ukushima  [under construction]

C.  Health Effects of Microwaves, including Cell Phones and Cell Towers, and Electromagnetic Pollution – Non-Ionizing Radiation

I.  Lai Henry, Comet Assay and Single-Strand and Double-Strand Breakage Caused by Non-Ionizing Radiation.

electromagnetic and radiofrequency radiation RF

Lai, H. and N.P. Singh. (1995) "Acute Low-Intensity Microwave Exposure Increases DNA Single-Strand Breaks in Rat Brain Cells."Bioelectromagnetics 16: 207-210.

Lai, Henry (2000a). "Biological Effects of Radiofrequency Radiation from Wireless Transmission Towers." In Levitt (2000) 65-74. See also

Lai, Henry. "Microwaves Break DNA in Brain; Cellular Phone Industry Skeptical." Microwave News 14, no. 6 (November/December 1994).


Lai, H. and Singh, N.P. (1997a) : "Acute exposures to a 60 Hz magnetic field increases DNA strand breaks in rat brain cells". Bioelectromagnetics 18: 156-165.,%20Singh,%201997.pdf,%20Singh,%201997.pdf


p. 160

Fig. 6. Photographs of single-strand break DNA migration pattern of individual brain cells from

rats exposed to bucking condition (0.1 mT) (a) or magnetic fields of 0.1 mT (b), 0.25 mT (c),

and 0.5 mT (d). x 400.




Fig. 12.  60 Hz Magnetic Field and DNA Strand Breaks


Fig. 12. Photographs of double-strand break DNA migration pattern of individual brain cells

from rats exposed to bucking condition (0.1 mT) (

a) or magnetic fields of 0.1 mT (

b), 0.25 mT

(c), and 0.5 mT (d).x 400.

Lai, H. and N.P. Singh. (1997b) "Melatonin and a Spin-Trap Compound Block Radiofrequency Electromagnetic Radiation-Induced DNA Strand Breaks in Rat Brain Cell." Bioelectromagnetics 18, no. 6 (1997) 446-54.


Lai, H., and Singh, N.P. (1997c) "Melatonin and N-tert-butyl-a-phenylnitrone Block 60 Hz magnetic field-induced DNA single- and double-strands Breaks in Rat Brain Cells." Journal of Pineal Research 22:152-162.

Magnetic-Field-Induced DNA Strand Breaks in Brain Cells of the Rat

HENRY LAI & NARENDRA P SINGH / Environmental Health Perspectives v.112, n.6, 1may04

[All figures below references]


Lai, H. "Non-Ionizing Electromagnetic Fields and Spatial Learning and Memory Functions." In Bersani (1999) 101-103.


Neurological Effects of Non-Ionizing

Electromagnetic Fields

2014 Supplement

Henry Lai


Lai, H. and Singh, N.P., 1996a: "Reply to "Comment on 'Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells' ". Bioelectromagnetics 17: 166.

Lai, H. and N.P. Singh (1996). "Single and double strand DNA breaks in rat brain cells after acute exposure to radiofrequency electromagnetic radiation." J Radiation Biology 69: 513-521.


More citations:

Does MW Radiation Affect Gene Expression, Apoptotic Level, and Cell Cycle Progression of Human SH-SY5Y Neuroblastoma Cells?


May 2016 · Cell biochemistry and biophysics

Handan Kayhan· Meric Arda Esmekaya· Atiye Seda Yar Saglam· […] · Nesrin Seyhan


Can Cell Phones Damage DNA and Cause Cancer? Dr. Henry Lai

Uploaded on Feb 26, 2012

WiFi in Schools






This image is from:




WiFi in Schools





Dr. Henry Lai, from the University of Washington, gives a talk on the genetic effects of cell phones and Radiofrequency radiation.”


Lai, Henry. "Fig. 1. Unexposed control, The bundle is simply DNA."





DNA Damage at Below Safe

Cell Phone Radiation Levels



Lai, Henry. "Fig. 2. X-ray calibration: After 6.4 rads. DNA strand breaks are evident.."

Previous link no longer valid.

Lai, Henry. "Fig. 3. X-ray calibration: After 25.6 rads. DNA strand breaks are now very obvious.."






Lai, Henry. "Fig. 4 Assay showing effect of 2 hrs of microwave exposure (2.45GHz) at a SAR (absorption) level of 0.6 W/kg [about cellphone handset levels]. DNA strand breaks are also obvious."






