EFFECTS OF ELECTROMAGNETIC FIELDS ON DEVELOPMENT
Developing organisms are highly sensitive to physical and chemical agents. For example, the teratologic effects of embryonic or fetal exposures to ionizing radiation that do not produce overt damage to adults are well documented.1 Developing organisms are therefore often used as indicators of biologic effects produced by exposure to various agents.
Various studies have examined the effects of electromagnetic fields (EMFs) on developing organisms, but most have been conducted under conditions different from those associated with operation of the GWEN system. Many of the studies have used nonmammals, including fish, drosophila, and chickens. For example, Zimmerman et al.2 reported that exposure of fertilized sea urchin eggs to a 60-Hz, 0.1-mT field for 24 h delayed development by about 1 h; no other developmental abnormalities were found. Cameron et al.3 found developmental delays in fish embryos, but no gross abnormalities; several possible mechanisms for the developmental delays were postulated including changes in transcription, alterations in mass migration of cells, and changes in cellular free calcium--but additional data are needed to evaluate the suggestions.
Delgado and co-workers4,5,6,7 aroused a great deal of interest among investigators working with EMF when they exposed fertilized chicken eggs to pulsed magnetic fields with repetition frequencies of 10, 100, and 1,000 Hz at intensities of 0.12, 1.2, and 12 µT. They found dramatic effects of the exposures; exposure to the 100-Hz 1.2-µT field produced the greatest effects. There was a generalized inhibition of development. Brain vesicles, the auditory pit, the neural tube, the foregut, heart vessels, and somites were all affected; the cephalic nervous system was the most sensitive, and the heart the least. They also compared various pulse shapes and modalities for effects on development. They used pulses of 0.4, 1.0, 10.4, 13.9, and 104 µT with rise and fall times of 100 µsec, a declining plateau, and long-duration postpulse negative amplitude. Exposure at 0.4 µT resulted in a slight decrease in incidence of developmental abnormalities. Exposures at 1.0 and 13.9 µT produced a 50-77% incidence of abnormalities. The 13.9-µT group had an increased incidence of heart and vessel abnormalities and a delay in development. Heart and vessel abnormalities were also found in the 1.0 µT group.
Other groups of eggs were exposed to a square-wave pulse of 0.4 µT with a 2-µsec rise and fall time; this exposure regimen resulted in an 83% incidence of abnormal embryos, compared with 35% in the controls. Another exposure regimen used a generally square wave of 1.0 µT with rise and fall times originally reported as 42 µsec, but later corrected to 1.7 µsec; this resulted in a 71% incidence of abnormalities vs. a 17% incidence in the controls. The use of the 0.4-µT pulse produced increases in
abnormalities in all five embryonic systems examined--the cephalic nervous system, truncal nervous system, heart, vessels, and somites. Particularly obvious were the short truncal nervous systems with large open folds and abnormal torsion of the embryos. In addition, the embryos exposed to 0.4 µT were more advanced than the normal controls or the controls with abnormalities. The advance in development was estimated to be 8-9 h. In contrast, embryos exposed to 1.0 µT showed a delay in development of approximately 10 h. Of some concern in the latter study is the apparent lack of double-blind evaluation of the embryos. The noncontinuity or lack of a dose-response relation is also of concern, despite the general consideration of “windows ” in the EMF area.
Leal et al.6 analyzed their data on chick development relative to the intensity of the earth's horizontal magnetic field. They suggested that the incidence of abnormalities in their control animals increased as the field increased and resulted in a lower apparent excess of abnormalities in exposed animals. The roughly even split in their data from 13 experiments between those which showed an increased incidence of abnormalities after exposure to pulsed magnetic fields and those which showed a decreased incidence did not give credibility to their suggestion. Chacon et al.7 extended the studies by exposing fertilized eggs to a bipolar pulse with a 1-µT amplitude, 2-µsec rise and fall times, 500-µsec width, and 30-Hz repetition rate. Eggs were placed with their narrow ends toward the west. Examination of embryos was blind. The incidence of abnormal embryos was not significantly affected by EMF exposure, although the incidence of malformed or underdeveloped optic vesicles appeared to be higher in exposed embryos. The proportion of nondeveloping eggs was larger in the exposed group.
