The Largest Security-Cleared Career Network for Defense and Intelligence Jobs - JOIN NOW


Reports - Assessment of Public Health Concerns Associated with Pave Paws Radar Installations

Assessment of Public Health Concerns Associated with Pave Paws Radar Installations

Report Prepared for

The Massachusetts Department of Public Health

November 1, 1999


Linda S. Erdreich, Ph.D.

Om P. Gandhi, Sc.D.

Henry Lai, Ph.D.

Marvin C. Ziskin, M.D.

Table of Contents Page

  1. Introduction and Background
  2. Conclusions from Experimental Studies
  3. Conclusions from Epidemiological Studies
  4. 3.1 Scientific Procedures for Assessing Potential Human Risk

    3.2 Evaluating Epidemiological Studies of RFR Exposures and Cancer

    3.3 Recent Epidemiological Studies

  5. Discussion and Summary
  6. References
  7. Approval of Document by Expert Panel


The Expert Panel was asked to provide information to the Massachusetts Department of Public Health (MDPH) on how to assess the public health implications of exposure to radiofrequency electromagnetic radiation (RFR) from the PAVE PAWS radar antenna. Cape Cod residents have expressed concern regarding the possibility of adverse health effects from long-term low level exposures to the emissions from PAVE PAWS. These concerns have been exacerbated by reports of higher cancer rates on Cape Cod compared to the rest of Massachusetts [MDPH, 1999]. At a public meeting in Sandwich, MA on February 16, 1999, local residents have referred to several laboratory studies, epidemiology studies, and reviews, both published and unpublished, that cause them to question whether exposures from PAVE PAWS can affect the health of people on Cape Cod.

The charge from the MDPH to the expert panel was to review existing information regarding the potential health effects from exposure to radiofrequency electromagnetic radiation (RFR) from the Cape Cod PAVE PAWS radar installation. In particular, the panel should:

(1) Determine if existing PAVE PAWS RFR data is adequate to estimate exposure potential health effects on Cape Cod;

(2) If not, make recommendations for how to collect or estimate exposure that can be applied epidemiologically to identify the public health implication of PAVE PAWS on Cape Cod;

(3) Assuming adequate data is available, make recommendation for how to assess the public health implications from exposure; and

(4) Prepare a report that includes the above recommendations and a summary of the current scientific understanding of the health effects, particularly cancer, from exposure to the type of RFR emitted from PAVE PAWS and the aspects of RFR (i.e., peak or average power levels, pulse or constant exposure, etc) seemingly most responsible for the various health effects.

In response to the first and second charges, the Panel decided that additional measurements of exposure levels (power densities) in the vicinity of the PAVE PAWS installation would be necessary to estimate the potential health effects to the local community. It was recommended by the Panel that the measurements should be performed by experienced personnel approved by both the community and the MDPH. Measurements should be performed with proper equipment at six to twelve different locations being sure to include points of interest to the public, as well as the likely locations of maximum exposure to the public. The measurements should not be limited to just those frequencies emitted by PAVE PAWS, but should include a detailed frequency analysis of the RF spectrum from 30 kHz to 30 GHz. The latter is important to ascertain the total RFR environment to which the public is exposed. An interim report detailing the above points was submitted to the MDPH in August, 1999.

The second charge from MDPH to this Panel requests a recommendation on how to collect data to assess exposure "that can be applied epidemiologically to identify the public health implications of PAVE PAWS on Cape Cod". The recommendation in the Interim Report for a study delineating areas of higher and lower exposure in comparison to background will assist the MDPH: 1) in assessing the potential health risks from exposure, and 2) in determining the need for, and in planning epidemiological follow-up studies. The recommended measurements strategy was designed as a screening strategy, to limit the use of resources until more is known, and therefore is not likely to provide direct information for specific case-control or cohort studies of Cape Cod. For example, for any identified exposure sources, PAVE PAWS or other, systematic sampling may be needed based on distance from the source. In addition, if the measurements identify other RF sources, then additional measurements may be needed. Measurements can be used to evaluate the reliability of calculations, and to dpetermine whether calculations can be used to develop more extensive information on exposure potential.

Epidemiology studies generally require systematic measurements to estimate exposures of individuals. However, the proposed measurement strategy is designed to capture maximum exposures, and does not include systematic measurements to characterize population exposure by town or census tracts. The MDPH did support an epidemiology study of cancer for different towns and census tracts [Upper Cape Cod Cancer Incidence Review, June 1999]. Although cancer rates assessed by geopolitical areas (census tracts) in epidemiological studies cannot be directly linked to cause and effect, such studies provide a basis for defining priorities for additional study. Geographic correlations can be facilitated and refined by the use of geographic information systems (GIS), which permit precise mapping of disease and areas of exposure.

The measurement survey that has been recommended will enable the MDPH to assess exposure intensity in comparison to background levels in various environments. In health risk assessments, environmental levels that are compliant with existing standards or exposure limits, or are within the range of background levels (levels commonly found in areas removed from the influence of specific sources) are not generally regarded as having public health implications. Residents on the Cape have questioned some of these exposure limits, and for that reason may want to ensure that exposures are below these guidance limits, or to assess how they compare with background levels. One approach used to assess the implications of potential exposures is to calculate the ratio of measured or calculated exposure estimates to recommended exposure limits.

For nearly all environment exposures, average exposure over time is used as a practical measure of exposure, provided there is no experimental evidence that suggests otherwise. RFR intensities are highest close to the source, and decrease with increasing distance. The pulsed nature of the PAVE PAWS signal generates high intensity of extremely short duration. However, during the pulse, RFR intensities are relatively high. Therefore, peak levels are of interest, and the available information on peak levels should be examined. However, there are no convincing experimental data indicating any adverse health effect at levels below national guidelines. Experimental studies involving pulsed RFR have shown 'microwave hearing' as the only non-thermal effect presently widely accepted by the scientific community This transient effect is an auditory sensation 'heard' upon exposure to very high intensity pulsed fields. The threshold is approximately 0.6 μJ/g/pulse or approximately 600 W/kg. There are no known or expected sequellae.

The movement of the beam means that RFR levels at a given point in space and time, whether measured or calculated, are not constant, but are changing. The RFR produced by the PAVE PAWS main beam or by its side lobes at any location at ground level is not continuous, but varies over time. To avoid underestimating exposure, exposure assessments, whether by calculation or measurement, should be based on the level when the beam is present.

The remainder of this report is the response of the Panel to the third and fourth charge. In order to do so in a fashion that responds to the primary charge to the Panel - to assess the public health implications of exposure to radiofrequency electromagnetic radiation (RFR) from the PAVE PAWS radar antenna - it is necessary to define what we know and what is not known about potential health effects from RFR (the scientific evidence assessment); and to then identify reasonable measures to take this information into account (the public health policy assessment). The foundation of available scientific evidence is sufficient to make interim public health recommendations by this Panel, even if it does not establish that conclusive scientific evidence is present.