Comet Assay


Solange Costa, João Paulo Teixeira, in Encyclopedia of Toxicology (Third Edition), 2014.





1)  Resolution of Denial of Conditional Use ermit (CUP) # PL2014-518 Cell Site At

Maple Hill Park, Diamond Bar, CA.

2)  Bio-initiative 2012, A Rationale for iologically Based Exposure Standard for Low Intensity Electromagnetic Radiation


Dr. Ronald Herberman, Director of the University of Pittsburgh Cancer Institute (UPCI) and the UPMC Cancer Center.  He is also Associate Vice Chancellor for cancer research within the School of Medicine, Department of Health Sciences


This is a modification of the iconic illustration made in 1996 by Om Gandhi, Professor and Chairman of Department of Electrical Engineering at the University of Utah, Salt Lake City. Dr. Herberman worked with Gandhi to turn the illustration into a three-dimensional model that estimates the absorption of electromagnetic radiation.


Fact: DNA damage at below safe cell phone radiation levels -

DNA Damage at Below Safe Cell Phone Radiation Levels l

In a ground breaking series of experiments between 1994–1998, Dr. Henry Lai and Dr. NP Singh demonstrated convincingly that moderate levels of microwave (2.45 GHz) radiation (below that of cell phone radiation levels) for exposure of 2 hours, could increase the frequency of single-strand DNA break in brain cells of live animals.


Accumulative and long term DNA disruption may lead to cancer cell development


Unexposed control. The bundle is simply DNA

Fig.2 X-ray calibration: After 25.6 rads. DNA

strand breaks are now very obvious

p. 7 n.4dnamw




Fig.4 Assay showing effect of 2 hrs of microwave exposure (2.45GHz) at a SAR (absorption) level of 0.6 W/kg [about cell phone radiation levels] DNA strand breaks re also obvious. 


These images result from fluorescent molecules attached to the end of each DNA strand at a break point, and so are best seen in the negative.

Figure 4 was captured by Dr Lai and Singh, and it shows the results of a comet assay at power densities about one-fifth those previously thought to cause adverse biological effects. These exposures were only for a short time, and they used radio power-densities well below those said to be ‘ionizing’ (having the power to break chemical/material bonds).


Singh NP, Lai H. (1998) 60 Hz magnetic field exposure induces DNA crosslinks in rat brain

cells. Mutat Res 400:313-320.

from Public - City Clerk Internet Site - City of Los Angeles

May 16, 2005



To :

His Excellency Ban Ki - moon, Secretary - General of the United Nations

Honorable Dr. Margaret Chan, Director-General of the World Health Organization

Honorable Achim Steiner, Executive Director

Of the U.N. Environmental Programme

U.N. Member Nations

International Appeal: Scientists call for Protection from Non-ionizing Electromagnetic Field Exposure



Lai H, Singh NP. 1997. Acute exposure to a 60 Hz magnetic field increases DNA strand

breaks in rat brain cells.  Bioelectromagnetics


Comet Assay

“The Comet Assay, also called single cell gel electrophoresis (SCGE), is a sensitive and rapid technique for quantifying and analyzing DNA damage in individual cells. As such, this is one of the techniques used in the area of cancer research for the evaluation of genotoxicity and effectiveness of chemoprevention. Swedish researchers Östling & Johansson developed this technique in 1984.1 Singh, et al., later modified this technique, in 1988, as the Alkaline Comet Assay.2 The resulting image that is obtained resembles a "comet" with a distinct head and tail. The head is composed of intact DNA, while the tail consists of damaged (single-strand or double-strand breaks) or broken pieces of DNA. While most of the applications of the Comet Assay have been to study animal eukaryotes, there have been reports of successful application in the study of plant cells.

“Individual cells are embedded in a thin agarose gel on a microscope slide. All cellular proteins are then removed from the cells by lysing. The DNA is allowed to unwind under alkaline/neutral conditions. Following the unwinding, the DNA undergoes electrophoresis, allowing the broken DNA fragments or damaged DNA to migrate away from the nucleus. After staining with a DNA-specific fluorescent dye such as ethidium bromide or propidium iodide, the gel is read for amount of fluorescence in head and tail and length of tail. The extent of DNA liberated from the head of the comet is directly proportional to the amount of DNA damage.

