Criticism of NIOH Report From Environ Intl. Corporation, USA

Review of Scientific Methods
and Findings for
Final Report of The

Investigation of Unusual
Illnesses Allegedly Produced by
Endosulfan Exposure in Padre
Village of Kasargod District
(N. Kerala)
Prepared for:
Velsicol Chemical, LLC
Prepared by:
ENVIRON International Corporation
Tampa, Florida
Date:
March 27, 2012
Scientific Review NIOH Endosulfan Study
Contents
Page
Executive Summary
1
1 Introduction 3
1.1 Background 3
1.2 Information Sources 3
2 Comments on Analytical Data Quality 5

2.1 Excluded Sample Results 5
2.2 Raw Data from RTI Release Not Matching Results Presented in Report 6
2.3 Detection Limits 8
2.4 Chromatographic Peak Identification 9
2.5 Random Noise Fluctuations 10
2.6 Calibration Data 11
2.7 QA/QC Data 11
3 Survey Design Comments 13

3.1 Study Design Considerations 14
3.2 Confounding Factors and Alternate Interpretations 15
3.3 Size of Study Groups 16
4 Comments on Endosulfan Exposure and Effects 18

4.1 Endosulfan Levels Consistent With Background 18
4.2 Samples Excluded from Journal Publication 20
4.3 Obvious Alternate Explanations Not Discussed 21
4.4 Recorded Observations Not Biologically Relevant 22
5 Conclusions 25
List of Attachments
Attachment A Curricula Vitae
i
Executive Summary
This report evaluates the scientific methods, conduct, interpretations and conclusion of a report
titled Final Report of The Investigation of Unusual Illnesses Allegedly Produced by Endosulfan
Exposure in Padre Village of Kasargod District (N. Kerala) conducted by the Indian National
Institute of Occupational Health (NIOH). This is a project report of a study regarding
environmental and human health conditions in an area near cashew plantations where there
has been a history of aerial application of the pesticide endosulfan. The report covers
environmental sampling of soil, water, sediment and other materials. It also includes a survey
used to obtain information about human health conditions and follow-up testing involving
physical examinations and blood sampling for endosulfan and hormonal analyses. The report
reaches broad and strong conclusions that human health conditions grouped under three
headings (neurobehavioral disorders, male reproductive system abnormalities, and congenital
malformations in females) are more prevalent in Padre village (the study population), near the
sprayed plantations, than in a reference village approximately 25 km distant where this
endosulfan application method was reportedly not used. The report goes so far as to conclude
that endosulfan is the most probable cause of the conditions documented in the report.
The evaluation of this report covers the study design, the analytical chemistry methods and the
relevance of the findings to endosulfan effects. First, a necessary limitation of the study design
employed to evaluate human health conditions, termed a survey study, is that it cannot reach
conclusions regarding the causes of effects noted. This method is generally accepted as
suitable solely for preliminary hypothesis generation. Based solely on the study design
selected, ascribing endosulfan as the most probable cause of the conditions recorded is not a
scientifically valid conclusion, even; without considering the quality of its conduct and findings.
When we do consider the analyses conducted and the interpretations, however, serious
limitations and inadequacies emerge. There were serious omissions and errors in the
computation and presentation of the analytical results for endosulfan in environmental samples.
In fact, there was not even confirmation that the measurements made were actually endosulfan.
Lack of confirmation, calibration and quality assurance/quality control information are such that
these results would commonly be rejected by environmental regulatory agencies and would not
be considered reliable for characterizing human health risks for any type of regulatory or judicial
action.
The survey method as conducted to obtain information regarding human health conditions does
not conform to the generally accepted requirements for epidemiological studies and is
insufficient for reaching a conclusion that endosulfan effects are observed in Padre village.
Substantial sources of potential bias were not prevented or considered in the analysis, and then
were not discussed in the report as possible sources of uncertainty and limitations. The
comparisons were frequently simplistic and, in some cases, presented in ways that served to
mask or overlook information that would have weakened the conclusion of adverse effects
occurring more prevalently in Padre village. The epidemiological results obtained and the
1
analyses conducted also to not meet the standards commonly required for studies used to
support regulatory or judicial action.
The effects reported to be linked to endosulfan are not biologically plausible as toxicological
responses to the low, background levels of endosulfan found. The congenital conditions
highlighted for male reproductive effects, in fact, are not even found in excess among the boys
from Padre village. And, the measurements characterized to reflect neurobehavioral disorders
are not generally accepted as direct markers of such effects. The interpretations stretch highly
uncertain and highly subjective tests into such serious terms as disorders, abnormalities, and
malformations. The results do not support the presence of elevated rates of such conditions in
Padre village. The analyses and interpretations do not meet generally accepted scientific
standards for establishing chemical exposures as an explanation for purported health effects.
Finally, there were significant and serious discrepancies in some cases between the raw data
obtained through a Right to Information request, the presentations made in the report, and the
subsequent presentations made in a journal article published from the study. Sample results
were excluded, transcription errors were made and numbers of subjects were changed in ways
that served to make the conclusions of the report and the journal article in particular stronger. In
conclusion, the NIOH Report cannot be used to draw a causal connection meeting generally
accepted scientific standards between endosulfan exposure and various reported symptoms
and outcomes because of the limitations of the design, the uncertainties and inadequacies of
the analyses, and the lack of concordance between the reported findings and actual adverse
health conditions.
2
1 Introduction
This report provides a critical review of the study prepared by the National Institute of
Occupational Health (NIOH), Indian Council of Medical Research, titled Final Report of The
Investigation of Unusual Illnesses Allegedly Produced by Endosulfan Exposure in Padre Village
of Kasargod District (N. Kerala) (hereafter referred to as the NIOH Report).
1.1 Background
The NIOH Report was prepared in response to several reports in the press of unusual diseases
in residents of small villages in the Kasargod district of Northern Kerala. The villages are
located below hilltop cashew plantations that have been treated for control of tea mosquitoes by
aerially spraying with endosulfan insecticide two to three times a year for over 20 years (NIOH,
2002; Saiyed, 2003).
At the request of the Indian Council of Medical Research (ICMR), a three-member team from
NIOH visited the area in August 2001 and recommended following up their visit with an
epidemiological study to investigate the prevalence of disease in school children from the
targeted population and a nearby control population. The field study was conducted from
September 24 to October 7, 2001 with the following objectives (NIOH Report page 5):
To confirm the reported disease pattern in the exposed populations and evaluate the
magnitude of the problem by comparison with control populations through a well
designed epidemiological study.
To search for etiological factors if the exposed populations show abnormal disease
patterns and generate a hypothesis.
To confirm the presence of endosulfan residues in environmental and biological samples

and estimate their levels.
An initial draft (the First Report) was promised by December 2001 and a final version of the
report (the NIOH Report) was published in July 2002. The final NIOH Report included additional
analyses of drinking water and soil samples collected in June, 2002, after the initial report.
1.2 Information Sources