In order to examine the possible health effects of exposure to the radiation of the PAVE PAWS radars, we need to consider the interaction of various features and parameters of radiofrequency radiation (RFR) exposure on biological systems. Both animal experimental studies and human epidemiological studies are important. In our review of the literature we have considered all pertinent articles, including those mentioned by members of the community that have not been published in the peer-reviewed literature (e.g. Cherry, 1998; Firstenberg, 1993). Reviews by other scientists provid>

Transfer interrupted!

are based on our own comprehensive review of the data. The available data suggest a complex reaction. Many parameters of RFR exposure, including intensity, frequency, duration, waveform, frequency- and amplitude-modulation, are important determinants of biological responses. Therefore, great caution should be taken in applying the existing research results to evaluate the possible effect of exposure to RFR from the PAVE PAWS radar system. In addition, exposure to the PAVE PAWS radiation is a long-term exposure to low intensity RFR, of whose health effects we know little if anything.


The intensity (or power intensity) of RFR in the environment is measured in units such as mW/cm2. However, the intensity provides little information on the biological consequence unless the amount of energy absorbed by the irradiated object is known. This is generally given as the specific absorption rate (SAR), which is the rate of energy absorbed by a unit mass (e.g., one kg of tissue) of the object, and usually expressed as W/kg. The rate of absorption and the pattern of distribution of RFR energy in an organism depend on many factors. The pattern of energy absorption inside an irradiated body is non-uniform, and biological responses are dependent on distribution of energy and on the body part that is affected [Lai et al., 1984, 1988].

In the case of the PAVE PAWS radar, because of the distance from the radar, the power densities that one would be exposed to, and thus, the SARs, are small. Most studies described in the literature used relatively high intensities of exposure and although they may not be sufficiently similar to the present consideration, they do provide information on thresholds of biological effects that are widely accepted by the scientific community. However, some studies also show effects at power density levels lower than those involved in heating living tissue. There is controversy over how these effects can occur, although it is beyond argument that bioeffects do occur across many RF frequencies and power intensities and SAR conditions. It is important to distinguish between a biological effect that has no apparent adverse health effect and a biological effect which does. It is not known if any of the low level effects are capable of producing adverse health effects. Nevertheless, it is important not to dismiss "small" power densities and SARs that may have potential effects.

It has been estimated that there are some 7000 to 10,000 scientific reports on the biological effects of RFR in the literature. The overwhelming majority report no harmful effects providing the exposures remain at or below an SAR value of 4 W/kg. At 4 W/kg, laboratory mammals demonstrate a temporary stoppage of pedal-pushing activity. At the frequencies emitted by PAVE PAWS, this would correspond to an intensity of approximately 10 mW/cm2. Exposure estimates and measurements regarding PAVE PAWS have been expressed in microwatts per square centimeter; 10 mW/cm2 = 10,000 mW/cm2.

In order not to overlook anything relevant to PAVE PAWS, the Panel has considered a number of studies investigating effects of low-intensity RFR. The following are some examples: Kwee and Raskmark [1997] reported changes in cell proliferation (division) at SARs of 0.000021- 0.0021 W/kg; Salford et al [1997] reported increase in blood-brain barrier permeability in mice exposed at 0.0004 W/kg; Navakatikian and Tomashevskaya [1994] reported a change in avoidance conditioned reflux in rats after 0.5 hr of exposure to RFR at 0.0027 W/kg and a drop in testosterone at 0.027 W/kg; Veyret et al. [1991 reported a change in immunological functions after RFR exposure at 0.015 W/kg; Ray and Behari [1990] reported a decrease in eating and drinking behavior in rats exposed to 0.0317 W/kg; Dutta et al. [1989] reported changes in calcium metabolism in cells exposed to RFR at 0.05-0.005 W/kg; Phillips et al. [1998] observed DNA damage at 0.024-0.0024 W/kg; Magnras and Xenos [1997] reported a decrease in reproductive functions in mice exposed to RFR intensities of 160-1053 nW/cm2 (the SAR was not calculated); and Chiang et al [1989] reported a change in white blood cell functions in humans exposed to a 4 W/cm2 field . It must be pointed out that most of the above studies investigated the effect of a single episode of RFR exposure for varying durations of exposure, but not long-term chronic exposure. Also, other studies failed to observe these effects at much higher intensities. Another important parameter to consider is the frequency of RFR. Frequency is analogous to the color of a light bulb, and intensity is its wattage. There is a question of whether the effects of RFR of one frequency are different from those of another frequency. The answer to this question depends on the mechanism involved. Nearly all of the known adverse effects of RFR are due to temperature elevation of the exposed part, and for this the pertinent quantity is the SAR, regardless of the frequency employed. The question of frequency is vital If there are any harmful effects that could be frequency-specific. This also calls into question whether existing research data on the biological effects of RFR can apply to the case of PAVE PAWS, as most previous research studied frequencies different from those used in the radar system.

It must be pointed out that data showing different frequencies producing different effects, or an effect occurring at one frequency and not at another, are sparse. An example is the study by Sanders et al [1984] who observed that RFR at frequencies of 200 and 591 MHz, but not at 2450 MHz, produced effects on energy metabolism in neural tissue. There are also several studies that showed different frequencies of RFR producing different effects [D'Andrea et al., 1979, 1980; de Lorge and Ezell, 1980; Thomas et al., 1975]. It is not certain whether these differences were actually due to differences in the distribution of energy absorption in the body of the exposed animal at the various frequencies. However, some studies showed frequency-window effects, i.e., an effect is only observed at a certain range of frequencies and not at higher or lower ranges [Bawin et al., 1975; Blackman et al., 1979, 1980a,b, 1989; Chang et al., 1982; Dutta et al., 1984, 1989, 1992; Lin-Liu and Adey, l982; Oscar and Hawkins, 1977; Sheppard et al., 1979]. These results may suggest that the frequency of an RFR can be a factor in determining the biological outcome of exposure.

On the other hand, there are many more studies showing that different frequencies can produce the same effect. For example, changes in blood-brain barrier have been reported after exposure to RFRs of 915 MHz [Salford et al., 1994]; 1200 MHz [Frey et al., 1975], 1300 MHz [Oscar and Hawkin, 1977], 2450 and 2800 MHz [Albert, 1977], and effects on calcium have been reported at 50 MHz [Blackman et al., 1980b], 147 MHz [Bawin et al., 1975; Blackman et al., 1980a; Dutta et al., 1989], 450 MHz [Sheppard et al., 1979], and 915 MHz [Dutta et al., 1984]. If there is any difference in effects among different frequencies, it is a difference in quantity and not in quality. There are few studies on the frequencies (~400 MHz) used in the PAVE PAWS radars. One study specially designed to address this question is the study by Toler et al. [1997]. In that study, mice were exposed for 21 months (22 hr/day, 7 days/week) to a 435 MHz pulse-wave (1.0 s pulse width, 1 kHz pulse rate) at an SAR of 0.32 W/kg. The investigators did not find a significant increase in cancer in mice chronically exposed to the radiation. The only biological finding was that there was a statistically significant increase in the exposed animals of bilateral ovarian stromal tumors. Another related study is that of Lyle et al (1983) showing that exposure to sinusoidally amplitude-modulated RFR at nonthermal levels can reduce immune function in cells. A 450-MHz radiofrequency field was modulated with a 60 Hz ELF field. Tests showed that the unmodulated carrier wave of 450 MHz by itself had no effect, and modulation frequencies of 40, 16 and 3 Hz had progressively smaller effects than 60 Hz. Peak suppression of the lymphocyte effectiveness (immune function effectiveness) was seen at 60 Hz modulation.