Maffeo et al.8 attempted to repeat the experiments of Delgado et al. by exposing fertilized chicken eggs to 1.2- or 12-µT pulsed fields at 100 or 1,000 Hz for 48 h. No differences were found between sham-exposed and exposed eggs. In some replicates, controls (not sham-exposed) had a higher incidence of abnormalities than did the shamexposed or exposed eggs. There seemed to be a high degree of variability among replicates.
Maffeo et al.9 attempted to repeat the work of Ubeda et al. on effects of pulse shape on chick-embryo development. They used a 1-µT field with a 42-µsec rise and fall time and 0-5 msec pulse duration. The repetition rate was 100 Hz. Positive controls were x-irradiated with 1,552 rads. Exposure to EMF did not alter the incidence of abnormalities. Exposure to x rays consistently produced abnormalities.
Juutilainen and colleagues also studied the effects of magnetic fields on chickembryo development.10,11,12 Juutilainen et al.10 compared 100-Hz sinusoidal, square (unipolar and bipolar), and pulsed waveforms at field strengths of 0.1 - 80 A/m (0.12 -96 µT). The incidence of abnormal embryos was increased by exposure to all waveforms at or above 1 A/m except the unipolar square wave. The anterior part of the neural tube was particularly sensitive, but in the most severe cases the whole
embryo was malformed. Development may have been delayed by the 0.1 A/m unipolar waveform, but not by other waveforms or at other field strengths. There was no evidence of an intensity window for production of abnormalities, but the data suggested a threshold at about 1 A/m. There also were no differences between effects produced by the sinusoidal, square, and pulsed fields. Although the unipolar and bipolar waveforms generate identical electric fields, no abnormalities were found with the unipolar waveform; this suggests that it might not be induced fields that are responsible for the effects.
Juutilainen and Saali11 used a sinusoidal field with frequencies of 1, 10, 16.7, 30, 1,000, 10,000, and 100,000 Hz to study the effects of frequency on development. Field strengths of 0.1, 1, 10, and 100 A/m were used. The incidence of abnormalities increased in groups exposed to fields of 1 A/m or greater at 16.7-100,000 Hz. There did not appear to be a dose-response relation above 1 A/m level, nor did there appear to be a window above 16.7 Hz. None of the fields affected the stage of development.
Juutilainen et al.12 further examined the role of field strength on chick development by exposing embryos to a 50-Hz field of varied magnetic intensity. Again, field strengths below 1 A/m did not affect the incidence of abnormalities. However, all field strengths of 1 A/m and above increased the incidence of abnormalities from approximately 16% to 29-36%. The stage of development was unaffected. In general, the affected animals in this and other studies by the Juutilainen group had neural tube defects, half of which, were classified as mild and half as severe.
The difference in results obtained by various investigators led to a comparative study among six laboratories. The study, dubbed “Operation Henhouse,” was funded by the U.S. Office of Naval Research, the Ontario Ministry of Labor, the Spanish Ministry of Health, the Swedish National Institute of Occupational Health, the U.S. Food and Drug Administration, and the U.S. Environmental Protection Agency.13 The study involved laboratories in Canada, Spain, Sweden, and the United States. It was designed so that each laboratory would use identical equipment and protocols. They used an unipolar, pulsed magnetic field (500-µsec pulse duration, 100 pulses/sec, 1-µT peak flux density, and 2-µsec rise and fall time). The field was applied for 48 h, and then the eggs were evaluated for development, structure, and stage of maturity. Of the six laboratories, two had significantly higher incidences of abnormalities in the exposed group. Combining all the data from all six laboratories led to an overall increase in the incidence of abnormalities that was statistically significant. Other measures did not differ between exposed and control groups.
Martin14 had reported an increased incidence of malformations in chick development when eggs were exposed to an unipolar, 60-Hz, 1-µT magnetic field. In a later experiment, however, Martin found no differences in incidences of malformations or death between exposed and control eggs when 60-Hz, 3-µT unipolar, bipolar, or split-sine waves were used.