In completing our review we relied in part on information provided in:
The NIOH Report (NIOH, 2002);

An initial draft of the NIOH Report (hereafter referred to as the First Report)(NIOH,
undated); and
A companion paper published in Environmental Health Perspectives (Saiyed et al.,
2003) along with comments on the paper (Abraham, 2004; Indulkar, 2004) and the
authors response (Saiyed, 2004) published in the same journal.
3
In addition, a limited amount of information was provided in response to the request by Mr. B.
Mallesham under the RTI Act 2005. The RTI response included 100 pages of material
including:
93 pages of Gas Chromatography-Electron Capture Detection (GC-ECD) output

corresponding to 2 soil samples analyzed on May 30, 2002 (Soil001.CHI and
Soil002.CHI); 2 water samples analyzed on December 13, 2001 (Water002.CHI and
Water003.CHI); 1 blank sample analyzed on November 21, 2002 (Blank001.CHI); and 4
standard samples analyzed on October 29, 2001 (VK013.CHI and VK014.CHI), October
31, 2001 (VK017.CHI) and December 6, 2001 (Std001.CHI).
1 laboratory notebook page (unsigned and undated) describing the extraction and clean-
up procedure for analysis of endosulfan in soils.
6 partially masked laboratory notebook pages (unsigned and undated) with limited
standard and sample information.
4
2 Comments on Analytical Data Quality

The NIOH Report presents the results of analytical chemistry testing used to measure
endosulfan concentrations from samples of soil, sediment, water and human blood. The report
uses these results to make comparisons between the environmental conditions in the Padre
village area, hypothesized to be impacted by aerial applications of endosulfan, and a reference
area (Meenja Panchayath village) approximately 25 km away where this type of application was
reportedly not used. The report uses the results from blood samples to make comparisons
between children from the study versus reference areas. These analytical data are, thus, the
critical foundation upon which the comparisons attempting to link endosulfan to the observations
in Padre village depend.
In our review we identified a number of issues in the way the analytical chemistry tests were
conducted and interpreted that affected the quality and reliability of the analytical data. These
issues were of a nature and extent that preclude the analytical results being considered valid
according to the standards required by governmental regulatory agencies. The results are also
unreliable to the extent that they do not meet the generally accepted standards for use in
guiding scientific interpretations of environmental or public health conditions. These issues
include:
Selected data have been excluded from the NIOH Report without explanation.
Information obtained from NIOH under the Right to Information Act reveals
inconsistencies between the raw data compared to the summary results presented in the
NIOH Report.
The reporting of endosulfan in water and soil at concentrations well below the minimum
detection limit of 1 to 3 ppb and the large numbers of peaks reported in the blank and
standard reference samples suggests that random peaks due to electronic noise were
routinely misinterpreted as endosulfan peaks.
Chromatographic peak identification is based solely on retention time no mass
spectrometry confirmation was performed on any of the study samples because
endosulfan concentrations were too low to confirm by GC/MS.
No calibration data are presented and there is no explanation as to how concentrations
in the samples were calculated from instrument readings.
Results from QA/QC samples and analyses required for the analytical method are not
provided, a condition which frequently results in regulatory agencies rejecting and not
relying upon analytical data.
2.1 Excluded Sample Results

Table 1 of the NIOH Report (page 14) provides levels of endosulfan in water samples collected
in 2001. Data are presented for six samples (3 well, 1 suranga, 1 stream and 1 pond);
presumably, though not specified to be from the study area. Concentrations ranged from
0.0022 to 0.0416 ppb for the individual isomers (-endosulfan, -endosulfan) and the
degradation product (endosulfan sulfate). While Table 1 contains data for six samples,
5
Annexure 6 of the NIOH Report (page 82) notes that a total of seven samples were collected
from the exposed area (Village Vaninagar Padre) and three samples from the reference area
(Miyapadavu, Meenja Gram Panchayat). Thus, it appears that selected data, including
apparently all of the results from the reference area, have been excluded from the NIOH Report
without explanation. Excluding the results from the reference area precludes any comparison
between the reference and study areas and any valid scientific representation whether the
conditions differ between the areas.
Similarly, Table 1-A of the NIOH Report (page 15) provides summary data for endosulfan
residues in soil samples collected in 2001. The table indicates that eight samples were
collected from the study area and 2 samples were collected from the reference area. However,
Annexure 6 (page 82) states that eight soil samples were collected in polyethylene bags from
the exposed area (Village Vaninagar Padre) and three samples from the control area
(Miyapadavu, Meenja Gram Panchayat). Once again, selected data are omitted from the NIOH
Report without explanation. The fact that only sample results from the reference area were
omitted (i.e., the study and reference areas were apparently treated differently) impairs the
scientifically interpretations that can be reached.
In addition, the description provided in the NIOH Report suggests that the soil samples were
likely not collected at locations useful for comparisons between groups of people from the study
village compared to the reference area. The soil sampling locations described for the study
area were not in the village itself, where the children reside, but from the cashew plantations
750 meters or more upslope from the village (page 12). The specific location relative to the
village is not described for the reference area, but there was reportedly no endosulfan spraying
in this area anyway. Comparisons between soil results from the plantations, in the one case,
versus the village, in the other case, are not reflective of the potential exposure differences for
school children.
2.2 Raw Data from RTI Release Not Matching Results Presented in Report
Raw data obtained from NIOH under the Right to Information Act, 2005 indicate that the
summary statistics for endosulfan levels in soil (mean and standard deviation) presented in
Table 4 on page 18 of the NIOH Report contain numerous calculation errors leading to
inaccurate conclusions as itemized below:
The mean -endosulfan concentration reported for the study area (0.274 ppb) in Table 4
is actually the mean -endosulfan concentration measured for the reference area. The
mean -endosulfan concentration reported for the study area should be reported as
0.222 according to the raw data. Note that if the values from the raw data were
presented in the table, the soil sample results from the study area (0.222 ppb) would be
shown to be lower than the results from the reference area (0.274 ppb). Currently, the
report refers to this table to substantiate the statement that the levels were higher in
study area as compared to reference area (page 16). The raw data contradict this
conclusion.
6
Accordingly, total endosulfan concentrations in the top layer of soil, which is the layer
where the greatest potential exposures would occur, are also reported inaccurately.
According to the raw data provided by NIOH, the mean total endosulfan concentration in
the upper soil layer in the study area was 0.242 ppb compared to a mean concentration
of 0.303 ppb in the reference area. Again, the concentration found in the study area for
total endosulfan is lower, not higher than that found in the reference area, similarly
contradicting the study conclusion quoted above.
For the middle layer of soil, the raw data provided by NIOH show that the mean
concentration of -endosulfan was 0.104 ppb in the study area compared to 0.184 in the
reference area. Contrary to the study conclusion, this difference is not statistically
significant (p = 0.15) at the 95% confidence level, and the study area is, again, lower
than the reference area. Table 4 has these values switched and incorrectly reports a
value of 0.089 ppb instead of 0.104 ppb as derived from the raw data.
In total, 16 out of 24 summary statistics reported in Table 4 of the NIOH Report (66% of
the values) differed from summary statistics calculated from the raw data sheets
obtained from NIOH under the Right to Information Act, 2005 (see Table 1).
Additionally, simple editing and oversight review of the report during its production
should have revealed the presence of errors and need for careful evaluation. There is
no need for access to the raw data to catch that obviously erroneous information is
presented in this table. For example, total endosulfan levels are reported to be less than
-endosulfan levels in some cases, which is impossible.
Table 1. Differences Between Summary Statistics Reported in Table 4 of NIOH