Another important question regarding the biological effects of RFR is whether the effects are cumulative, i.e., after chronic exposure, will a biological system adapt to the perturbation and, with continued exposure, its homeostasis will break down leading to irreparable damage? The question is important in considering the PAVE PAWS chronic exposure situation. Depending on the responses studied in the experiments, several outcomes have been reported. (1) An effect was observed only after prolonged (or repeated) exposure, but not after one period of exposure [e.g., Baranski, 1972; Baranski and Edelwejn, 1974; Mitchell et al., 1977; Takashima et al., 1979]; (2) an effect disappeared after prolonged exposure suggesting habituation [e.g., Johnson et al., 1983; Lai et al., 1992]; and (3) different effects were observed after different durations of exposure [e.g., Baranski, 1972; Dumansky and Shandala, 1974; Grin, 1974; Lai et al., 1989; Servantie et al., 1974; Snyder, 1971]. Cumulative exposure to long-term, low intensity RFR may have the potential to produce biological and potential health effects. Related to this is that various lines of evidence suggest that responses to RFR could be a stress response [Lai, 1992; Lai et al., 1987]. A recent study has reported that low intensity RFR can activate genes for the production of stress proteins (heat shock protein) [Daniells et al, 1998]. The production of heat shock protein is considered a protective response to further stress. Stress effects can cumulate over time and involve first adaptation and then an eventual breakdown of homeostatic processes when the stress persists. Although experimenters attempt to minimize the stress imposed on laboratory animals, the stress cannot be eliminated completely. This stress can be considerable if animals are restrained in laboratory experiments, regardless of whether or not they are exposed to RFR.

The consequences of a cumulative effect are particularly important in considering the risk of cancer. It is well known that x-rays and other forms of ionizing radiation are cumulative. That is, ionizing radiation insufficient to cause any harm in a single exposure will lead to an increased risk of cancer following multiple exposures. This results from the ability of the high intrinsic energy of ionizing radiation to dislodge electrons and ultimately cause DNA changes, which if not correctly repaired can lead to cancer. RFR is not ionizing. It does not possess sufficient intrinsic energy to cause ionization. However, an increased damage to macromolecules, such as DNA, might be caused indirectly, e.g., by an increase in free radicals in cells [Lai and Singh, 1997; Phelan et al., 1992] or a change in enzymatic mechanisms [Daniells et al, 1998; Litovitz et al., 1993, 1997; Singh et al., 1994].

An important conclusion of the research is that modulated, or pulsed, RFR seems to be more effective in producing an effect. It can also elicit a different effect when compared with continuous-wave radiation of the same frequency [Arber and Lin, 1985; Baranski, 1972; Frey and Feld, 1975; Frey et al., 1975; Lai et al., 1988; Oscar and Hawkins, 1977; Sanders et al., 1985, see also review by Juutilainen and de Seze, 1998]. This conclusion is important, since PAVE PAWS signals are modulated signals. Another point which may be relevant to the PAVE PAWS situation is that RFR has been reported to synergistically interact with drugs [Lai, 1992; Lai et al., 1987], medicine [Kues et al., 1992] and carcinogens [see reviews of Juutilainen and Lang, 1997; Verschaeve and Maes, 1998].

Therefore, frequency, intensity, and exposure duration can affect the response to RFR, and these factors can interact with each other and produce different effects. In addition, in order to understand the biological consequence of RFR exposure, one must know whether the effect is cumulative, whether compensatory responses result, and when homeostasis will break down. For example, the different results of the following studies are related to the complex interactions to very different experimental designs: an increase in a variety of cancer types but no single type [Chou et al., 1992], an increase in lymphoma in a genetically altered mouse [Repacholi et al., 1997], a decrease in brain cancer following promotion [Adey et al., 1999], and no significant effect on cancer in a strain prone to breast cancer [Frei et al., 1999] have all been reported in studies of animals exposed to RFR. Care should be taken in applying the existing research results to evaluate the possible effects of radiation from PAVE PAWS.

Conclusions should consider all of the data, and to the extent possible, to avoid personal biases. Additionally, the scientific merit and credibility of research publications needs to be considered. In our review of the available data on the biological effects of RFR, we conclude that there is no definitive scientific evidence to claim that the anticipated low RFR levels from PAVE PAWS could cause any harmful effect to the public. But at the same time, there is suggestive scientific evidence that RFR produces bioeffects at much lower intensities than previously known. The scientific evidence cannot answer the question conclusively whether the PAVE PAWS radar will or will not cause harmful effects to humans in the community. Although Science can prove that something is harmful, it can not prove that something is safe, if safe is defined as zero risk for any effect or change. The question that is always present in making these policy decisions is then, "what do we do about public health when the possibility of harm cannot be totally ruled out?" The approach taken by several federal and public health agencies is to assess the weight of the evidence regarding public health. Policy decisions should include balancing the scientific weight of the evidence for risks, the human consequences of these risks, and the nature and extent of uncertainty against the known benefits and costs. This will be discussed in the Discussion and Summary sections.


The epidemiological studies of exposures to RFR reviewed by this Panel are pertinent to questions of health, particularly cancer. Several of these studies are of populations exposed to radars of various types.


SCIENTIFIC STANDARD FOR DECISION-MAKING: Standard procedures in epidemiology and health risk assessment can be used to respond to the charge to evaluate and summarize the "...current scientific understanding of the health effects, particularly cancer, from exposure to the type of RFR emitted from PAVE PAWS...". Hill's criteria, also recognized as the Surgeon General's criteria, are widely used in public health as the basis of an approach to assess cause and effect from scientific studies [Rothman, 1998; Susser, 1991]. The principle for these criteria as guidance is that the more firmly these criteria are met by the data, the more convincing is the evidence that observed statistical associations indicate cause and effect. These criteria overlap the standard risk assessment approach and the weight of evidence approach, because they include an assessment of the biological plausibility, which is rooted mostly in laboratory data. The weight of the evidence approach to risk assessment is followed by the World Health Organization (WHO) International Program for Chemical Safety; and the US Environmental Protection Agency [IARC, 1995; WHO, 1993]; USEPA, 1996].

PUBLIC HEALTH CRITERIA: In contrast to this scientific standard, which requires conclusive scientific evidence before there is an action (the action is the development of general consensus among scientists of a health risk), public health criteria for taking action on RFR exposures is developed using different standards. Good public health principles select for some level of action, even interim action, to avoid potentially risky exposures, based on the available scientific evidence, and updated as further knowledge is acquired. Prudent avoidance, or prudently limiting or avoiding exposures to possible and probable health risks is a firmly established public health principle, but it must be balanced with respect to the benefit/risk ratio. It is also necessary to consider all sources of environmental hazard in deciding which sources are most important to reduce. Public policy is nearly always made without absolute certainty of the outcome. To "err on the side of caution" when faced with uncertain science, with matters of great public concern, with potentially grave health hazards, and with involuntariness of exposure is the expression of prudent avoidance. It takes much wisdom to know how much caution is warranted; it ultimately depends on the benefit/risk ratio.