“The Comet Assay can be used to detect DNA damage caused by double strand breaks, single strand breaks, alkali labile sites, oxidative base damage, and DNA cross-linking with DNA or protein. The Comet Assay is also used to monitor DNA repair by living cells.3

Cited References

  1. Ostling, O., and Johanson, K.J., Microelectrophoretic study of radiation-induced DNA damages in individual mammalian cells. Biochem. Biophys. Res. Commun., 123, 291-8 (1984).
  2. Singh, N.P, et al., A simple technique for quantitation of low levels of DNA damage in individual cells. Exp. Cell Res., 175, 184-91 (1988).
  3. Collins, A.R., The comet assay for DNA damage and repair (Review). Molecular Biotechnology, 26, 249-261 (2004).
  4. Comet Assay Interest Group website

Review Articles and General References for Comet Assays

  1. Anderson D., et al., Comet assay responses as indicators of carcinogen exposure. (Review) Mutagenesis, 13, 539-555. (1998).
  2. Fairbairn, D.W., et al., The Comet assay: a comprehensive review. (Review) Mutat. Res., 339, 37-59 (1995).
  3. McKelvey-Martin, V.J., et al., The single cell gel electrophoresis assay (comet assay): A European review. (Review) Mutat. Res., 288, 47-63 (1993).
  4. Rojas, E., et al, Single cell gel electrophoresis. Methodology and applications. (Review) J. Chromatogr. B Biomed. Sci. Appl. 722, 225-254 (1999).
  5. Tice, R.R., et al., Single cell gel/comet assay: guidelines for in vitro and in vivo genetic toxicology testing. Environ Mol Mutagen, 35, 206-21 (2000).
  6. Comet Assay Forum website, Industrial Toxicology Research Centre, Lucknow, India.



[Fig. 3]







Measurement of DNA damage in PBLs and prostate cells from elderly dogs. The extent of DNA damage in PBLs and prostate cells was measured by single cell gel electrophoresis (alkaline Comet assay) as described by Singh (13). Under the assay conditions used in this experiment, comet tails reflect the electrophoretic migration of DNA fragments that result from strand breaks, alkali-labile sites, crosslinks, or base-excision repair sites (13). The extent of DNA damage was visually

scored in 100 randomly selected cells from each sample (50 cells from several different fields from each of two replicate slides) by one examiner who was blinded to the treatment group. SYBR Green 1 – stained nucleoids were examined at 200

magnification with an epifluorescent microscope. Each cell was visually scored on a 0 to 4 scale using a method described by Collins (42) as follows: no damage (type 0); mild to moderate (types 1 and 2), and extensive DNA damage (types 3 and 4). The extent of DNA damage within PBLs or prostate cells was expressed as the percentage of cells with extensive DNA damage (sum of cells that displayed type 3 or type 4 DNA damage). PBLs isolated from the whole blood of each dog (12) were assayed fresh without cryopreservation. Cytospin preparations confirmed that more than 90% of cells in this enriched cell population were lymphocytes; mean percent viability

(trypan blue exclusion) was 90%. The sensitivity of PBLs to oxidative stress was determined by measuring DNA damage

before and after exvivo challenge of PBLs with 25 Amol/L hydrogen peroxide (5 min, 4j

C). To assess endogenous DNA

damage in prostate cells, the prostate was collected from each dog at necropsy, and 50 to 80 mg of prostate tissue was placed

in 1 mL of cold HBSS containing 20 mmol/L EDTA and 10% DMSO (43). Tissue was then minced with fine scissors, and 50 AL of the resulting cell suspension was mixed with 1 mL of RPMI 1640 containing 10% fetal bovine serum for subsequent

electrophoresis. Cytospin preparations indicated that >90% of cells had epithelial cell morphology; mean percentage cell

viability estimated by trypan blue exclusion was 80%.  Histopathologic evaluation of formalin-fixed, step-sectioned prostate tissue sections revealed no foci of carcinoma in any of the dogs in this study population.”


This figure is from:

Noninvasive Prediction of Prostatic DNA Damage by Oxidative Stress Challenge of Peripheral Blood Lymphocytes

David J. Waters, Shuren Shen, Huiping Xu, Seema S. Kengeri, Dawn M. Cooley, Emily C. Chiang, Yu Chen, Deborah Schlittler, Carol Oteham, Gerald F. Combs Jr., Lawrence T. Glickman, J. Steven Morris and David G. Bostwick