Report and Summary Statistics Calculated from Raw Data
Soil Area Mean SD Difference

Layer (Yes/No)
Constituent Report Table 4 Raw Data
Top Study -endosulfan 0.274 0.161 0.222 0.133 Yes

-endosulfan 0.0018 0.004 0.018 0.039 Yes
Endosulfan sulfate 0.025 0.03 0.002 0.004 Yes
Total endosulfan 0.030 0.18 0.242 0.161 Yes
Reference -endosulfan 0.153 0.067 0.275 0.162 Yes
-endosulfan 0.002 0.004 0.002 0.005 No
7
Middle Study -endosulfan 0.183 0.076 0.184 0.077 No

-endosulfan 0.005 0.001 0.001 0.001 Yes
Endosulfan sulfate 0.008 0.018 0.008 0.018 No
Total endosulfan 0.191 0.08 0.192 0.089 No
-endosulfan ND 0.001 0.003 Yes
Lower Study -endosulfan 0.128 0.076 0.128 0.077 No
-endosulfan ND ND No
Endosulfan sulfate 0.012 0.028 0.012 0.029 No
-endosulfan ND ND No
Endosulfan sulfate 0.0005 0.001 ND Yes
2.3 Detection Limits

The minimum detection limits cited on page 84 (Annexure 6) for -endosulfan, -endosulfan and
endosulfan sulfate are 1, 1, and 3 pg/ml, respectively. A concentration of 1 pg/ml is equivalent
to 0.001 ppb (1 part per trillion [ppt]) and 3 pg/ml is equivalent to 0.003 ppb (3 ppt). There is no
description as to how these detection limits were determined and the specified levels do not
match those stated twice in other locations in the Final and First Report. The levels on page 84
appear to be the erroneous units for several reasons:
1) Elsewhere in Annexure 6 of the Final Report (page 86) the detection limits for analysis of
-endosulfan, -endosulfan and endosulfan sulfate by GC-ECD are reported as 1, 1 and
3 pg/l, respectively equivalent to 1, 1, and 3 ppb.
2) The minimum detection limits for -endosulfan, -endosulfan and endosulfan sulfate
cited in the First Report (page 61) are given as 1, 1, and 3 pg/l, respectively also
equivalent to 1, 1, and 3 ppb.
3) Detection limits of 1-3 ppb would be consistent with the method detection limits reported
elsewhere for water samples using EPA Method 508. Achieving detection limits in the
range of 1-3 ppt (1 pg/ml) with the volumes of material (500 ml for water) used in this
study and no chromatographic cleanup step would be extraordinary, and is highly
unlikely.
4) Further, the records showing computations of concentrations from serum samples
obtained under the RTI request show that a reference standard concentration of 200 ppb
was used in these computations. If the GC/ECD method was actually achieving 1-3 ppt
8
detection limits, instead of 1-3 ppb, selecting a standard of 200 ppb would have been
unusual.
There is a clear discrepancy of 1000-fold between the detection limits specified on page 84
compared to those listed on page 86. We have considered the possibility that this discrepancy
is just a lack of clarity related to the conversion between the concentration found in the hexane
diluent compared to the detection limit for the original sample of serum or water. We have also
reviewed information provided in response to the RTI request that suggests the values of 1-3
ppt to be correct due to the mathematical conversion to account for concentration of the extracts
from the samples.
However, based on the detection limits being twice specified by the authors to be 1-3 ppb, the
reasonable expectations of the GC/ECD method, and the chromatograms and information
provided in the RTI response, we have concluded that it is more likely that the statement
indicating 1-3 ppt on page 84 is in error and that 1-3 ppb (1-3 pg/l) endosulfan in serum or
water is more likely the correct detection limit. If sample detection limits of 1-3 ppt were actually
achieved with the water samples, this would need to be clearly explained and specified.
Throughout the descriptions of the method and detection limits, there is no information at all
regarding extraction methods and detection limits for the solid materials sampled (soil,
sediment, leaves). Detection limits for these types of materials are frequently less sensitive
than those for water samples, however no in-depth comparison can be made and the validity of
the soil and sediment results cannot be assessed without a description of the method, amount
of material extracted and the detection limits achieved.
2.4 Chromatographic Peak Identification

Annexure 6 to the NIOH Report includes a description of Confirmation Tests sing gas
chromatography mass spectrometry (GC/MS). Whereas gas chromatography using an
electron capture detector (GC-ECD the primary method used to analyze study and reference
population samples) relies on retention time for non-specific compound identification, GC/MS
provides specific identification of compounds through mass spectral analysis.
To attempt to verify the GC-ECD analysis of serum samples from the study population and
document that they were reporting results for endosulfan specifically, the authors analyzed
standard endosulfan samples and serum samples from an individual poisoned with endosulfan
along with serum samples from the study population by GC/MS. However, this approach was
flawed because the levels of endosulfan in serum samples from the study population were
below the limit of detection for the GC/MS instrument, which was reported to be 100 pg/l or
100 ppb (NIOH Report, page 86). Using this instrument/method, no endosulfan was detectable
in the blood samples from the study population via the specific, GC/MS method.
Moreover, the chromatography column used in the GC/MS analysis (a 30m x 0.25 mm id DB-5
column) differed from the column used in the GC-ECD analyses (a 60m x 0.25 mm HP5
column) such that endosulfan retention times in the GC/MS analysis (ranging from 28.8 to 32.5
minutes) were much shorter than the endosulfan retention times reported for the longer 60 m
9
column used in the GC-ECD analyses (ranging from 38.9 to 67.0 minutes). Because the
retention times did not match between the two methods, the GC/MS results could not even
serve to substantiate that the peaks measured in the study population samples via GC/ECD
were likely to be endosulfan. The confirmation method capable of specifically identifying
endosulfan failed to detect this compound in the serum samples from the study population and
the endosulfan standard peaks did not match the retention time peaks quantified as
endosulfan from the GC/ECD analyses of the study population.
Note that EPA Method 508 warns in particular about potential interference from phthalate esters
presenting a major problem when using an electron capture detector. Phthalates are
plasticizers (the serum samples were stored in plastic) and are also extremely common at low,
background levels in human blood samples. Because no independent confirmation of peak
identification was performed, there is no way to determine if phthalate ester interference was
contributing to the GC/ECD signal interpreted to be endosulfan.
2.5 Random Noise Fluctuations

