given that treatment for a single case of brain cancer can cost between $100,000 for radiation therapy alone and up to $1 million depending on drug costs, resources to address this illness are already in short supply and not universally available in either developing or developed countries. Significant additional shortages in oncology services are expected at the current growth of cancer. No other environmental carcinogen has produced evidence of an increased risk in just one decade. Empirical data have shown a difference in the dielectric properties of tissues as a function of age, mostly due to the higher water content in children's tissues. High resolution computerized models based on human imaging data suggest that children are indeed more susceptible to the effects of EMF exposure at microwave frequencies. If the increased brain cancer risk found in young users in these recent studies does apply at the global level, the gap between supply and demand for oncology services will continue to widen. Many nations, phone manufacturers, and expert groups, advise prevention in light of these concerns by taking the simple precaution of "distance" to minimize exposures to the brain and body. We note than brain cancer is the proverbial "tip of the iceberg"; the rest of the body is also showing effects other than cancers.

7.
Electromagn Biol Med ; 31(1): 34-51, 2012 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-21999884

RESUMO

The existing cell phone certification process uses a plastic model of the head called the Specific Anthropomorphic Mannequin (SAM), representing the top 10% of U.S. military recruits in 1989 and greatly underestimating the Specific Absorption Rate (SAR) for typical mobile phone users, especially children. A superior computer simulation certification process has been approved by the Federal Communications Commission (FCC) but is not employed to certify cell phones. In the United States, the FCC determines maximum allowed exposures. Many countries, especially European Union members, use the "guidelines" of International Commission on Non-Ionizing Radiation Protection (ICNIRP), a non governmental agency. Radiofrequency (RF) exposure to a head smaller than SAM will absorb a relatively higher SAR. Also, SAM uses a fluid having the average electrical properties of the head that cannot indicate differential absorption of specific brain tissue, nor absorption in children or smaller adults. The SAR for a 10-year old is up to 153% higher than the SAR for the SAM model. When electrical properties are considered, a child's head's absorption can be over two times greater, and absorption of the skull's bone marrow can be ten times greater than adults. Therefore, a new certification process is needed that incorporates different modes of use, head sizes, and tissue properties. Anatomically based models should be employed in revising safety standards for these ubiquitous modern devices and standards should be set by accountable, independent groups.


Assuntos
Telefone Celular/normas , Exposição Ambiental/normas , Doses de Radiação , Animais , Certificação , Criança , Simulação por Computador , Humanos , Lesões por Radiação/epidemiologia
9.
Environ Health Perspect ; 116(11): 1439-42, 2008 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-19057693

RESUMO

BACKGROUND: Chemical carcinogenesis bioassays in animals have long been recognized and accepted as valid predictors of potential cancer hazards to humans. Most rodent bioassays begin several weeks after birth and expose animals to chemicals or other substances, including workplace and environmental pollutants, for 2 years. New findings indicate the need to extend the timing and duration of exposures used in the rodent bioassay. OBJECTIVES: In this Commentary, we propose that the sensitivity of chemical carcinogenesis bio-assays would be enhanced by exposing rodents beginning in utero and continuing for 30 months (130 weeks) or until their natural deaths at up to about 3 years. DISCUSSION: Studies of three chemicals of different structures and uses-aspartame, cadmium, and toluene-suggest that exposing experimental animals in utero and continuing exposure for 30 months or until their natural deaths increase the sensitivity of bioassays, avoid false-negative results, and strengthen the value and validity of results for regulatory agencies. CONCLUSIONS: Government agencies, drug companies, and the chemical industry should conduct and compare the results of 2-year bioassays of known carcinogens or chemicals for which there is equivocal evidence of carcinogenicity with longer-term studies, with and without in utero exposure. If studies longer than 2 years and/or with in utero exposure are found to better identify potential human carcinogens, then regulatory agencies should promptly revise their testing guidelines, which were established in the 1960s and early 1970s. Changing the timing and dosing of the animal bioassay would enhance protection of workers and consumers who are exposed to potentially dangerous workplace or home contaminants, pollutants, drugs, food additives, and other chemicals throughout their lives.


Assuntos
Bioensaio , Carcinógenos/toxicidade , Poluentes Ambientais/toxicidade , Animais , Testes de Carcinogenicidade
11.
Environ Health Perspect ; 115(6): 941-6, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17589604

RESUMO

BACKGROUND: The expected ratio of male to female births is generally believed to be 1.05, also described as the male proportion of 0.515. OBJECTIVES: We describe trends in sex ratio at birth and in fetal deaths in the United States, in African Americans and in whites, and in Japan, two industrial countries with well-characterized health data infrastructures, and we speculate about possible explanations. METHODS: Public health records from national statistical agencies were assembled to create information on sex ratio at birth and in fetal deaths in the United States (1970-2002) and Japan (1970-1999), using SPSS. RESULTS: Sex ratio at birth has declined significantly in Japan and in U.S. whites, but not for African Americans, for whom sex ratio remains significantly lower than that of whites. The male proportion of fetal death has increased overall in Japan and in the United States. CONCLUSIONS: Sex ratio declines are equivalent to a shift from male to female births of 135,000 white males in the United States and 127,000 males in Japan. Known and hypothesized risk factors for reduced sex ratio at birth and in fetal deaths cannot account fully for recent trends or racial or national differences. Whether avoidable environmental or other factors--such as widespread exposure to metalloestrogens or other known or suspected endocrine-disrupting materials, changes in parental age, obesity, assisted reproduction, or nutrition--may account for some of these patterns is a matter that merits serious concern.


Assuntos
Morte Fetal/epidemiologia , Razão de Masculinidade , Negro ou Afro-Americano , Povo Asiático , Feminino , Morte Fetal/induzido quimicamente , Humanos , Recém-Nascido , Japão/epidemiologia , Modelos Lineares , Masculino , Fatores de Risco , Estados Unidos/epidemiologia , População Branca
12.
Int J Occup Environ Health ; 11(2): 199-201, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-15875896

RESUMO

Epidemiologic methods only seldom identify causes of childhood cancer associated with relative risks below a factor of 1 1/2-2. Children are at risk of exposure to over 15,000 high-production-volume chemicals and are certainly exposed to many carcinogens. The individual impacts of most of these agents are too small to be detected, but collectively these unrecognized factors are potentially important. Infants and children are exposed to higher levels of some environmental toxicants and may also be more sensitive. During intrauterine development and childhood, cells divide frequently, and the mutant frequency rises rapidly. Endocrine-related cancers or susceptibility to cancer may result from developmental exposures rather than from exposures existing at or near the time of diagnosis. That environmental exposures may be important causes of childhood cancers is indicated by associations of enzyme polymorphisms with risk.


Assuntos
Proteção da Criança , Exposição Ambiental , Poluentes Ambientais/efeitos adversos , Neoplasias/etiologia , Carcinógenos , Criança , Humanos , Polimorfismo Genético , Fatores de Risco
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