The response of developing mammal to EMF exposure has been less intensively examined than that of other animals. However, a few studies with mice and rats have examined the effect of electric or magnetic fields on the incidence of fetal abnormalities. Marino et al.15 reported decreased weight gains in mice prenatally and postnatally exposed to vertical (15-kV/m) or horizontal (10-kV/m) electric fields. The watering tubes were not grounded, so it is likely that microshocks influenced the growth of the mice.
Seto et al.16 examined the effects of a 60-Hz, 80-kV/m electric field on the fertility, fecundity, nurturing, survival, and sex ratio of rat offspring. There were no significant differences in any of those measures between exposed and sham-exposed animals through three generations of study. A third filial generation of females were bred and either exposed or sham-exposed until days 16-20 of gestation. They were then killed, and their offspring examined for teratologic changes. No malformations were found in either group, and sex ratios were the same in both groups.
In contrast with the results of Seto et al.,16 results of another study by the same group17 suggested that prenatal development in the rat was inhibited by exposure to a 60-Hz, 80-kV/m electric field. Earflap separation and eye-opening were delayed in exposed offspring. Time to vaginal opening was shortened by electric field exposure, and prenatally exposed males exhibited significantly fewer intromissions and ejaculations than did sham-exposed animals. The latter findings suggest that prenatal exposure to electric fields might have affected sexual differentiation.
Portet and Cabanes18 exposed rabbits to a 50-Hz electric field (50-kV/m) for 16 h/d in the last 2 wk of gestation and for 6 wk after birth. No differences between controls and exposed were found in serum concentrations, of glucose, triglycerides, or cholesterol. Plasma concentrations of thyroid, pituitary, and adrenal hormones were unaffected by exposure to the electric field. Adrenal cortisol was significantly lower in the exposed group, but, corticosterone was unaffected. Growth and development were not affected.
Frolen et al.19 studied the effects of a pulsed magnetic field on prenatal CBA mice; there were 154 control litters with 1,113 live fetuses and 211 exposed litters with 1,530 live fetuses. They characterized their fields as saw-toothed with a mean peak strength of 15 µT. The pulses had a frequency of 20 kHz with-45 µsec rise and 5-µsec fall times. Fetal mortality was increased in the exposed group, but the incidence of abnormalities did not differ between the two groups. The incidence of early resorptions was increased in the exposed group.
Stuchly et al.20 exposed female rats to a saw-tooth magnetic field similar to that produced by video display terminals for 2 wk before breeding and throughout pregnancy (7 h/d). The intensities were 5.7, 23, and 66 µT peak to peak. The duration of each
cycle was 56 µsec, and the fall time was 12 µsec. Exposure to the magnetic fields had no effect on incidence of malformations or resorptions.
Two large studies performed at the Battelle Pacific Northwest Laboratories have examined the effect of prenatal exposure to electric or magnetic fields on in utero development of the rat. The first study21 used 60-Hz electric fields of 0, 10, 65, and 130 kV/m. Animals were exposed for 19 h/d throughout gestation, and exposed pups were allowed to be born in the field. The number of pups and pup mortality were not affected by exposure. At weaning, two F1 females per litter were randomly selected and maintained under their own exposure conditions until 11 wk of age. They were then mated to unexposed males and continued in the field until day 20 of gestation. They were euthanatized, and the pups were examined for developmental abnormalities. There was no evidence of teratologic effects or other developmental abnormalities.
In the second Battelle study,22 female rats were mated and sperm-positive animals were randomly distributed among three groups. Exposures were to 0.09-µT (sham-exposed), 0.61-µT (low-exposure), or 1,000-µT (high-exposure) 60-Hz horizontal magnetic fields for 20 h/d from mating until day 20 of gestation. Replicate experiments were performed to provide approximately 180 litters per exposure group. A total of 7,903 fetuses were evaluated. There was no difference in incidence of malformations between exposed and control groups.
Sikov and coworkers23 exposed Hanford minature swine to a 60-Hz, 30 kV/m electric field for 20 h/d, 7 d/wk and compared their reproductive performance with that of sham-exposed animals. There was no effect of E-field exposure on the incidence of abnormalities in the first litters produced by the F0 females, although there was a suggestion that the exposed offspring fared slightly better than the controls. However, subsequent breeding of F0 females to produce an F1b generation or of F1a to produce an F2 generation resulted in a significantly increased incidence of malformations in the exposed animals. A subsequent breeding of F1 females to produce an F2b generation resulted in no differences in incidences of malformations between exposed and sham-exposed animals. The reasons for these inconsistencies were discussed, but a definite explanation was not given.