The number of distinct peaks reported in the chromatographic output provided in the RTI
response (including chromatographic data for the standard samples) ranged from 309 to 486.
Even the blank sample, which is expected to serve as the zero sample for the method,
contained integrated areas for 429 peaks. Because it is unlikely that the blank contained 429
contaminating compounds, this situation suggests that the software that serves to identify
peaks and measure their area was not calibrated to accurately distinguish real peaks from
random electronic noise fluctuation. The frequent reporting of results purported to be
endosulfan in water and soil at concentrations well below the minimum detection limit of 1 to 3
ppb (e.g., see data reported in Tables 1, 2, 3 and 4 of the NIOH Report) suggests that random
electronic noise may have been routinely misinterpreted as endosulfan peaks. In the absence
of independent confirmation of peak identification (performed via either GC/MS or dual column
chromatography), there is no way that apparent peaks corresponding to the thousandth of a ppb
range reported by the authors can be differentiated as actual responses to a specific chemical
versus simply electronic background fluctuation from the detector.
For example, endosulfan concentrations measured in water samples collected in 2001 are
reported in Table 1 (NIOH Report, page 14). Concentrations ranged from 0.0022 to 0.0667 ppb.
These concentrations are well below the reported detection limits of 1 to 3 ppb (currently
interpreted to be the correct final sample detection limits see Section 2.3, above) and suggest
that the authors may in fact be quantifying random noise fluctuations rather than true endosulfan
levels. In two of the samples, -endosulfan levels were greater than -endosulfan levels, which
is contrary to the expected relationship in which -endosulfan is the predominant isomer
detected (for example see page 45 of the NIOH Report). This further suggests that the peaks
quantified as -endosulfan and -endosulfan may have been neither and reflect instrument
electronic noise.
Table 2 of the NIOH Report (page 16) presents levels of endosulfan in drinking water. There
are no units presented in the table, however by comparison to other tables and the First Report,
10
it appears likely that the Report is listing values in ppb. Some values are listed as low as 0.0005
and 0.0004. Values of 0.0004 and 0.0005 ppb are below the minimum detection limits reported
in Annexure 6. Similarly, in Table 4 (page 18), which contains a summary of endosulfan levels
in soil samples collected in June 2002, mean endosulfan levels are also reported below the
detection limit.
2.6 Calibration Data

No mention is provided in the report regarding the method used to calibrate the GC/ECD
results, in other words, the calculations needed to convert retention peak areas to
concentrations of endosulfan. Calibration curves are not provided in an Annexure to the report.
Accordingly, there is considerable uncertainty as to how the sample concentrations were
determined.
No calibration curve demonstrating linearity of the detector response is presented.

There is no indication as to how many standards were used to construct the calibration
curve.
The lowest standard on a calibration curve should be approximately ten times the
method detection limit (i.e. around 10 ppb for this study); however, no standard in this
range was apparently run and the lowest standard used was apparently much higher,
i.e., 200 ppb.
While a multi-point calibration curve may have been generated at some point, the 6
partially masked laboratory notebook pages suggest that calculations of sample
concentrations were actually made using single-point calibration with a 1 ppm standard.
To be reliable, among other conditions, single-point calibration should be done using a
standard concentration that is within 20% of the expected sample concentration. In this
case, the study reported calculated concentrations in the sub-ppb range, thousands to
hundreds of thousands of times lower than the single standard (1 ppm) that was used for
calculations. Calculations based on this type of extreme extrapolation are highly
uncertain and such extrapolation would not be acceptable for typical regulatory agency
evaluations of analytical data.
2.7 QA/QC Data

No quality assurance/quality control (QA/QC) data are presented to assess the quality of the
analytical data presented in the NIOH Report. Annexure 6 provides descriptions of the
methodologies used for analysis of endosulfan residues. The method for endosulfan analysis is
said to be based on EPA method Section 5, A, (3), (a) but no actual reference is included and
this terminology appears to reflect some type of typographical error since a method number is
omitted. The method used is actually similar to EPA Method 508 Determination of Chlorinated
Pesticides in Water by Gas Chromatography with an Electron Capture Detector which also
11
involves liquid/liquid extraction with methylene chloride and analysis by GC-ECD, as done in
this study. 1
Results obtained from QA/QC samples are required to evaluate the accuracy and precision of
environmental data collected in a study. Method blanks, field blanks and equipment blanks are
used to evaluate issues with contamination. Laboratory duplicates, field duplicates and matrix
spike duplicates are used to evaluate the precision of the analyses. Surrogate spikes, matrix
spikes and external reference standards are used to establish the accuracy of the results. No
such data are presented in the NIOH Report and there are no indications in the report,
annexures or lab notes provided that such QA/QC testing was completed.
No blank data are presented in the report.

There is no indication that surrogate spikes were used in the analysis.
No matrix spike/matrix spike duplicate results are presented in the report.
There is no indication that any duplicate analyses were performed to assess
measurement reproducibility.
Without presentation of these QA/QC data, there is no way to affirm the reliability of the data
reported in the study. If such QA/QC analyses were not conducted, the study would not meet
the generally accepted scientific standards for environmental chemistry analyses. In this case,
the results would be rejected and not considered usable for scientific interpretations according
to the QA/QC requirements that apply for the U.S. EPA method employed.
1 U.S. EPA. 1995. Method 508 Determination of Chlorinated Pesticides in Water by Gas Chromatography with an
Electron Capture Detector Revision 3.1. Edited by J.W. Munch. National Exposure Research Laboratory, Office
of Research and Development, Cincinnati, OH.
12
3 Survey Design Comments

The NIOH Report specifies that one of its objectives is to evaluate disease patterns through a
well designed epidemiological study (page 7). However, the study described in the report is, in
fact, a simple survey of children in two populations, one from Padre village, near the plantations
sprayed with endosulfan and another from a reference village where such spraying had
reportedly not occurred nearby. The study was implemented rapidly, over approximately 2
weeks in 2001, and involved numbers of participants that ultimately proved too small to provide
useful numbers of the conditions reported. Under generally accepted methods for the design
and conduct of epidemiological studies 2, surveys can only serve as preliminary tools to generate
hypotheses and do not serve as a basis for reaching conclusions about the causes of health
effects. The study by its own design cannot serve as the basis for conclusion regarding an
etiological link (causation) for endosulfan producing the conditions observed. Even for the
modest goal of hypothesis generation, the design and conduct of the study presented in the
NIOH report was not adequately reliable to produce scientific findings suitable for regulatory or
judicial uses or action.
Similar to the analytical chemistry results serving as the foundation upon which comparisons of
environmental conditions rest, the survey and follow-up testing are the foundation upon which
the entire interpretation of potential human health effects relies. And, similarly, this foundation is
inadequate for the uses to which it is stretched.
The validity and strength of epidemiological study results depend on the study design, data
quality and completeness. Factors determining the quality and usefulness of epidemiological
studies include the ability to avoid bias, control for potential confounding variables, and including
sufficient numbers of exposed and non-exposed cases to limit imprecision due to small
numbers. Issues relating to these factors in the NIOH study include:
The study design is a survey, which cannot be used to determine causation, and the
strength of the statistical analyses presented cannot be validated because details on the
population base and how the participants reflect their respective communities are
lacking.
The study fails to account for or discuss the numerous sources of potential bias.
The study fails to address, account for or discuss known and suspected causes of the
numerous outcomes evaluated, known as confounding variables.
Small percentages of surveyed populations participated in some tests conducted for the
study.
2
Kleinbaum, Kupper and Morgenstern, 1982; Epidemiological Research: Principals and Quantitative
Methods. Van Nostrand Reinhold; Rothman, Greenland and Lash, 2008; Modern Epidemiology,
Lippincott Williams & Wilkins
13
3.1 Study Design Considerations