A major toxicological principle applied in circumstances other than RFR (chemicals, ionizing radiation) is the importance of amount of exposure. The capability of a substance to cause harm depends on dose, and higher doses produce more frequent or more severe responses (e.g. Fan and Chang, 1996). This is important because it governs the design and interpretation of both epidemiological and laboratory research in traditional toxicology [IARC, 1995; WHO, 1994; USEPA, 1996]. However, this approach has been questioned as applicable for RFR, since there may be non-linear responses.


Our review of epidemiology studies related to RF exposure concentrated on those regarding cancer that were published in the peer reviewed scientific literature. All studies published in scientific journals were reviewed, as well as two unpublished epidemiological studies [Lilienfeld et al, 1978; Hill, 1988]. These two studies were included because they reported detailed descriptions of methods used, are of acceptable design, and have been evaluated in other papers and reports, including those of Federal agencies such as the Environmental Protection Agency. The study by Hill deals with occupational exposure to radars. Studies of power frequency fields, at 50 or 60 Hertz were excluded, because these fields have different characteristics than RF and hence not relevant. Less weight was given to studies where exposure is estimated only by occupation, or from a job title obtained from the death certificate. Reports of clusters have also been excluded, as these are not useful for directly assessing cause and effect, although such reports may prompt further analytical studies if a common factor can be identified [Rothman, 1990; CDC, 1991]

Some epidemiological studies of people potentially exposed to RFR have reported risk ratios above 1.0 for some types of cancer, whereas others have not. Other characteristics of the individual epidemiology studies of RFR should be considered in order to evaluate the study's results, such as the type of study design, response rate, the size of the study population, methods for selection of study participants, control of potential confounding factors.

The studies that were reviewed regarding cancer are included in the reference list, and the criteria for review are described above. The following discussion is a summary of our review, with somewhat more discussion allocated to studies published recently, or to those that appear to be the basis of discussion and public concern.


Descriptive statistics, such as disease rates for various age, race, gender groups or geographic areas, provide important public health information by describing the distribution of disease in populations. Epidemiological studies, or geographical correlation studies, link descriptive statistics of a specified group of people to estimates of exposure. Geographical correlation studies are generally viewed as less informative than case-control or cohort studies for determining cause and effect, because they do not examine data at an individual level. However, studies of epidemiological design involving RF, particularly a few recent studies, have been brought to the attention of the public and presented as evidence for cause and effect, for example on the Internet (e.g. Cherry, 1998). In these studies, rates of leukemia were compared among populations at different distances from high power TV or radio transmission antenna towers1. In published reviews, some authors highlight the positive associations reported in correlation studies; Goldsmith [1995] cites these epidemiological studies as a basis for concern, but clearly states that it is an opinion piece and not a balanced assessment.

Correlation studies have several limitations, so that it can be misleading to single out risk ratios from a study of RFR sources and present them out of context. In addition, these studies can be misleading if the reader does not know about, or does not recognize the importance of related studies that have been published. For example, Dolk et al published two studies in the same journal in 1997 [Dolk et al, 1997a, b]. The first considered one broadcast tower, and the second considered 20 broadcast towers, so these two studies must be considered together. The study by Hocking et al [1996] was followed by a more detailed and complete assessment by McKenzie et al [1998].

Studies in England: The study of a single tower in England reported a weak association for adult leukemia, but reported no difference in childhood cancers [Dolk et al, 1997a]. The researchers wrote "no causal implications can be made from a single cluster investigation of this kind." To better evaluate the observed correlation, the researchers in London extended their analysis to examine the population around 20 different towers transmitting TV or FM frequencies [Dolk et al, 1997b]. In this larger study, no correlation was seen between the rate of childhood leukemia, or brain cancer, with distance from the transmitters. The rate of adult leukemia showed some decline with distance, which could be taken to suggest a link with the towers; however, the rate was not increased in the areas within two kilometers from the transmitter, where RF levels would be greater.

Studies in Australia: In Australia, the populations were identified by the geopolitical units, the local government area (LGA) [Hocking et al, 1996; McKenzie et al, 1998]. The first study reported that leukemia was higher in children and adults who lived in the inner area, less than 2 kilometers (about 1.2 miles) from the center of a group of three towers [Hocking et al, 1996]. Hocking et al [1996] defined the outer radius by including all LGA's north of the towers, and excluding the LGA's to the south. Other scientists in Australia re-analyzed the cancer data, including the LGA's to the south as well as those to the north [McKenzie et al, 1998]. No correlation was seen for calculated RF level and incidence of childhood leukemia. Only one of the three LGA's in the inner group had an increased incidence rate. This LGA resulted largely from cases diagnosed before TV transmission was introduced, when exposure in the area was the lowest.

Other Studies of Leukemia: The results of geographic correlation studies in Australia and the U.S. taken together do not support a link between proximity to RF sources and leukemia in children or adults. The U.S. Embassy study in Moscow [Lilienfeld et al. 1978] reported risk ratios for adults and for children that are above one, but these estimates are quite imprecise because they are based on only one or two cases and chance cannot be ruled out. Tynes et al. [1992] reported an increased risk ratio for leukemia in male workers. In that study no exposure levels at the workplaces were reported, and the authors acknowledge that confounding factors may have played a role. These researchers studied female radio and telegraph operators and did not find evidence for an association with leukemia [Tynes et al., 1996].

Studies of Military Workers: A study of Polish military workers [Szmigielski, 1996] merited intense scrutiny because of the strong statistical associations reported. This was a study of the cancers that were reported over a 15-year period in a cohort of about 127,800 Polish military personnel. Szmigielski reported strong associations between RF exposure and several types of cancer and cancer overall. However, the design included a major source of bias in reporting exposure [Elwood, 1999]. The methods in analysis and reporting of data are not consistent with standard epidemiological methods; the number of cases observed and expected are not given, and the report provides no evidence that adjustments were made for the age differences between the exposed and comparison groups. Because basic data is absent, and the methods used are inadequate, it is difficult to accept the results as valid. By way of comparison, note that Robinette et al's study [1980] of personnel on U.S. Navy ships and Garland's two studies of U.S. Navy personnel also assessed cancer in military workers. Garland et al. [1988, 1990] found no increased rates of disease in the study of newly diagnosed cases (incidence) of lymphoma and of leukemia in a cohort of U.S. Naval personnel. Although exposure was estimated only by job title, the group was fairly large and the epidemiological methods were well described and adequate.

Studies of All Types of Cancer: Few environmental exposures or known causes of cancer increase all types of cancer. However, observed increases in total cancer would suggest that further study is needed to determine whether a specific type of cancer may increase. Several of the epidemiology studies report decreases in total cancer [Hill, 1988; Milham, 1988]. The decrease reported by Lilienfeld et al. [1978] may be chance, and its value limited by the relative short time and small size of the study. The workers studied by Hill were less likely to have been exposed to confounding factors and were followed for a long period of time, yet the risk ratio does not indicate a positive association. Tynes et al. [1996] reports a small increase in a study of women radio and telegraph operators. Based on the evidence available to date, there is no consistent or credible epidemiological evidence to suggest that long term RF exposure increases cancer overall.

