Dr George Carlo has released the following comments as his reaction 

to the Essex EHS study in absence of the results findings:

'The following comments relate to the interpretation of the results of the Essex study.

1.  Based on what we have learned from our clinical experiences and the symptoms 

reported by patients in our registry, a key to the integrity of the 

Essex study is in how a 'sensitive' person was defined at the outset.  We 

believe that the pathology of these sensitivities is cell membrane based, 

but that the same pathology is present in conditions including multiple 

chemical sensitivities, alcoholism, drug addiction, and neuro-behavioral 

syndromes like ADHD and Autism.  In addition, there appears to be a familial 

predisposition component that involves inability to clear metals from the 

system through methylation and an inability to adapt to oxidative stress.  

Thus, the definition of patients selected in the Essex study is a key 

point.  And, in the analyses, it would be important to categorize the 

patients on the severity scale in terms of these other conditions that have 

similar underlying pathology.  The point is that there is a continuum we are 

seeing in terms of severity of effects, and the level of hypersensitivity to 

the various types of EMR also scales along that continuum.  Thus, without 

either controlling for these other conditions statistically or through 

subject category restriction, it is likely that associations that are 

present would not be identified.....false negative findings because of 

imprecision in the measurement of the dependent variables.  That is one of 

the main difficulty with the majority of provocation studies that have been 

done.  Measurement imprecision and bias toward the null.

2.  The other key is that depending on the severity of the 

hypersensitivity...and that in large part is related to the points raised 

above....different EMR effect windows will have varying effects on the 

persons being provoked with EMR.  Thus, the EMR that is used in the exposure 

scenario needs to be precisely defined as well.  We know, for example, that 

ELF operates through a field intensity dependent mechanism that exerts 

direct magnetic effect on tissue (including disruption of gap-junction 

intercellular communication) and thus the ensuing pathology.  But there is a 

threshold for ELF effects.  RF has two different pathology mechanism 

components:  raw microwaves or RFR act through thermal mechanisms dependent 

on field intensity -- there is a thermal effects threshold;  microwaves that 

carry information from wireless devices act through a biological mechanism 

that is triggered as a protective cellular response -- for this response, 

there is no threshold.  Thus, in the Essex study, the provocation exposures 

would have needed to be defined along these effect windows, otherwise there 

is a likely bias also toward false negative findings because of the lack of 

precison in the measurement of the independent variables.  For example, from 

what they define, the question of base station 'on or off' is key.  For the 

effect windows of ELF and raw microwaves, 'on or off' would have an effect 

if there was adequate field intensity to provoke the mechanistic pathways -- 

in other words to go above the threshold.  However, for the information 

carrying radio waves, there would have to be talking on the signal or there 

would be no biological protective pathway triggered.  It is the modulation 

associated with the carried information that we now know triggers the 

non-thermal effect pathways.  So, without talking on the signal, 

the biological pathway would not be triggered.  The result in the study 

would be a false-negative finding.

3.  Overall, the electrohypersensitivity response is dependent then on the 

severity of the patients cellular pathology -- and that from all sources 

including the conditions detailed in Number 1 above.  The observed response 

is also dependent on the mechanism that the EMR exposure provocation likely 

will act through.  At this point, we don't believe that a precise enough 

definition of the conditions in the patients recruited to allow for proper 

controlling.  We don't believe that the exposure provocations were defined 

well enough in terms of EMR effect windows and the likely pathological 

pathways triggered by the provocations. 

Because of the imprecision in the measurements in the Essex study, any 

findings showing 'no effect' are likely false negative or the result of the 

study not being able to pick up the real underlying pathology.  Any finding 

showing an 'effect' is likely an underestimation of the actual effect 

because the study is biased toward the null or 'no effect' finding.'

__________________



Dr. George L. Carlo 

Science and Public Policy Institute 

1101 Pennsylvania Ave. NW -- 7th Floor 

Washington, D.C. 20004 

www.sppionline.org 
202-756-7744 

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