The NIOH Report fails to describe how the actual participants were selected, or to provide the
total number of subjects in each village who would be eligible for inclusion. Without this
information, it is not possible to consider whether those included are representative of children
in the corresponding villages. Thus, it is not possible to ascertain the extent to which selection
forces were operating, resulting in the 619 and 416 in the study and referent groups,
respectively (page 8).
Limited information on the methods of recruitment is provided, and whether these efforts were
comparable and similarly extensive in each location is not discussed. The introduction of the
report describes anecdotal reporting of cases of illness in this area, which would be expected to
sensitize the population in the study village as compared to the reference village. This
situation can lead to differential reporting and participation in a study, thus biasing findings due
to over-reporting in the study village. If different methods were used to recruit participants
between the communities and if the study village was aware of what was under
investigation, any analyses would be subject to potential bias.
Methods to survey/interview participants are described to include staff training (page 9).
However, the staff was apparently not blinded to the exposure status of the two groups, and
since the assessments included subjective characterizations, the extent to which observer bias
has been introduced is not known. Given that abnormalities were subjectively identified by the
staff, and no criteria are provided that define major abnormalities, the potential for intensive
scrutiny or differential inclusion of children in the study group is high. This could lead to the
appearance of a greater number of abnormalities in the study group.
This factor is particularly relevant with regard to the Sexual Maturity Rating (SMR) scoring for
male subjects. While Annexure 3 contains tables presumably used to train and guide project
staff on the specific criteria and corresponding scores for girls (page 70-71), no such tables are
provided for boys. The lack of specific and consistent grading categories for boys increases the
likelihood of differential scoring by different examiners and increases the potential of observer
bias. Also, the proforma questionnaire for boys calls for two SMR scores to be recorded, one
for pubic hair and one for external genitalia and testes (page 65). No line is provided for a
separate discrete score corresponding to stage of penis development. However, in the
analyses that were presented in the report, separate SMR scores are presented in the following
categories: pubic hair, penis, and testes. Given a direction on the questionnaire form to score
external genitalia and testes collectively, there is substantial potential for errors and
uncertainty attempting to separate this into separate scores for penis versus testes development
later in the analysis phase, particularly if the observers were not provided a table with the
scoring criteria.
A questionnaire is provided in the NIOH Report; however, the report states (page 9) that the
parents were interviewed in one of four local languages. The possible misunderstandings and
14
misinterpretations resulting from translation of the health questions into local languages from
English may in fact be substantial, especially if there is no comparable term for the symptoms
listed on pages 60 and 61. Bias can be introduced by the interviewers attempts to explain or
translate from English, and if these explanations are more detailed or extensive for the study
group, a bias toward over-reporting can result. However, the report does not indicate how many
participants were issued the questionnaire in each of the languages, nor does the report discuss
any of the challenges involved in the translation or understanding of the symptoms in each of
the languages.
3.2 Confounding Factors and Alternate Interpretations

A significant confounding variable in this study important to a number of the analyses presented
is the inherent age difference between the groups of children from the two villages. The
average age of the reference population is about 10.5 years, compared to 12 years in the study
population (Table 7). In the pre-pubescent and pre-teen years, there can be significant
differences in growth, maturation, development, and learning that are simply a function of how
children develop. Lack of discussion of how an age difference would be expected to affect such
outcomes is a serious oversight in qualifying the interpretation of the results presented.
The report also failed to provide data describing the ethnic differences among the populations
studied, which could reflect real differences in socio-economics, nutrition, or genetics that might
affect health measures if not considered in the analysis. The limited narrative discussion of
this topic does not provide sufficient information to exclude cultural factors as playing a role in
the differences subsequently found in the survey. The suggestion that because differences in
height and weight were not statistically significant between the groups, the nutritional status is
comparable (page 21) is not substantiated, and cannot be assumed to be a non-factor in other
outcomes assessed. Also, the lack of significance for the reported differences in height and
weight is likely due to the statistical method chosen and failure to stratify the groups by age.
This factor is discussed further below (Section 4.3).
Other possible confounding variables include differential diets, hereditary (genetic) factors
associated with certain ethnicities, quality of teaching between the schools, and family factors
that might differentially influence a childs performance in school. The lack of acknowledgement
and control for these and other confounding variables is one of the most serious flaws in the
study.
The presentation of neurobehavioral problems is similarly lacking a discussion of alternative

explanations for the results reported (Table 9). Again, the children in the two study populations
are of different ages, and thus, the comparison of learning disabilities and class retention have
not considered the affect of age, differences in school teaching standards, possible bias on the
part of teachers identifying more disabilities among the study village, or family and home
factors that may be affecting learning and classroom behavior. The lack of consideration of age
and other extenuating factors and possible teacher bias are also ignored in reporting
findings in Tables 10 and 11, the latter based on very small numbers
15
3.3 Size of Study Groups