Studies of Brain Cancer: Most cohort studies have not reported convincing associations between RF exposure and brain cancer. As discussed above, the weak association reported by Szymigielski does not appear to be based on reliable data. Of three case-control studies, one reported a risk ratio above one for occupations involving RFR exposure [Thomas et al., 1987]. The authors clearly noted the likelihood of confounding from chemicals in these occupations. Grayson [1996] reported an increased risk ratio for the surrogate measure of exposure - occupations more likely than others to incur exposure above the standard. No cases of brain cancer were found in the Moscow embassy cohort [Lilienfeld et al., 1978], or in Navy personnel on ships [Robinette et al, 1980]. If RF exposure contributed to brain cancer, one would expect a higher risk in cell phone users, because RF exposure from cell phones is manifold higher and more localized to the head than the exposures in other studies. The case-control study by Hardell et al. [1999] of cell phones provides no convincing evidence for a risk for brain cancer. However, the authors also pointed out that the sample size in their study was small and there may not have been enough time for cancer to develop.

Studies of Breast Cancer: Several studies have been completed regarding "EMF" and breast cancer in women and in men, but most pertain to electrical workers and power frequency fields. Few studies considered RFR specifically, and therefore they provide limited information for assessing cause and effect. Demers reported a non-significant association for men in communications and broadcasting. Tynes et al. [1996] reported a risk ratio slightly above one for breast cancer in women who worked as radio and telegraph operators aboard ships. He noted that these women were exposed to light at night, which is known to decrease melatonin levels. Because decreased melatonin is hypothesized as a risk factor for breast cancer, light at night may play a role as a confounder. Several studies have examined the association between different occupations and breast cancer. Pollan [1999], for example, reported a positive association with breast cancer for radio and telegraph operators. Lilienfeld's mortality study reported an increased risk ratio that may have been due to chance.

None of the epidemiology studies provided information on individual RF exposures, thus misclassification bias may lead to underestimation of an association if one exists, or provide misleading information. These studies also provide limited information because bias, chance, and confounding cannot be ruled out. However, laboratory studies can provide additional information regarding breast cancer. Several long-term studies used mammary-tumor prone animals, and exposed the animals for nearly their entire lifetime. The lack of evidence for a carcinogenic effect in these studies, such as one in which mice were exposed at 1 watt per kilogram over lifetime, is pertinent for weighing the evidence suggesting any relationship between RF and breast cancer [Frei et al, 1999]. Szmigielski et al., 1982 reported that female rats exposed to 2450-MHz microwaves, the same frequency as that used by Frei et al., developed mammary tumors faster and at a significantly greater number than sham-exposed controls. The increase occurred in animals exposed to 15 mW/cm2; but at 5 mW/cm2, the cancer rate was the same as in confinement stressed controls.


The epidemiology studies consist mainly of occupational studies in adults, and epidemiological studies. Many of the occupational studies clearly included opportunity for exposure to RFR levels higher than the recommended exposure limits, and thus much higher than levels calculated as being associated with PAVE PAWS. In these studies, risk ratios greater than one when reported are imprecise so chance cannot be ruled out, and sufficiently small so that the presence of confounding factors cannot be ruled out as a possible cause. Therefore, the epidemiological studies do not support the idea that RFR exposure increases the occurrence of cancer in general or any specific type of cancer. Nevertheless, there are deficiencies in the exposure assessment in all of the studies, and limitations such as small sample size or short follow-up time in some of the studies [e.g. Lagorio et al., 1997; Muhm, 1992].

Public health decisions are informed by data from a variety of sources, and laboratory studies can be used to address some of the gaps and uncertainties regarding RFR and cancer. In health risk assessments, laboratory studies that use standard bioassay methods and well studied rodent models for cancer provide evidence on whether the long-term low level exposure can cause cancer or other adverse effects in mammals. Genotoxicity bioassays, which provide information on mutagenicity, are considered as well. Such studies of RFR have been reviewed and we conclude that the weight of evidence supporting a causal association between RFR exposure and cancer is weak.

There are a number of publications that report biological effects after exposure to RFR levels lower than the 'safe' limits given in national standards. These studies have been carefully reviewed and evaluated with respect to their credibility, their scientific merit, and the implications for potential health risks. It has been estimated that there are from 7000 to 10,000 published reports on RFR effects in the scientific literature, but only a handful report adverse health effects occurring at intensities below nationally accepted safe levels. Attempts to reproduce these findings have yielded conflicting results. There are no known and accepted physical mechanisms that can account for any of the adverse biological effects reported to occur at such low intensities. It is the opinion of this panel that the evidence for these "low level" (<10 microwatt/cm2) effects does not reach a level sufficient to justify claims of any health hazard

Therefore, the Panel recognizes that in the face of scientific uncertainty and some evidence pointing to a possible problem, it is prudent for the MDPH to take interim action to limit public exposure to PAVE PAWS RFR, according to prudent avoidance and the precautionary principle, to levels considered safe by national standards, until such time as there is 1) good characterization of RFR exposure in the community, and 2) better scientific evidence to define the nature and magnitude of the health hazard, if any. If, with better scientific information, the evidence reaches the level sufficient to justify claims of a health hazard, it will be necessary to readjust their policy (the permissible safe limits) consistent with:

  1. the likelihood and severity of an adverse effect,
  2. exposure levels from Radio, TV and other RFR sources present in the environment
  3. the risk of not having the security afforded by the PAVE PAWS, and
  4. the benefit/risk ratio.


Adey, W.R., Byus, C.V., Cain, C.D., Higgins, R.J., Jones, R.A., Kean, C.J., Kuster, N., MacMurray, A., Stagg, R.B., Zimmerman, G., Phillips, J.L., Haggren, W. Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer 344 rats chronically exposed to 836 MHz modulated microwaves. Radiat Res 152:293-302, 1999.

Albert, E.N. Light and electron microscopic observations on the blood-brain-barrier after microwave irradiation, in: "Symposium on Biological Effects and Measurement of Radio Frequency Microwaves," D.G. Hazzard, ed., HEW Publication (FDA) 77-8026, Rockville, MD, 1977.

Arber, S.L., Lin, J.C. Microwave-induced changes in nerve cells: effects of modulation and temperature. Bioelectromagnetics 6:257-270, 1985.

Baranski, S. Histological and histochemical effects of microwave irradiation on the central nervous system of rabbits and guinea pigs. Am. J. Physiol. Med. 51:182-190, 1972.

Baranski, S., Edelwejn, Z. Pharmacological analysis of microwave effects on the central nervous system in experimental animals, in: "Biological Effects and Health Hazards of Microwave Radiation: Proceedings of an International Symposium," P. Czerski, et al., eds., Polish Medical Publishers, Warsaw, 1974.

Bawin, S.M., Kaczmarek, L..K.., Adey, W.R. Effects of modulated VHF fields on the central nervous system. Ann. N.Y. Acad. Sci .247:74-81, 1975.