Wertheimer and Leeper24 reported that women exposed to increased 60-Hz electromagnetic fields, either from sleeping on waterbeds or under electric blankets or from exposure to ceiling-cable heat, had a greater incidence of spontaneous abortions than women who did not use waterbeds or electric blankets or who had other forms of heating in their homes. In the case of the ceiling heat, no differences were found until the data were stratified on the basis of seasonal exposures; that is, the rate of abortions went up when the amount of heating increased (expressed as percent change from previous month). However, the correlation was very weak when the actual numbers of heating degree days were used for comparison.
The use of visual display terminals (VDTs), which produced EMFs of 3-30 kHz, has been suggested to affect pregnancy outcome adversely. Interest in the possible relationship between VDT use and pregnancy outcome was stimulated in part by a report of a high percentage of spontaneous abortions among women working in the Dallas computer center of Sears, Roebuck and Company (NIOSH Report EPI-80-113-2, Atlanta, GA, 1981). Abortions reportedly occurred after conceptions that took place between May 1979 and June 1980. That observation was followed by a similar report of abortions in workers in Southern Bell's central computer facility in Atlanta (HETA 83-329-1498, Cincinnati, OH, 1984). The two clusters of high rates of spontaneous abortions were investigated by the National Institute for Occupational Safety and Health (NIOSH), and a number of factors were evaluated for their possible contribution to the increased rate of spontaneous abortion. The investigations at each site concluded that there was no correlation between VDT use and spontaneous abortion. No other factor could be positively identified as contributing to the problem, the NIOSH investigators concluded that chance occurrence was the most reasonable explanation in both situations. Goldhaber et al.25 used data from the Kaiser Permanente system and found that women in some job classifications who used VDTs more than 20 h/wk had a higher incidence of abortions.
Several other studies have failed to find evidence of a relationship between VDT use and fetal loss. Kurppa et al.26 performed a case-control study with data in the Finnish National Registry of Congenital Malformations. They found no association between VDT use and birth defects. McDonald et al.27 examined data on a large number of pregnancies in Montreal hospitals for the period 1982-1984 with interview techniques; they found no association of birth defects or spontaneous abortions with VDT use. Ericson and Kallen28 used the Swedish Registry of Congenital Malformations and identified three cohorts of women who had high, medium, and low probability of using video display equipment during 1980-1981. Their analysis did not identify significant differences in incidences of malformations or perinatal deaths among the three cohorts, although there was a weak trend for more spontaneous abortions in the group with highest VDT exposure. However, comparison of pregnancy outcomes during 1980-1981 with data from 1976-1977 did not show any consistent pattern, despite the large increase in computerization that had occurred in the workplace. The same investigators29 performed a case-control study with data from their cohort study. They found a weak association between VDT use and birth defects, but found that the association was not significant when stress and smoking were taken into account. Bryant and Love,30 in a case-control study involving 334 cases of spontaneous abortion, found no evidence that VDT use influenced the rate of abortion. Studies on a large population of telephone workers (Schnorr et al.31) provided strong evidence that exposure to VDTs during pregnancy had no effect on the pregnancy outcome.
Some studies performed to examine the developmental effects of RF and microwave radiation have been reviewed by Lary and Conover32 and O'Connor.33 Most of the early experimental studies were performed at 2,450 MHz, the operating
frequency of many microwave ovens, and at levels that induced some heating. Lary et al.34,35,36,37 have explored the relationship between RF exposures and developmental changes with different frequencies and magnitudes of exposure. They established that abnormalities in development are related to maternal hyperthermia and not to some direct effect of RF radiation on the embryo or fetus. Rugh and McManaway38 and Schmidt et al.39 also provided evidence that developmental abnormalities did not result from the direct action of RF radiation. Evidence from the studies of Lary and colleagues and others generally indicates that maternal colonic temperatures need to reach 41°C or higher before mortality and malformations are increased. However, some studies 40,41,42 have found increased prenatal mortality and decreased fetal body weight at maternal colonic temperatures as low as 39.5°C, and others 43,44 found no effects at 40.3 - 40.6°C. The data of Lary et al.36 indicate that the duration of temperature increase in the dam influences the effects. Moreover, the sensitivity of the embryo to various noxious agents varies widely with the stage of gestation. Such factors might help to explain the different observations. Developmental abnormalities found after RF irradiation were usually those associated with the head and included micrognathia, agnathia, microtia, anotia, exencephaly, encephalocele, and facial aplasia. The results indicate that the malformations resulted from increased heat load and that prolongation of increased temperatures exacerbated the effects. The results are in general agreement with those of other studies of the effects of hyperthermia on mammalian development.
