Brain Cancer Symptoms
Brain cancer with induction periods of less than 10 years in young military radar workersElihu D. Richter CASE REPORTS. Previously, (1) we reported that 6 young patients had cancers (i.e., melanoma of the eye, seminoma, nasopharyngeal cancer, breast cancer, pituitary adenoma, and non-Hodgkin's lymphoma) that occurred following high or prolonged occupational exposures to radar in the military. Given that there were other cases of cancer among young coworkers, we used a linear model of risk to suggest a precautionary threshold for no detectable increase in risk, ranging from--10 [micro]w/[cm.sup.2] to 100 [micro]w/[cm.sup.2] for all cancers, and from 1 [micro]w/[cm.sup.2] to 10 [micro]w/[cm.sup.2] for specific cancers.
In this article, we report on 5 young patients with cancer of the brain with an induction period of less than 10 yr following occupational exposure to radar in military settings. In 4 patients, age of onset was under 30 yr, and in 3 patients the induction periods were less than 5 yr; 1 patient had already died at the time of publication. Exposures were generally unregulated, monitoring was lax, and exposures were based on detection thresholds that exceeded 100 [micro]w/[cm.sup.2]. The patients, listed by year of first exposure, are listed in Table 1. The tumors appeared in the first 4 patients prior to the advent of cell phone use in Israel. The remaining 1 patient did not own a cell phone prior to diagnosis.
Comments
Subsequent to Zaret's (2) first report of 2 individuals with astrocytoma in a group of 18 radar-exposed workers, Goldsmith (3) reanalyzed the Moscow Embassy data and showed increased risks for brain cancer from exposure to radar/microwaves in adult dependents. In addition, there have been suggestions that there are increased risks of brain cancer in subgroups of naval (4) and air force electronic radar technicians. (5,6)
Szmigielski et al. (7) reported increased risks for brain cancer in Polish military personnel who were exposed to radar; this is the only such study that contained reported exposure estimates. It is generally assumed that episodes of brain cancer that appear after latent periods of less than 10 yr are merely coincidental associations, not sentinel indicators of causation. In an authoritative text on brain cancer and occupational exposures, and specifically on exposure to radiofrequency fields from cell phones, it was stated that "in adult humans, all known environmental carcinogens, including radiation, require a latency period usually more than 10 and often more than 20 years." (8) Such a statement ignores the well-established epidemiologic observation that short induction periods following high exposures in certain individuals are a recognized indicator of impending group risk. (9-11) With respect to leukemia and multiple myeloma, latencies between first exposure to benzene and death can be as brief as 2-3.5 yr. (12)
We suggest that the earlier-reported individual cases characterized by short latencies in young persons with high military occupational exposures serve as indicators of impending increased group risk for exposures to radiofrequency fields/microwaves. If the brain tumors we report are causally related to prior exposures, then induction periods can be very brief, and growth of brain tumors can be extremely rapid. This statement applies to brain tumors from other exposures also. We have seen other patients--1 with astrocytoma and another with medulloblastoma (both deceased)--whose brain tumors presented within 5 yr of the first exposures to high levels of solvents. Furthermore, if exposures are high, induction periods may be brief for clusters of patients with several types of tumors.
All of the aforementioned points about risks from military exposures to radar state the case for the reduction of work exposures of individuals to the lowest achievable levels, and they should guide our evaluations of recent reports on hazards and risks from exposure to radiofrequency fields from cell phones. The use of cell phones represents the first time in history that humans are carrying out a mass "experiment" in which possibly hundreds of millions of individuals are holding a source of radiofrequency fields that produce field strengths that sometimes reach several hundred [micro]w/[cm.sup.2], and the fields are in direct contact with the side of each individual's head.