Blackman, C.F., Elder, J.A., Weil, C.M., Benane, S.G., Eichinger, D.C., House, D.E. Induction of calcium-ion efflux from brain tissue by radiofrequency radiation: effects of modulation frequency and field strength. Radio Sci. 14:93-98,1979.

Blackman, C.F., Benane, S.G., Elder, J.A., House, D.E., Lampe, J.A., Faulk, J.M. Induction of calcium ion efflux from brain tissue by radiofrequency radiation: effect of sample number and modulation frequency on the power-density window. Bioelectromagnetics 1:35-43, 1980a.

Blackman, C.F., Benane, S.G., Joines, W.T., Hollis, M.A., House, D.E. Calcium ion efflux from brain tissue: power density versus internal field-intensity dependencies at 50-MHz RF radiation. Bioelectromagnetics 1:277-283, 1980b.

Blackman, C.F., Kinney, L.S., House, D.E., Joines, W.T. Multiple power density windows and their possible origin. Bioelectromagnetics 10:115-128, 1989.

Brusick, D., Albertini, R., McRee, D., Peterson, D.,Williams, G, Hanawalt, P., Preston, J. Genotoxicity of radiofrequency radiation. Environ Mol Mutagen. 32:1-16, 1998.

Centers For Disease Control. Guidelines for Investigating Clusters of Health Events. Morbidity and Mortality Weekly Report; U.S. Department of Health and Human Services. Vol. 39. No. RR-11. 1990

Chang, B.K., Huang, A.T., Joines, W.T., Kramer, R.S. The effect of microwave radiation (1.0 GHz) on the blood-brain-barrier. Radio Sci. 17:165-168, 1982.

Cherry, N. Criticism of the proposal to adopt the ICNIRP guidelines for cell sites in New Zealand. Lincoln University; DR 98627PubCo-039, 1998.

Chiang, H., Yao, G.D., Fang, Q.S. Wang, K.Q., Lu, D.Z. and Zhou, Y.K. Health effects of environmental electromagnetic fields. J. Bioelectri., 8: 127-131, 1989.

Chou, C.K., Guy, A.W., Kunz, L.L., Johnson, R.B., Crowley, J.J., Krupp, J.H. Long-term, low-level microwave irradiation of rats. Bioelectromagnetics13:469-96, 1992

D'Andrea, J.A., Gandhi, O.P., Lords, J.L., Durney, C.H., Johnson, C.C., Astle, L.. Physiological and behavioral effects of chronic exposure to 2450-MHz microwaves. J. Microwave Power 14:351-362, 1979.

D'Andrea, J.A.., Gandhi, O.P., Lords. J.L., Durney, C.H., Astle, L.., Stensaas, L.J., Schoenberg, A.A. Physiological and behavioral effects of prolonged exposure to 915 MHz microwaves. J. Microwave Power 15:123-135, 1980.

Daniells, C., Duce, I., Thomas, D., Sewell, P., Tattersell, J., de Pomerai, D. Transgenic nematodes as biomonitors of microwave-induced stress. Mutat Res. 399:55-64, 1998.

de Lorge, J., Ezell, C.S. Observing-responses of rats exposed to 1.28- and 5.62-GHz microwaves. Bioelectromagnetics 1:183-198, 1980.

Dolk, H., Shaddock, G., Walls, P., Grundy, C., Thakrar, B., Kleinschmidt, I., Elliott, P. Cancer Incidence near radio and television transmitters in Great Britain. Am. J. Epidemiol. 145(1): 1-9, 1997a.

Dolk, H., Elliott, P., Shaddick, G., Walls, P., Thakrar, B. Cancer incidence near radio and television transmitters in Great Britain. Am. J. Epidemiol. 145(1):10-17, 1997b.

Dumansky, J.D., Shandala, M.G. The biologic action and hygienic significance of electromagnetic fields of super high and ultra high frequencies in densely populated areas, in: "Biologic Effects and Health Hazard of Microwave Radiation: Proceedings of an International Symposium," P. Czerski, et al., eds., Polish Medical Publishers, Warsaw, 1974.

Dutta, S.K., Subramoniam, A., Ghosh, B., Parshad, R. Microwave radiation-induced calcium ion efflux from human neuroblastoma cells in culture. Bioelectromagnetics 5:71-78, 1984.

Dutta, S.K., Ghosh, B., Blackman, C.F. Radiofrequency radiation-induced calcium ion efflux enhancement from human and other neuroblastoma cells in culture. Bioelectromagnetics 10:197-202, 1989.

Dutta, S.K., Das, K., Ghosh, B., Blackman, C.F. Dose dependence of acetylcholinesterase activity in neuroblastoma cells exposed to modulated radiofrequency electromagnetic radiation. Bioelectromagnetics 13:317-322, 1992.

Elwood, J.M. A critical review of epidemiologic studies of radiofrequency exposure and human cancer. Environ. Health Perspect. 107:155-168, 1999.

Fan, A.M., Chang, L.W. (eds) Toxicology and risk assessment, principles, methods, and applications. New York: Marcel Dekker, Inc .1995.

Firstenberg, A. Microwaving our planet: the environmental impact of the wireless revolution. Brooklyn, NY: 85 pp. 1996.

Frei, M.R., Jauchem , J.R., Dusch, S.J., Merritt, J.H., Berger, R.E., Stedham, M.A . Chronic, low-level (1.0 W/kg) exposure of mice prone to mammary cancer to 2450 MHz microwaves. Radiat. Res.150:568-76, 1998.

Frey, A.H., Feld, S.R. Avoidance by rats of illumination with low power nonionizing electromagnetic radiation. J. Comp. Physol. Psychol. 89:183-188, 1975.

Frey, A.H., Feld, S.R., Frey, B. Neural function and behavior: defining the relationship. Ann. N. Y. Acad. Sci. 247:433-439, 1975.

Garland, F.C., Gorham, E. D., Garland, C. F., Ferns, J. A. Non-Hodgkin's Lymphomas in U.S. Navy personnel. Arch Environ. Health 43(6):425-429, 1988.

Garland, F.C., Shaw, E., Gorham, E.D., Garland, C.F., White, M.R., Sinsheimer, P.J. Incidence of leukemia in occupations with potential electromagnetic field exposure in United States Navy personnel. Am. J. Epidemiol; 132:293-303, 1990.

Goldsmith, J. R. Epidemiologic evidence of radio-frequency radiation (microwave) effects on health in military, broadcasting, and occupational studies. Int. J. Occup. Environ. Health 1(1):47-57, 1995.

Grayson, J.K.. Radiation exposure, socioeconomic status, and brain tumor risk in the United States Air Force: A nested case-control study. Am. J. Epidemiol. 143(5): 480-488, 1996.

Grin, A.N. Effects of microwaves on catecholamine metabolism in brain, US Joint Pub. Research Device Rep. JPRS 72606, 1974.

Hardell, L.., Nasman, A., Hallquist, A., Mild, K.H. Use of Cellular telephones and the risk for brain tumours; A case control study. Int. J. Oncol. 15(1):113-166, 1999.

Hill, D. A longitudinal study of a cohort with past exposure to radar: the MIT Radiation Laboratory follow-up study. [dissertation]. Ann Arbor, MI: University of Michigan Dissertation Service, 1988.