In most of the studies just cited, the frequencies used were substantially different from those produced by the GWEN system. VDTs emit fields with frequencies up to about 30 kHz, but that still is far below the GWEN frequencies. Juutilainen et al.10 used fields up to 100 kHz, thus coming closest to the GWEN frequency; moreover, the actual fields they used were at least in the same range as would be expected from GWEN. Their data indicated that malformations in chick embryos could be produced by exposure to a magnetic field with a threshold of approximately 1 A/m = 1.2 µT = 12 mG, which is about 20-times higher than the field at the GWEN perimeter fence. It is not clear that the chick-embryo system is indicative of what happens in mammals, but there are no studies of the effects of GWEN-frequency fields on mammalian development. The studies of Seto et al.,16 Portet and Cabanes,18 and Rommereim et al.21 with ELF electric fields have provided convincing evidence that exposure to these fields during gestation does not produce teratological changes. It is well documented that higher-frequency (radiofrequency, RF) fields are capable of inducing profound developmental changes. However, the evidence is very convincing that such effects are related to tissue heating by EMF fields.
Results of some of the studies with chick embryos suggest that exposure to lowintensity magnetic fields can cause developmental abnormalities, but there is not much evidence that these results are relevant to GWEN fields or to mammals. Examination of the literature does not reveal any studies performed with developing mammalian systems under conditions similar to those to be encountered with GWEN. However,
1. Brent, R. 1980. Radiation teratogenesis. Teratology 21 : 281-298.
2. Zimmerman, S., A. M. Zimmerman, W. D. Winters, and I. L. Cameron. 1990. Influence of 60-Hz magnetic fields on sea urchin development. Bioelectromagnetics 11 : 37-45.
3. Cameron, I. L., K. E. Hunter, and W. D. Winters. 1985. Retardation of embryogenesis by extremely low frequency 60-Hz electromagnetic fields. Physiol. Chem. Phys. Med. NMR 17 : 135-138.
4. Delgado, J. M. R., J. Leal, J. L. Monteagudo, and M. G. Gracia. 1982. Embryological changes induced by weak, extremely low frequency electromagnetic fields. J. Anat. 134 : 533-551.
5. Ubeda, A., J. Leal, M. A. Trillo, M. A. Jimenez, and J. M. R. Delgado. 1983. Pulse shape of magnetic fields influences chick embryogenesis. J. Anat. 137 : 513-536.
6. Leal, J., K. Shamsaifar, M. A. Trillo, A. Ubeda, V. Abraira, and L. Chacon. 1989. Embryonic development and weak changes of the geomagnetic field. J. Bioelectricity 7 : 141-153.
7. Chacon, L., M. A. Trillo, A. Ubeda, and J. Leal. 1990. A 30-Hz pulsed magnetic field can stop early embryonic development . J. Bioelectricity 9 : 61-66.
8. Maffeo, S., M. W. Miller, and E. L. Carstensen. 1984. Lack of effect of weak low frequency electromagnetic fields on chick embryogenesis. J. Anat. 139 : 613-618.
9. Maffeo, S., A. A. Brayman, M. W. Miller, E. L. Carstensen, V. Ciaravino, and C. Cox. 1988. Weak low frequency electromagnetic fields and chick embryogenesis: failure to reproduce positive findings. J. Anat. 157 : 101-104.
10. Juutilainen, J., M. Harri, K. Saali, and T. Lahtinen. 1986. Effects of 100-Hz magnetic fields with various waveforms on the development of chick embryos. Radiat. Environ. Biophys. 25 : 65-74.