Most of the simple tabulations of findings presented in the report show that less than the full
number of participants in each group responded or participated. While incomplete participation
and failure to complete multiple components of a study occur frequently, this limits the
interpretation of what is presented. Also, when findings are only available for small percentages
of study participants, the uncertainty and potential bias become much greater. The report does
not report or attempt to evaluate the scale of uncertainty that resulted from these factors.
Uncertainty analyses are a common component of epidemiological studies and methods to
evaluate the statistical limitations resulting from the low response rates for various endpoints
were readily available. Examples include:
Chromosomal analyses presented for 2% of reference group and 5% of study group.
Serum samples obtained from 26% study group and 20% reference group (page 10).
Prevalence of seizure disorders presented for 41% reference girls and 42% study
group girls (Table 12).
There is additional potential for selection bias as the children for whom blood samples were
taken (page 10) or sexual maturity examinations done are a small sub-set of each study group
(Tables 16 and 18). Any interpretation of comparisons of these small subgroups is not
meaningful, and cannot be assumed to represent the whole eligible study population.
Another issue creating uncertainty related to the selected sub-groups for certain tests is the
difference in participation rates between the study and reference populations. When differing
proportions of groups choose to participate, there is the potential that it is occurring because of
a desire to self-select, either for or against participation. Large differences in participation rate
include:
IQ surrogate testing 57% reference group participation compared to 82% participation

from the Padre village study population (Table 10).
Sexual maturity rating examinations 70% participation from boys in the reference
village compared to 53% participation from boys in the study group (Table 18).
The numbers of children who are compared in the various tables are not sufficient to draw
causal conclusions. The analyses are simplistic and do not all represent the full number of
participants in each evaluation. For example, Table 14 includes less than half of both the study
and referent populations; there is no basis to conclude the majority of girls for whom there is no
information are in fact distributed in the same way as what is given.
The results that are presented stratified by age include findings in some age groups that are too
small to be meaningful. Table 14, for example, presents results for the age distribution of
menstruating girls showing higher numbers and proportions of girls menstruating among the
older girls from Padre village. However, only eight 15-year old girls were included from the
16
reference village, compared with 23 girls of this age from Padre village. Thus, each individual
girl from the reference village has a larger influence on the statistics compared to the Padre
village group. With this type of sample size difference, the status of just a couple of girls in the
reference group has large effect on the apparent difference between the villages. Also, the
statistic presented, an odds ratio, is dependent upon the groups being compared not having
such confounders present. Since the odds ratio compares girls from the reference village that
are younger on average than the Padre village girls, the effect of age can influence comparisons
that have been purported to be affected by environmental factors.
In another example, results of chromosomal analyses presented in Table 22 include 8 reference

and 29 or 21 study participants (for two different measurements). Thus, comparisons cannot be
reasonably characterized as being reflective of the two overall populations results are
provided from less than 2% of the reference population versus 5% of the study population. With
such a small number from the reference population, the lack of chromosomal abnormalities
among these few children is not a useful basis for comparison. Also, the report states It may
be noted that the chromosomal abnormalities like dicentric chromosome and chromosome
exchange were observed in two each of the study subjects. Drawing note to this
observation implies such small numbers are significant to interpretations when such minimal
observations are not generally accepted as scientifically relevant.
17
4 Comments on Endosulfan Exposure and Effects

One of the specified objectives of the NIOH study was to evaluate etiological factors that could
explain the health conditions observed in the study population; in other words, to evaluate
potential causes. There are specific generally accepted requirements for evaluating potential
causation in toxicological or epidemiological studies and these include the requirement that
purported effects be biologically plausible. In the context of a survey, this means that observed
conditions being evaluated must be consistent with the biological responses that occur from a
putative cause, in this case endosulfan. Also, evaluating causation specifically requires
consideration of possible alternate explanations for observations.
We have evaluated how the conditions and health effects reported in the NIOH Report relate to
the toxicological characteristics of endosulfan and whether the findings reported can
substantiate an etiological (causal) role for endosulfan. We have identified issues with the
relevance of the survey and follow-up testing of a nature and degree that the report does not
meet the standards typical for studies establishing causation for use in regulatory or judicial
actions. The issues include the following areas:
The endosulfan levels measured in blood samples from the study population in Padre
village were within the expected range reported in other studies, making this a weak
candidate cause for conditions in the village.
Age differences between the study group and reference group are an obvious potential
cause of differences in hormone levels that was not fully addressed.
Observations purportedly associated with neurobehavioral conditions and congenital

conditions are insensitive and not toxicologically relevant.
4.1 Endosulfan Levels Consistent With Background

Endosulfan levels in blood samples from the study group are typical of general background
levels found in other populations exposed through routine environmental and dietary sources
(i.e., no specific source such as aerial spraying). In and of itself, this circumstance makes
endosulfan a difficult candidate to establish as the cause of conditions in Padre village, since
there is no indication that exposures are substantially different than experienced elsewhere.
Additionally, the computation of values from the reference population generated levels that are
unusually low in comparison to expected background levels. Together, these circumstances
suggest it is more likely there is something out of the ordinary about the computed values from
the reference village than the results from Padre village. Comparisons made between these
reference group results and the results from Padre village are, thus, weakened by the
uncertainty inherent in the former being inconsistent with other scientific studies.
Endosulfan testing results were presented for blood serum samples collected from sub-groups
of the children studied in each village. These sub-groups were not selected randomly and are
stated to be an outcome of the willingness of parents and children to consent to blood sampling.
Results are reported for approximately 1 out of 5 children studied in the reference village and 1
18
out of 4 children studied in Padre village. The difference in participation rates suggests that
parents in Padre village were more likely to consent, potentially because they were more
sensitized to concerns regarding endosulfan. This highlights the potential for selection bias
affecting the outcome of comparisons based on the serum sample results.
The NIOH Report references Table 5 stating that endosulfan residues were found in 85% and
78% of female and male subjects, respectively of study area; whereas they were found in 34%
and 29% of female and male subjects in the reference group (page 16). First, there appears to
be a typographical error in Table 5, because the percentages stated to be from the study area
are actually shown in the table as being from the reference area and vice versa. In this case,
based on comparison of the subgroup sizes subsequently reported in the published version of
the study (Saiyed et al., 2003), it appears that the error is in the table heading, as opposed to
the text explanation. Additionally, this statement fails to make clear that the percentages do not
actually apply to the overall subject groups, but only the non-randomly selected subgroups.
Thus, endosulfan was not actually detected in 85% of the 619 subjects from Padre village,
rather in 85% of the 97 children who provided blood samples.
The NIOH Report presents serum levels of -endosulfan, -endosulfan and endosulfan sulfate
grouped by gender of the children (Table 6). No units are shown or mentioned in the text,
however, by comparison to the published version (Saiyed et al., 2003) it appears that they are
likely presented in parts per billion. Combining the males and females, the average result for
the group from the reference village is approximately 1 ppb, while the overall average for the
study group from Padre village is between 9-10 ppb.
Interestingly, it is the results from the reference group that appear unusual compared to other
studies. Because of its wide usage in parts of the world, there are routinely found background
levels of endosulfan in human blood, even in the absence of specific exposures such as the
aerial spraying being investigated around Padre village. Results from a study conducted in four
Punjab villages found average levels of -endosulfan and -endosulfan of approximately 5 ppb
in human blood samples (Mathur et al., 2005). A study in Spain reported an average total of
approximately 9 ppb for -endosulfan, -endosulfan and endosulfan sulfate combined in
umbilical cord blood from newborns, and even higher levels of other endosulfan metabolites not
accounted for in the NIOH study (Cerrillo et al., 2005). These results suggest that background
levels should have been expected to be in the 5-10 ppb range where exposures were general
environmental and dietary sources of endosulfan. The results from the Padre village group
appear to be within the range of routine background endosulfan levels found in other
populations. The reported values for this village do not stand out as being obviously elevated
due to exposures from the aerial spraying patterns on the plantations in the area.
Conversely, the reported average values of approximately 1ppb in the reference area appear
low relative to expected background and suggest the need to obtain the raw data from these
measurements to ascertain how non-detect values were handled in computing the averages.
The report does not specify whether averages were computed only using detected values. With
19
more than 2/3rd non-detected samples from the reference village, the approach used to deal
with censored values is important to consider.
Further information suggesting the potential impacts of including samples below detection limits
in the analyses emerges by referring to the First Report. Table 2 (page 12) in the First Report
provides a listing of individual serum sample results for 22 individuals from Padre village. This
version of the report specifies that at that point, 170 children from Padre village had been
sampled, but no individual nor summary information is presented for the remaining children. For
serum samples, the specified detection limit was 3 ppb for endosulfan sulfate. Three children
are listed to have values lower than this (1.57, 2.79 and 2,9 ppb) in the table. The quantification
of these results is uncertain if they are below the minimum detection limit for the method. In the
Final Report, no individual measurements are provided, just summary information such as the
mean, which is influenced by the manner in which censored values (below detection limits) are
included. The handling of the reported values below detection limits is not specified. They
should have been treated as non-detects.
4.2 Samples Excluded from Journal Publication