Hocking, B. Gordon, I.R., Grain, H.L., Hatfield, G.E. Cancer incidence and mortality and proximity to TV towers. Med. J. Aust. 165(2):601-605,1996.

Institute of Electrical and Electronics Engineers, Inc. (IEEE). Safety Levels with Respect to Human Exposure to Radio Frequency Electromagnetic Fields, 3 kHz to 300 GHz. IEEE C95.1-1991 (Revision of ANSI C95.-1982), 1992.

IARC, IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Some naturally occurring substances: food items and constituents, heterocyclic aromatic amines and mycotoxins. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 56, International Agency for Research on Cancer (IARC), Distributed by the World Health Organization (WHO), IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, Lyon, June 9-16, 1993.

International Agency for Research on Cancer; IARC, Lyon, France. ISBN 92-832-12630, 1995.

International Commission on Non-Ionizing Radiation Protection. Guidelines for limiting exposure to time-varying electric, magnetic, and electromagnetic fields (up to 300 GHz). Health Physics; vol. 74: 494-522, 1998.J. Occup. Med. 34(3):287-292, 1992.

Johnson, R.B., Spackman, D., Crowley, J., Thompson, D., Chou, C.K., Kunz, L.L., Guy, A.W. Effects of long-term low-level radiofrequency radiation exposure on rats, vol. 4, open field behavior and corticosterone, USAFSAM-TR83-42, Report of USAF School of Aerospace Medicine, Brooks AFB, San Antonio, TX.

Juutilainen J., Lang, S. Genotoxic, carcinogenic and teratogenic effects of electromagnetic fields, introduction and overview. Mutat Res. 387:165-171, 1997.

Juutilainen, J., de Seze, R. Biological effects of amplitude-oulated radiofrequecy radiation. Scand. J. Work Environ. Health 24: 245-254, 1998.

Kues, H.A., Monahan, J.C., D'Anna, S.A., McLeod, D.S., Lutty, G.A., Koslov, S. Increased sensitivity of the non-human primate eye to microwave radiation following ophthalmic drug pretreatment. Bioelectromagnetics 13:379-93, 1992.

Kwee S.; Raskmark, P. Radiofrequency electromagnetic fields and cell proliferation. Presented at the Second World Congress for Electricity and Magnetism in Biology and Medicine, June 8-13, 1997 in Bologna, Italy.

Lagorio, S., Rossi, S., Vecchia, P., De Santis, M., Bastianini, L., Fusilli, M., Ferrucci, A., Desideri, E., Comba, P. Mortality of plastic-ware workers exposed to radiofrequencies. Bioelectromagnetics 18:418-421, 1997.

Lai, H. Research on the neurological effects of nonionizing radiation at the University of Washington. Bioelectromagnetics 13:513-526; 1992.

Lai, H., Singh, N.P. Melatonin and a spin-trap compound blocked radiofrequency radiation-induced DNA strand breaks in rat brain cells. Bioelectromagnetics 18:446-454, 1997.

Lai, H., Horita, A., Chou, C.K., Guy, A.W. A review of microwave irradiation and actions of psychoactive drugs. IEEE Eng. Med. Biol. 6(1):31-36, 1987.

Lai, H., Horita, A., Chou, C.K., Guy, A.W. Acute low-level microwave irradiation and the actions of pentobarbital: effects of exposure orientation. Bioelectromagnetics 5:203-212; 1984.

Lai, H., Horita, A., Guy, A.W. Acute low-level microwave exposure and central cholinergic activity: studies on irradiation parameters. Bioelectromagnetics 9:355-362, 1988.

Lai, H., Carino, M.A., Horita, A., Guy, A.W. Low-level microwave irradiation and central cholinergic systems. Pharmac. Biochem. Behav. 33:131-138, 1989.

Lai, H., Carino, M.A., Horita, A., Guy, A.W. Single vs repeated microwave exposure: effects on benzodiazepine receptors in the brain of the rat. Bioelectromagnetics 13:57-66, 1992.

Lilienfeld, A M, Tonascia, J., Tonascia, S., Libauer, C. H., Cauthen, G. M., Markowitz, J. A., Weida, S. Foreign service status study: evaluation of health status of foreign service and other employees from selected eastern European posts. NTIS Document No. PB-28B 163/9GA; 436 pp. Dept. of State, Washington DC, Final Report, Contract No. 6025- 619073, 1978.

Lin-Liu, S., Adey, W.R. Low frequency amplitude modulated microwave fields change calcium efflux rate from synaptosomes. Bioelectromagnetics 3:309-322, 1982.

Litovitz, T.A., Krause, D., Mullins, J.M.. The role of coherence time in the effect of microwaves on ornithine decarboxylase activity. Bioelectromagnetics 14: 395-403, 1993.

Litovitz, T.A., Penafiel, L.M ., Farrel, J.M., Krause, K ., Meister, R., Mullins, J.M. Bioeffects induced by exposure to microwaves are mitigated by superposition of ELF noise. Bioelectromagnetics 18: 422-430, 1997.

Lyle, D.B., Schechter, P., Adey, W.R., Lundak, R.L. Suppression of T-lymphocyte cytotoxicity following exposure to sinusoidally amplitude-modulated fields. Bioelectromagnetics 4(3):281-92, 1983.

Magras, I.N., Xenos, T.D. RF radiation-induced changes in the prenatal development of mice. Bioelectromagnetics 18:455-461, 1997.

Massachusetts Department of Public Health. Upper Cape Cod cancer incidence review 1986-1994. Bureau of Environmental Health Assessment Environmental Epidemiology Unit. June 1999.

McKenzie, D.R., Yin, Y., Morrell, S. Childhood incidence of acute lymphoblastic leukemia and exposure to broadcast radiation in Sydney -- a second look. Aust. New Zealand J. Pub. Health, 22:360-367, 1998.

Milham, S., Jr. Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies. Am. J. Epidemiol. 127:50-54, 1988.

Mitchell, D.S., Switzer, W.G., Bronaugh, E.L. Hyperactivity and disruption of operant behavior in rats after multiple exposure to microwave radiation. Radio Sci. 12(6):263-271,1977.

Moulder, J.E., Erdreich, L..S., Malyapa, R.S., Merritt, J., Pickard, W.F., Vijayalaxmi. Cell phones and cancer: what is the evidence for a connection? Radiat Res; 151(5): 513-531, 1999.

Muhm, J. M. Mortality investigation of workers in an electromagnetic pulse test program. J. Occup.Med.34:287-292, 1992.

Navakatikian, M.A., Tomashevskaya, L.A. Phasic Behavioral and Endocrine Effects of Microwaves of Nonthermal Intensity by Carpenter DO and Ayrapetyan S, editors. Biological Effects of Electric and Magnetic Fields. Volume 1, published by Academic Press, Inc. New York, 1994, pp. 303-312.

Oscar, K.J., Hawkins, T.D. Microwave alteration of the blood-brain-barrier system of rats. Brain Res. 126:281-293, 1977.

Phelan, A.M., Lange, D.G., Kues, H.A., Lutty, G.A. Modification of membrane fluidity in melanin-containing cells by low-level microwave radiation. Bioelectromagnetic 13:131-46, 1992.