11. Juutilainen, J., and K. Saali. 1986. Development of chick embryos in 1 Hz to 100 kHz magnetic fields. Radiat. Environ. Biophys. 25 : 135-140.
12. Juutilainen, J., E. Laara, and K. Saali. 1987. Relationship between field strength and abnormal development in chick embryos exposed to 50 Hz magnetic fields. Int. J. Radiat. Biol. 52 : 787-793.
13. Berman, E., L. Chacon, D. House, B. A. Koch, W. E. Koch, J. Leal, S. Lovtrup, E. Mantiply, A. H. Martin, G. I. Martucci, K. H. Mild, J. C. Monahan, M. Sandstrom, K. Shamsaifar, R. Tell, M. A. Trillo, A. Ubeda, and P. Wagner. 1990. Development of chicken embryos in a pulsed magnetic field. Bioelectromagnetics 11 : 169-187.
14. Martin, A. H. 1992. Development of chicken embryos following exposure to 60-Hz magnetic fields with differing waveforms. Bioelectromagnetics 13 : 223-230.
15. Marino, A. A., R. O. Becker, and B. Ullrich. 1976. The effect of continuous exposure to low frequency electric fields on three generations of mice: a pilot study. Experientia 32 : 565-566.
16. Seto, Y. J., D. Majeau-Chargois, J. R. Lymangrover, W. P. Dunlap, E. F. Walker, and S. T. Hsieh. 1984. Investigation of fertility and in utero effects in rats chronically exposed to a high-intensity 60-Hz electric field. IEEE Trans. Biomed. Eng. BME 31 : 693-701.
17. Burack, G. D., Y. J. Seto, S. T. Hsieh, and J. L. Dunlap. 1984. The effects of prenatal exposure to a 60-Hz high-intensity electric field on postnatal development and sexual differentiation. J. Bioelectricity 3 : 451-467.
18. Portet, R., and J. Cabanes. 1988. Development of young rats and rabbits exposed to a strong electric field. Bioelectromagnetics 9 : 95-104.
19. Frolen, H., B. M. Svendenstal, P. Bierke, and H. Fellner-Feldegg. 1987. Repetition of a study of the effect of pulsed magnetic fields on the development of fetuses in mice. Swedish University of Agricultural Sciences, Uppsala. Project SSI 346,86. Final Report, June 1987.
20. Stuchly, M. A., J. Ruddick, D. Villeneuve, K. Robinson, B. Reed, D. W. Lecuyer, K. Tan, and J. Wong. 1988. Teratological assessment of exposure to time-varying magnetic fields . Teratology 38 : 461-466.
21. Rommereim, D. N., R. L. Rommereim, M. R. Sikov, R. L. Buschbom, and L. E. Anderson. 1990. Reproduction, growth, and development of rats during chronic exposure to multiple field strengths of 60-Hz electric fields. Fund. Appl. Toxicol. 14 : 608-621.
22. Rommereim, D. N., R. L. Rommereim, D. L. Miller, R. L. Buschbom, and L. E. Anderson. 1993. Developmental toxicology evaluation of 60-Hz horizontal magnetic fields in rats. Current Topics in Occupational Health Fund (in press).
23. Sikov, M. R., J. L. Beamer, D. N. Rommereim, R. L. Buschbom, W. T. Kaune, and R. D. Phillips. 1987. Evaluations of reproduction and dvelopment in Hanford miniature swine exposed to 60-Hz electric fields. Pp. 379-393 in Interaction of Biological Systems with Static and ELF Electric and Magnetic Fields. eds. L.E. Anderson, B. J. Kelman, and R. J. Weigel. Pacific Northwest Laboratory, Richland, WA.
24. Wertheimer, N., and E. Leeper. 1989. Fetal loss associated with two seasonal sources of electromagnetic field exposure. Am. J. Epidemiol. 129 : 220-224.
25. Goldhaber, M. K., M. R. Polen, and R. A. Hiatt. 1988. The risk of miscarriage and birth defects among women who use visual display terminals during pregnancy. Am. J. Indust. Med. 13 : 695-706.