Frey (13) called attention to the limited power of recent epidemiological studies of brain cancer and prior use of cell phones, inasmuch as the studies were based on small numbers and short latencies for the elimination of increased risks--a point the authors of these studies (14,15) and editorialists (16) themselves make. Lai and Singh (17) reported experimental findings on effects of radiofrequency on deoxyribonucleic acid breaks. Gandhi et al. (18) and Schornborn et al. (19) have presented models on the geometry of the gradient of diffusion of microwave energy into the brain from side of use. Weinberger and Richter (20) have suggested that the frequencies for transmission and reception by cellular telephones (900 MHz and 1,800 MHz) exploit the head as a lossy resonator.
What, then, is to be made of reports of brain cancers following short latencies in persons who use cell phones? Hardell et al. (21) reported that 13 patients developed brain cancer on the same side of their head reportedly used for cell phone activities. Eight of the patients had induction periods of less than 5 yr (5 were under the age of 50 yr), and 2 individuals had induction periods between 5 and 9 yr. In a case-control study conducted subsequently, Hardell et al. (22) suggested that the risk for brain cancer increases on the same side of the head a cell phone is used. We suggest the hypothesis that brief latent periods for brain cancer from radar, as well as from radiofrequency in individual cell phone users, predict the likelihood of impending increased risks for brain cancer from the radiofrequency of cell phones. If, however, latencies for ipsilateral tumors of the brain are briefer than for contralateral tumors, we would have even stronger evidence for a very early indicator of risk.
Epidemiology will enhance its effectiveness as a tool for the early detection and prevention of hazardous exposures to carcinogens when it recognizes that the first signs of increased risks come from cases with brief latency periods following high exposures--before there are detectable increases in group risk. When such cases follow exposures for which there is experimental evidence for a genotoxic effect, precautionary measures are indicated.
Submitted for publication April 12, 2002; revised; accepted for publication July 5, 2002.
Requests for reprints should be sent to Dr. Elihu D. Richter, The Joseph H. and Belle R. Braun Hebrew University--Hadassah, School of Public Health and Community Medicine, P.O.B. 12272, Jerusalem 9920, Israel. E-mail: elir@cc.huji.ac.il
Table 1.--Case Reports for 5 Young Patients with Cancer of the Brain,
with an Induction Period < 10 yr Following Occupational Exposure to
Radar in Military Settings
Age at Symptoms
first when exposed or
Patient Years of exposure symptoms leading
no. exposure (yr) Job, tasks, exposure to diagnosis
1 1980-1982 19 Radar technician; Headache, vision
supervised direction problems, loss of
of firing. memory.
2 1982-1996 29 Senior engineer. Numbness and
18-GHz signal tingling, left
generators, power up side of face,
to 100 W; microwave left hand
communication
systems with radio-
frequencies (10-100
W). Communication
systems and large
antenna arrays. ELF
from mainframe.
3 1987-1992 20 Technician, communi- Asymptomatic;
cation equipment diagnosis made
(i.e., radios) with after concussion
power sources of was diagnosed
0.01-1 W in MHz to GHz in connection
range. Radiofrequency with a motor-
fields/ microwaves cycle accident.
(30-88 MHz) at very
high transmission
power--up to 300 W.
4 1987-1991 20 Technician-supervisor. No information
Active and passive on symptoms
instruments for trans-
mitting and receiving
radiofrequency. A co-
worker who was the
same age committed
suicide.
5 1995-1998 18 Technician. Receiving Gait disturbance,
and transmitting dysmetria, and
antennas; radar nets nystagmus
and wave guides;
electronic equipment
and generators.
Current age
Induction Age at in 2002
Patient Year of period diagnosis or age (yr)
no. Diagnosis diagnosis (yr) (yr) at death
1 Cystic 1982 2 21 41
astrocytoma
(surgery).
2 Invasive 1990 8 37 47
pituitary
adenoma
(surgery).
3 Neurocytoma, 1994 7 27-28 35
left ventricle,
on septum
pellucidum
(surgery)
4 Probably 1991 3 23-24 29 *
glioblastoma
brain stem
(MRI).
5 Medullo- 1998 3 21 25
blastoma right
posterior fossa
with obstructive
hydrocephalus
(surgery).
Notes: GHz = gigahertz, W = watts, MHz = megahertz, MRI = magnetic
resonance imaging, and ELF = extremely low frequency.