The NIOH study is dated 24 July 2002. A journal article presenting some of the data and results
from the study, particularly focusing on the results for the males, was submitted for publication
on 10 February 2003 (Saiyed et al., 2003). With regard to the blood sample results, there are
notable differences in the datasets presented in these two documents. While endosulfan blood
levels for 97 boys from Padre village are summarized in the NIOH report, the published article
includes results from only 70 boys from the study village. The average total endosulfan level in
the published version is 7.47 ppb, compared to 8.71 ppb in Table 6 of the NIOH Report. This
suggests that the endosulfan results from the 27 boys excluded from the journal publication
were actually a bit higher, on average. The omission of results from these boys is curious since
it reduces the apparent elevation of endosulfan in boys from Padre village. This suggests that
there was some compelling reason that the results from these 27 boys were not considered
suitable for publication, opening up the possibility that data quality issues were recognized
between the release of the NIOH Report and subsequent journal publication. In comparison,
results from 48 boys from the reference village appeared in the NIOH Report and only 3 of
these were excluded in the dataset for the publication, which included results from 45 reference
village boys. The outcome that the exclusions occurred to such differing degrees between the
groups further suggests there was some factor specific to the detected levels reported in the
NIOH Report for the study village that was reconsidered. Also, the published article does not
disclose that the results presented are a selected subset of samples from the larger NIOH study
or explain the basis for excluding samples.
Another unusual quantitative outcome is the reporting of the frequency of detecting endosulfan
among the tested samples stated in the journal article, endosulfan was detected in serum
samples of 78% of the children in the study group and 29% of the children in the control group
(page 1961). These are exactly the same values stated in the NIOH Report and presented in
Table 5, albeit apparently reversed. It seems extraordinarily unlikely that the percentages of
samples with detected levels of endosulfan could have been identical once 27 study group and
20
3 control group boys were dropped. This raises a question as to whether the published
statement regarding the frequency of detection is accurate based on the smaller dataset or
whether it might have referred to the larger dataset from the NIOH study, which was not
disclosed in the article. Presenting summary statistics, such as the frequency of detection, using
a different number and group of samples than those described in the materials and methods
section of a submitted journal article would be inconsistent with expected transparency in
scientific publishing.
4.3 Obvious Alternate Explanations Not Discussed

The data presented in Table 7 show that the girls from Padre Village were older, taller and
heavier than the corresponding groups from the reference village. The average age of the study
group (12.0 years) is a full year-and-one-half older than the average age of the reference village
girls (10.5 years). Particularly at these peri-pubescent ages, such a difference is an obvious
alternative factor in hormone levels. Additionally, the girls from Padre village were 19% heavier
on average than the girls from the reference village (30.8 kg vs. 25.9 kg). This difference also
suggests the obvious possibility that the overall group of girls from Padre village was at a more
advanced stage of puberty.
The NIOH report does acknowledge the age difference stating, the mean age of the study
group is higher as compared to reference population (page 19). However, the report also goes
on to conclude that the sex-wise distribution is comparable in study and reference groups
(page 19). Such a conclusion in light of a 1.5-year age difference and 5 kg weight difference
does not appear adequately supported.
The NIOH study reports that levels of Luteinizing Hormone (LH), progesterone and estradiol
were higher in the female study group from Padre village compared to the reference village
(Tables 26, 29 and 30). This is the outcome that you would expect with such hormones from an
older group of peri-pubescent girls and it substantiates that the position stated in the report that
the groups from the different villages can be considered comparable is subject to challenge.
Both the NIOH Report and the subsequent journal publication (Saiyed et al., 2003) focus
extensively on results relating to male reproductive development, particularly testosterone levels
and SMR scoring for the boys. However, results relating to both of these parameters are also
not adequately considered with regard to alternate explanations. For the SMR scoring, the
failure to provide scoring criteria, failure to blind the observers, and small differences in a
subjective score indicate the obvious potential for differences to be explained by observer bias.
For the testosterone results, the report and publication acknowledge that age is a controlling
factor, but suggest that residence in Padre village is also a statistically relevant factor.
However, the statistical testing and information that would allow a reviewer to evaluate the
relative importance of these two different causes is not presented.
SMR scoring involves assigning a categorical value of 1 to 5 based on certain observable

characteristics related to sexual maturity. In the report, the differences reported fall
predominantly between scores of 2 and 3 and separate scores for pubic hair, penis and testes
21
are presented in tables and figures. The values for penis development cannot be considered
reliable because the questionnaire provided to examiners did not even call for a separate score
for penis development. It is not clear how the analysts obtained such values.
The scores and differences between the study and reference groups for testes development
illustrate the subjective nature and high uncertainty of using this parameter. While the criteria
employed by project staff for boys were not disclosed in the report or its annexures, a common
version of the Tanner SMR criteria relating to development of the testes and scrotum is:
SMR Score 2 Enlargement of scrotum and testis, reddening and change of texture of
scrotum
SMR Score 3 Growth of testes and scrotum
Particularly for examiners seeing a patient for the first time, differentiating between whether the
boy qualifies for a score of 3 versus 2 is obviously subjective and uncertain.
The differences tabulated (Table 18) and plotted (Figure 3) between the study and reference
groups show that the Padre village boys aged 12, 13, 14, and 15 scored approximately 0.5 SMR
point lower than the corresponding aged boys from the reference village. In other words, the
difference reported to be significant corresponds to something about halfway between
enlargement versus growth of the testes and scrotum. Also, there are small numbers of boys
of each age, ranging from only 5 to 14 with SMR scores of 2 or higher. In the context of these
minor differences, unintended observer bias is an obvious possibility that should have been
addressed. Providing consistent scoring charts and using examiners blinded to the village of
residence for each boy were critical when interpretations depended on such fine distinctions.
The NIOH Report states levels of testosterone were lower in the study group as compared to
reference population in the same age group (page 37). This statement is not a precise
representation of the results in Table 28 because for boys of some ages, the levels were
actually lower in the reference group. Looking at boys older than 10, the table shows that the
11 year olds were essentially equivalent between the villages, the reference village boys had a
clearly lower average testosterone level for ages 12 and 15 and the Padre village boys had a
clearly lower average for ages 13, 14 and 16. And, the 16-year old group from Padre village
included only two boys. This type of inconsistent pattern based on small numbers is not a clear
indication of effects in Padre village. Statistical analyses intended to help differentiate between
the obvious effect of age on testosterone production and a possible effect of location (i.e.,
village of residence) were apparently conducted. However, the summary information presented
is not sufficient to determine the relative contribution of these two factors or to reanalyze the
data to confirm the report findings.
4.4 Recorded Observations Not Biologically Relevant