26. Kurppa, K., P. C. Holmberg, K. Rantala, T. Nurminen, and L. Saxen. 1985. Birth defects and exposure to video display terminals during pregnancy . Scand. J. Work Environ. Health 11 : 353-356.
27. McDonald, A. D., N. M. Cherry, C. Delorme, and J. C. McDonald. 1986. Visual display units and pregnancy: evidence from the Montreal survey . J. Occup. Med. 28 : 1226-1231.
28. Ericson, A., and B. Kallen. 1986a. An epidemiological study of work with video screens and pregnancy outcome. I. A registry study. Am. J. Indust. Med. 9 : 447-457.
29. Ericson, A., and B. Kallen. 1986b. An epidemiological study of work with video screens and pregnancy outcome: II. A case-control study. Am. J. Indust. Med. 9 : 459-475.
30. Bryant, H. E., and E. J. Love. 1989. Video display terminal use and spontaneous abortion risk. Int. J. Epidemiol. 18 : 132-138.
31. Schnorr, T. M., B. A. Grajewski, R. W. Hornung, M. J.Thun, G. M. Egeland, W. E. Murray, D. L. Conover, and W. E. Halperin. 1991. Video display terminals and the risk of spontaneous abortion. N. Engl. J. Med. 324 : 727-733.
32. Lary, J. M., and D. L. Conover. 1987. Teratogenic effects of radiofrequency radiation. IEEE Eng. Med. Biol. Mag. Vol. 6 (March) : 42-46.
33. O'Connor, M. E. 1990. Teratogenesis: nonionizing electromagnetic fields. Pp. 358-372 in Biological Effects and Medical Applications of Electromagnetic Energy , O. P. Gandhi, ed. Englewood Cliffs, N J : Prentice Hall.
34. Lary, J. M., D. L. Conover, E. D. Foley, and P. L. Hanser. 1982. Teratogenic effects of 27.12 MHz radiofrequency radiation in rats . Teratology 26 : 299-309.
35. Lary, J. M., D. L. Conover, P. H. Johnson, and J. R. Burg. 1983. Teratogenicity of 27.12-MHz radiation in rats is related to duration hyperthermic exposure. Bioelectromagnetics 4 : 249-255.
36. Lary, J. M., D. L. Conover, and P. H. Johnson. 1983. Absence of embryotoxic effects from low-level (nonthermal) exposure of rats to 100 MHz radiofrequency radiation. Scand. J. Work Environ. Health 9 : 120-127.
37. Lary, J. M., D. L. Conover, P. H. Johnson, and R. W. Hornung. 1986. Dose-response relationship between body temperature and birth defects in radiofrequency-irradiated rats. Bioelectromagnetics 7 : 141-149.
38. Rugh, R., and M. McManaway. 1976. Anesthesia as an effective agent against the production of congenital anomalies in mouse fetuses exposed to electromagnetic radiation. J. Exp. Zool. 197 : 363-368.
39. Schmidt, R. E., J. H. Merritt, and K. H. Hardy. 1984. In utero exposure to low-level microwaves does not affect rat foetal development. Int. J. Radiat. Biol. 46 : 383-386.
40. Michaelson, S. M., R. Guillet, and F. W. Hegeness. 1978. Influence of microwave exposure on functional maturation of the rat . Pp. 300-316 in Developmental Toxicology of Energy- related Pollutants, D. D. Mahlum, M. R. Sikov, P. L. Hackett, F. D. Andrew, eds. DoE Symposium Series 47, Washington, D.C.
41. Nawrot, P. S., D. I. McRee, and R. W. Staples. 1981. Effects of 2.45 GHz CW microwave radiation on embryofetal development in mice. Teratology 24 : 303-314.
42. Berman, E., H. B. Carter, and D. House. 1982. Observations of Syrian hamster fetuses after exposure to 2450 MHz microwaves. J. Microwave Power 17 : 107-112.
43. Chernovetz, M., D. Justensen, N. King, et al. 1975. Teratology, survival, and reversal learning after fetal irradiation of mice by 2450-MHz microwave energy. J. Microwave Power 10 : 391-409.
44. Berman, E., H. B. Carter, and D. House. 1981. Observations of rat fetuses after irradiation with 2450-MHz (CW) microwaves. J. Microwave Power 16 : 9-13.