Phillips, J.L., Ivaschuk, O., Ishida-Jones, T., Jones, R.A., Campbell-Beachler, M., Haggren, W. DNA Damage in Molt-4 T-lymphoblastoid cells exposed to cellular telephone radiofrequency fields in vitro.

Bioelectrochem. Bioenerg. 45:103-110, 1998.

Pollan, M; Gustavsson, P. High-risk occupations for breast cancer in the Swedish female working populations. Am J of Public Health. 89(6): 875-81, 1999.

Ray, S., Behari, J. Physiological changes in rats after exposure to low levels of microwaves. Radiat. Res. 123:199-202, 1990.

Repacholi, M.H., Basten, A., Gebski, V., Noonan, D., Finnie, J., Harris, A.W. Lymphomas in E-Pim1 transgenic mice exposed to pulsed 900-MHz electromagnetic fields. Radiat. Res. 147:631-40, 1997.

Robinette, C.D., Silverman, C., Jablon, S. Effects upon health of occupational exposure to microwave radiation (radar). Am. J. Epidemiol. 112:39-53, 1980.

Rothman, K.J. Keynote presentation a sobering start for the cluster busters' conference. Am. J. Epidemiol. 132:S6-S13, 1990.

Rothman, K.J, Greenland, S. Modern epidemiology. Philadelphia, PA: Lippincott-Raven Publishers, 1998.

Salford, L.G., Brun, A., Sturesson, K., Eberhardt, J.L., Persson, B.T. Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation, continuous wave and modulated at 8, 16, 50, and 200 Hz. Microsc. Res. Tech. 27(6):535-542, 1994.

Salford L.G. et al, Blood brain barrier permeability in rats exposed to electromagnetic fields from a GSM wireless communication transmitter. Abstract in Proceedings of the Second World Congress for Electricity and Magnetism in Biology and Medicine, Bologna, Italy, June 1997.

Sanders, A.P.; Joines, W.T.; Allis, J.W. The differential effect of 200, 591, and 2450 MHz radiation on rat brain energy metabolism. Bioelectromagnetics 5:419-433; 1984.

Sanders, A.P., Joines, W.T., Allis, J.W. Effects of continuous-wave, puled, and sinusoidal-amplitude-modulated microwaves on brain energy metabolism. Bioelectromagnetics 6:89-97, 1985.

Servantie, B., Batharion, G., Joly, R., Servantie, A.M., Etienne, J., Dreyfus, P., Escoubet, P. Pharmacologic effects of a pulsed microwave field, in: "Biological Effects and Health Hazards of Microwave Radiation: Proceedings of an International Symposium," P. Czerski, et al., eds., Polish Medical Publishers, Warsaw, 1974.

Sheppard, A.R., Bawin, S.M., Adey, W.R. Models of long-range order in cerebral macro-molecules: effect of sub-ELF and of modulated VHF and UHF fields. Radio Sci. 14:141-145, 1979.

Singh, N., Rudra, N., Bansal, P., Mathur, R., Behari, J., Nayar, U. Poly ADP ribosylation as a possible mechanism of microwave--biointeraction. Indian J. Physiol. Pharmacol. 38:181-184, 1994

Snyder, S.H. The effect of microwave irradiation on the turnover rate of serotonin and norepinephrine and the effect of microwave metabolizing enzymes, Final Report, Contract No. DADA 17-69-C-9144, U.S. Army Medical Research and Development Command, Washington, DC (NTLT AD-729 161), 1971

Susser, M. What is a cause and how do we know one? a grammar for pragmatic epidemiology. Am. J. Epidemiol. 133:635-648, 1991.

Szmigielski, S. Cancer morbidity in subjects occupationally exposed to high frequency (radiofrequency and microwave) electromagnetic radiation. Sci. Total Environ. 180:9-17, 1996.

Szmigielski, S., Szudzinski, A., Pietraszek. A., Bielec, M., Janiak, M,. Wrembel, J.K. Accelerated development of spontaneous and benzopyrene-induced skin cancer in mice exposed to 2450-MHz microwave radiation. Bioelectromagnetics 3(2):179-191, 1982).

Takashima, S., Onaral, B., Schwan, H.P. Effects of modulated RF energy on the EEG of mammalian brain. Rad. Environ. Biophys. 16:15-27, 1979.

Thomas, J.R., Finch, E.D., Fulk, D.W., Burch, L.S. Effects of low level microwave radiation on behavioral baselines. Ann. N.Y. Acad Sci. 247:425-432, 1975.

Thomas, T.L., Stewart, P.A., Stemhagen, A., Correa, P., Norman, S.A., Bleecker, M.L., Hoover, R.N. Risk of astrocytic brain tumors associated with occupational chemical exposures. Scand. J. Work Environ. Health. 13(5):417-23, 1987.

Toler, J.C., Shelton, W.W., Frei, M.R., Merritt, J.H., Stedham, M.A. Long-term, low-level exposure of mice phone to mamary tumors to 435 MHz radiofrequency radiation. Rad. Res. 148: 227-234, 1997.

Tynes, T., Andersen, A., Langmark, F. Incidence of cancer in Norwegian workers potentially exposed to electromagnetic fields. Am. J. Epidemiol. 136(1):81-88, 1992.

Tynes, T., Hannevik, M., Andersen, A., Vistnes, A.l., Haldorsen, T. Incidence of breast cancer in Norwegian female radio and telegraph operators. Cancer Causes Control 7:197-204, 1996

U.S Environmental Protection Agency (EPA). Guidlines for carcinogen risk assessment. Washington, D.C., 1996.

U.S. Environmental Protection Agency (EPA). Biological Effects of Radiofrequency Radiation. Washington, DC., 1984.

Verschaeve, L., Maes, A. Genetic, carcinogenic and teratogenic effects of radiofrequency fields. Mutat. Res. 410:141-165, 1998.

Veyret, B., Bouthet, C., Deschaux, P., de Seze, R., Geffard, M., Joussot-Dubien, J., le Diraison, M., Moreau, J.M., Caristan, A. Antibody responses of mice exposed to low-power microwaves under combined, pulse and amplitude modulation. Bioelectromagnetics 12: 47-56, 1991.

World Health Organization (WHO). Environmental Health Criteria 137: Electromagnetic Fields (300 Hz to 300 GHz) Geneva: WHO Publications. 1993.


We, the authors of the document, Assessment of Public Health Concerns Associated with Pave Paws Radar Installations, hereby show our approval of its contents. Also, let it be known that this completes the work of the expert panel, and that upon acceptance of this document by the Massachusetts Department of Public Health, this panel will disband.

Linda S. Erdreich, Ph.D. Date

Bailey Research Associates, Inc.

Om P. Gandhi, Sc.D. Date

University of Utah

Henry Lai, Ph.D. Date

University of Washington

Marvin C. Ziskin, M.D. Date

Temple University Medical School


Click here to read report

Initial Report on the Environmental Health Assessment of the PAVE PAWS Radar at the MMR

Click here to read report

Assessment of Public Health Concerns Associated with Pave Paws Radar Installations

Click here to read report

PAVE PAWS Related Documents

Click here to read report

Join the mailing list