Cell Phone Radiation Exposure Limits and Engineering Solutions.

In the 1990s, the Institute of Electrical and Electronics Engineers (IEEE) restricted its risk assessment for human exposure to radiofrequency radiation (RFR) in seven ways: (1) Inappropriate focus on heat, ignoring sub-thermal effects. (2) Reliance on exposure experiments performed over very short times. (3) Overlooking time/amplitude characteristics of RFR signals.

Concordance between sites of tumor development in humans and in experimental animals for 111 agents that are carcinogenic to humans.

Since the inception of the in the early 1970s, this has developed 119 Volumes on more than 1000 agents for which there exists some evidence of cancer risk to humans. Of these, 120 agents were found to meet the criteria for classification as (Group 1). Volume 100 of the , compiled in 2008-2009 and published in 2012, provided a review and update of the 107 Group 1 agents identified as of 2009.

Commentary on the utility of the National Toxicology Program study on cell phone radiofrequency radiation data for assessing human health risks despite unfounded criticisms aimed at minimizing the findings of adverse health effects.

The National Toxicology Program (NTP) conducted two-year studies of cell phone radiation in rats and mice exposed to CDMA- or GSM-modulated radiofrequency radiation (RFR) at exposure intensities in the brain of rats that were similar to or only slightly higher than potential, localized human exposures from cell phones held next to the head. This study was designed to test the (null) hypothesis that cell phone radiation at non-thermal exposure intensities could not cause adverse health effects, and to provide dose-response data for any detected toxic or carcinogenic effects. Partial findings released from that study showed significantly increased incidences and/or trends for gliomas and glial cell hyperplasias in the brain and schwannomas and Schwann cell hyperplasias in the heart of exposed male rats.

Effect of cell phone radiofrequency radiation on body temperature in rodents: Pilot studies of the National Toxicology Program's reverberation chamber exposure system.

Radiofrequency radiation (RFR) causes heating, which can lead to detrimental biological effects. To characterize the effects of RFR exposure on body temperature in relation to animal size and pregnancy, a series of short-term toxicity studies was conducted in a unique RFR exposure system. Young and old B6C3F1 mice and young, old, and pregnant Harlan Sprague-Dawley rats were exposed to Global System for Mobile Communication (GSM) or Code Division Multiple Access (CDMA) RFR (rats = 900 MHz, mice = 1,900 MHz) at specific absorption rates (SARs) up to 12 W/kg for approximately 9 h a day for 5 days.

Commentary: IARC Monographs Program and public health under siege by corporate interests.

The International Agency for Research on Cancer (IARC) evaluates causes of cancer with help from independent international experts in an open and transparent manner. Countries, research and regulatory agencies, and other organizations adopt IARC evaluations for communication of human cancer hazards, and for strategies to prevent cancer. Scientists worldwide endorse IARC cancer evaluations and process.

Life-Time Dosimetric Assessment for Mice and Rats Exposed in Reverberation Chambers of the 2-Year NTP Cancer Bioassay Study on Cell Phone Radiation.

In this paper, we present the detailed life-time dosimetry analysis for rodents exposed in the reverberation exposure system designed for the two-year cancer bioassay study conducted by the National Toxicology Program of the National Institute of Environmental Health Sciences. The study required the well-controlled and characterized exposure of individually housed, unrestrained mice at 1900 MHz and rats at 900 MHz, frequencies chosen to give best uniformity exposure of organs and tissues. The wbSAR, the peak spatial SAR and the organ specific SAR as well as the uncertainty and variation due to the exposure environment, differences in the growth rates, and animal posture were assessed.

A Radio Frequency Radiation Exposure System for Rodents based on Reverberation Chambers.

In this paper we present the novel design features, their technical implementation, and an evaluation of the radio Frequency (RF) exposure systems developed for the National Toxicology Program (NTP) of the National Institute of Environmental Health Sciences (NIEHS) studies on the potential toxicity and carcinogenicity of 2nd and 3rd generation mobile-phone signals. The system requirements for this 2-year NTP cancer bioassay study were the tightly-controlled lifetime exposure of rodents (1568 rats and 1512 mice) to three power levels plus sham simulating typical daily, and higher, exposures of users of GSM and CDMA (IS95) signals. Reverberation chambers and animal housing were designed to allow extended exposure time per day for free-roaming individually-housed animals.

War on Carcinogens: industry disputes human relevance of chemicals causing cancer in laboratory animals based on unproven hypotheses, using kidney tumors as an example.