* Age at death.
References
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(2.) Zaret MM. Potential hazards of Hertzian radiation and tumors. NY State J Med 1977; 146.
(3.) Goldsmith JR. Epidemiologic evidence relevant to radar (microwave) effects. Environ Health Perspect 1997a; 105(suppl 6):1579-87.
(4.) Robinette CD, Silverman C, Jablon S. Effects upon health of occupational exposure to microwave radiation (radar). Am J Epidemiol 1980; 112(1):39-53.
(5.) Grayson JK, Lyons TJ. Cancer incidence in the United States Air Force. Aviat Space Environ Med 1996a; 67(2):101-04.
(6.) Grayson JK, Lyons TJ. Brain cancer, flying and socioeconomic status: a nested case-control study of USAF aircrew. Aviat Space Environ Med 1996b; 67(12):1152-54.
(7.) Szmigielski S, Sobiczewska E, Kubacki R. Carcinogenic potency of microwave radiation: overview of the problem and results of epidemiologic studies on Polish military personnel. Eur J Oncol 2001; 6(2):193-99.
(8.) Lantos PL, VandenBerg SR, Kleihues P. Tumors of the nervous system. In: Greenfeld's Neuropathology. Graham DI, Lantos PZ (Eds). London, UK: Hodder Group, 1997; p. 58, 6th ed.
(9.) Smith PG, Doll R. Mortality among patients with ankylosing spondylitis after a single treatment course with x-rays. Br Med J 1982; 284:449-60.
(10.) Whittemore AS. Age distribution of human cancer from carcinogenic exposures of various intensities. Am J Epidemiol 1977; 106:418-32.
(11.) Armenian HK, Lilienfeld AM. Distribution of incubation periods of neoplastic diseases. Am J Epidemiol 1974; 99:92-100.
(12.) Rinsky RA, Smith AB, Hornung R, et al. Benzene and leukemia. an epidemiologic risk assessment. N Engl J Med 1987; 316(17): 1044-50.
(13.) Frey AH. Hold the (cell) phone. Science 2002; 295(5554): 440-41.
(14.) Muscat J, Malkin M, Thompson S, et al. Handheld cellular telephone use and risk of brain cancer. JAMA 2000; 284:3001-07.
(15.) Inskip PD, Tarone RE, Hatch EE, et al. Cellular telephone use and brain tumors. N Engl J Med 2001; 344(2):79-86.
(16.) Trichopolous D, Adami H-O. Cellular telephonees and brain tumors. N Engl J Med 2001; 344(2):133-34.
(17.) Lai H, Singh NP. Single- and double-strand DNA breaks in rat brain cells after acute exposure to low-level radiofrequency electromagnetic radiation. Int J Radiat Biol 1996; 69:513-21.
(18.) Gandhi OP, Lazzi G, Furse CM. Electromagnetic absorption in the human head and neck for mobile telephones at 835 and 1900 MHz. Institute of Electrical and Electronic Engineers Trans Microwave Theory Tech 1996; 44:1884-97.
(19.) Schornborn F, Buckhardt M, Kuster N. Differences in energy absorption between heads of adults and children in the near field of sources. Health Phys 1998; 74:160-68.
(20.) Weinberger Z, Richter ED. Cellular telephones and effects on the brain. The head as an antenna and brain tissue as a radio receiver. Med Hypotheses (in press [January 2003]).
(21.) Hardell L, Nasman A, Pahlson A, et al. Use of cellular telephones and the risk for brain tumors: a case-control study. Int J Oncol 1999; 15(1):113-16.
(22.) Hardell L, Hallquist A, Hansson-Mild K, et al. Cellular and cordless telephones and the risk for brain tumours. Eur J Cancer Prey 2002; 11:377-86.
ELIHU D. RICHTER *
TAMAR BERMAN
OR LEVY
Unit of Occupational and Environmental Medicine
Hebrew University-Hadassah
Jerusalem, Israel
* The author has served as witness for 2 plaintiffs for the reported patients.
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