Evidence from studies in animals is essential for identifying chemicals likely to cause or contribute to many diseases in humans, including cancers. Yet, to avoid or delay the implementation of protective public health standards, the chemical industry typically denies cancer causation by agents they produce. The spurious arguments put forward to discount human relevance are often based on inadequately tested hypotheses or modes of action that fail to meet Bradford Hill criteria for causation.

MTBE: recent carcinogenicity studies.

MTBE, a gasoline oxygenate, has contaminated drinking water sources for many years. Carcinogenicity studies conducted in animals in the 1990s raised concerns of potential human health risks. Recent industry-sponsored studies have confirmed the carcinogenic effects of this agent and have identified additional sites of tumor induction (i.

Chemically exacerbated chronic progressive nephropathy not associated with renal tubular tumor induction in rats: an evaluation based on 60 carcinogenicity studies by the national toxicology program.

Chronic progressive nephropathy (CPN) is a common age-related degenerative-regenerative disease of the kidney that occurs in both sexes of most strains of rats. Recently, claims have been made that enhanced CPN is a mode of action for chemically induced kidney tumors in male rats and that renal tubular tumors (RTTs) induced by chemicals that concomitantly exacerbate CPN are not relevant for human cancer risk assessments. Although CPN is an observable histopathological lesion that may be modified by diet, the etiology of this disease and the mechanisms for its exacerbation by chemicals are unknown, and it fails to meet fundamental principles for defining carcinogenic modes of action and human relevance.

Environmental justice and primary prevention of cancer: the odyssey and legacy of lorenzo tomatis.

Lorenzo Tomatis [1929-2007] devoted his private and professional life to the betterment of mankind. As a physician, scientist, and humanitarian he championed against the plight of social injustice and promoted the obvious benefits of primary prevention of diseases compared to treatments that prevent or delay disease progression, especially occupational cancers. An avowed student and scholar of literature, the arts, the history of medicine and science, and chemical carcinogenesis, he believed in and wrote about these issues throughout his storied life.

Lorenzo Tomatis and primary prevention of environmental cancer.

The leading 20th century proponent for primary prevention of environmental cancer was Dr. Lorenzo Tomatis, the former Director of the International Agency for Research on Cancer and founder of the IARC Monographs program. This paper is dedicated to the memory of Dr.

Exposure to hexavalent chromium resulted in significantly higher tissue chromium burden compared with trivalent chromium following similar oral doses to male F344/N rats and female B6C3F1 mice.

In National Toxicology Program 2-year studies, hexavalent chromium [Cr(VI)] administered in drinking water was clearly carcinogenic in male and female rats and mice, resulting in small intestine epithelial neoplasms in mice at a dose equivalent to or within an order of magnitude of human doses that could result from consumption of chromium-contaminated drinking water, assuming that dose scales by body weight(3/4) (body weight raised to the 3/4 power). In contrast, exposure to trivalent chromium [Cr(III)] at much higher concentrations may have been carcinogenic in male rats but was not carcinogenic in mice or female rats. As part of these studies, total chromium was measured in tissues and excreta of additional groups of male rats and female mice.

Clarifying carcinogenicity of ethylbenzene.

Ethylbenzene has been evaluated for carcinogenic activity in Fischer rats and B6C3F1 mice exposed by inhalation (Chan et al., 1998; Chan, 1999) and in Sprague-Dawley rats after oral exposure (Maltoni et al., 1985,1997).

Hexavalent chromium is carcinogenic to F344/N rats and B6C3F1 mice after chronic oral exposure.

Background: Hexavalent chromium [Cr(VI)] is a human carcinogen after inhalation exposure. Humans also ingest Cr(VI) from contaminated drinking water and soil; however, limited data exist on the oral toxicity and carcinogenicity of Cr(VI).

Objective: We characterized the chronic oral toxicity and carcinogenicity of Cr(VI) in rodents.

Developmental neurotoxicity of perfluorinated chemicals modeled in vitro.

Background: The widespread detection of perfluoroalkyl acids and their derivatives in wildlife and humans, and their entry into the immature brain, raise increasing concern about whether these agents might be developmental neurotoxicants.

Objectives: We evaluated perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorooctane sulfonamide (PFOSA), and perfluorobutane sulfonate (PFBS) in undifferentiated and differentiating PC12 cells, a neuronotypic line used to characterize neurotoxicity.

Methods: We assessed inhibition of DNA synthesis, deficits in cell numbers and growth, oxidative stress, reduced cell viability, and shifts in differentiation toward or away from the dopamine (DA) and acetylcholine (ACh) neurotransmitter phenotypes.