The conclusions presented in the NIOH report specify that the study identified a higher
prevalence of neurobehavioral disorders, male reproductive system abnormalities, and
congenital malformations in females in the study group from Padre village. Interpreting the
22
findings of the study in these terms is inconsistent with both the results obtained and the
generally accepted meaning of these terms.
The results apparently categorized to indicate neurobehavioral disorders were 1) differential

scholastic performance, 2) differential performance in a test to draw a man, and 3) abnormal
behavior reported by teachers. None of these parameters are directly or uniquely indicative of a
biologically based neurobehavioral disorder. The report states the prevalence of arrogant and
aggressive behavior and restlessness were higher in the study group as compared to the
reference population (page 22). According to reporting by teachers for the 619 Padre village
children, 1.8% of them were arrogant, 1.3% were aggressive and 0.3% were restless. The
comparison made is to reporting from the teachers of the 416 reference village children among
whom there was not a single restless or aggressive child noted and only one child reported to
be arrogant. Such a finding is clearly a difference without meaning in the context of declaring
children to have neurobehavioral disorders. Given the awareness of the Padre village teachers
of the concerns regarding endosulfan, reporting bias is an obvious consideration, along with
some type of motivation to underreport that may be affecting the teachers of the apparently 415
near perfect children from the reference village. These endpoints are not appropriately sensitive
to identify actual clinically relevant disorders and are not indicators of endosulfan toxicology.
In addition to the reported differences in testosterone levels and SMR scoring discussed above,
the other observations apparently interpreted as male reproductive system abnormalities in the
report include two conditions reported in Table 12 undescended testes and congenital
hydrocele. Two cases of undescended testes were reported among 361 boys from Padre
village, amounting to 0.55% of the boys. This is a relatively common condition with a
prevalence of around 1% in boys over age 2. Higher rates are seen among newborns, but they
commonly resolve prior to age 2. The number of cases seen in Padre village is, thus, not
higher than would be expected. Curiously, Table 12 shows the fraction 2/361 and
parenthetically 1.55%. This incorrect calculation overstates the percentage by almost threefold
and makes the table entry appear higher than the general population rate of around 1%.
Congenital hydrocele is another common condition at birth, occurring in approximately 1-2% of

boys. Hydrocele refers to fluid accumulation around the testes and congential cases also
frequently resolve as the testes complete their descent and the scrotum becomes isolated from
the abdominal cavity, allowing the fluid to resorb. The report lists four cases of congenital
hydrocele, meaning the condition was present at birth, among 361 Padre village boys. This
amounts to 1.1% of the group, again not higher than expected.
In the published journal article version of the study (Saiyed et al., 2003), cases of a third
condition, congenital inguinal hernia, are included along with undescended testes and
congenital hydrocele, even though there is one case in each of the study and reference
populations. The article reports a total of 6 cases among these three conditions (omitting one of
the hydrocele cases for some reason) and, then computes a prevalence of 5.1% in Padre
village (abstract, page 1958) by revising the group size to report that they were observed among
117 subjects (6/117). Changing the denominator in this manner between the report version and
23
published version, and adding an extra case to the numerator from another condition for which
there is clearly no difference among the study and reference populations, thus computing a
higher prevalence rate from the same underlying study, is inconsistent with expectations of
scientific publishing.
While the conclusions of the report specify differences in female congenital conditions
collectively to be important, review of Table 12 shows that the only significant difference
between the two villages was noted for the non-specific grouping congenital heart disease.
Nine cases were noted among 258 girls from Padre village. Only one case was noted among
183 girls from the reference village. By segregating the girls in this manner the report shows an
apparent difference. However, congenital heart diseases in general are not particularly linked to
gender. And, among the boys, the prevalence of congenital heart disease is 3 times higher in
the reference village than in Padre village according to Table 12. The observations among the
boys are, thus, contradictory to the pattern observed with the girls. Since there is no biologically
reasonable basis or research suggesting that endosulfan affects cardiac development in
opposing manners between males and females, the observations collectively grouped as female
congenital conditions are not, in fact, relevant to establishing endosulfan as the cause. This is a
case where the difference is more likely a matter of chance related to the small number of
reported cases.
24
5 Conclusions
The NIOH report draws a series of conclusions including that there is a significantly higher
prevalence of neurobehavioral disorders, congenital malformations in females, and male
reproductive abnormalities in the Padre village area. The report also concludes that sufficient
information has been considered such that endosulfan exposure from aerial spraying in the
cashew plantations upslope from the village is the most probable cause of the health
conditions documented in the report.
These conclusions are not supported by the study design, methodologies, or results of the
investigation that was completed. The conclusions outreach the stated objectives of the study,
which specify that the survey approach was intended to serve to generate a hypothesis
regarding potential etiological factors. This objective was theoretically attainable, however the
survey method employed cannot, as a matter of generally accepted epidemiological science,
serve as the basis for determining causation from a single environmental factor. The design
and methods are suited solely for preliminary hypothesis generation. Therefore, the survey
could not, in the first place, support the conclusion reached regarding endosulfan as the
probable cause.
Review of the Final Report, the First Report, the information provided subsequent to an RTI
request and available scientific literature lead us to conclude that this investigation is impacted
by analytical limitations; computational errors; reporting and documentation errors and
omissions; and inadequately substantiated interpretations to such an extent that it is not
scientifically reliable. The uncertainties are sufficient that results from this investigation would
frequently be rejected by environmental regulatory agencies and excluded from consideration of
regulatory or judicial actions.
We recognized serious limitations in the analyses for endosulfan conducted on environmental

and blood samples. The failures to provide QA/QC documentation or confirm the presence of
endosulfan with a chemical-specific method and the implications of the large number of
apparent chromatographic peaks in the blank create uncertainties with regard to whether
endosulfan was even the compound detected in some samples with low reported
concentrations. The presentation of summary data alone, without appendices containing the full
set of results, makes it impossible to recreate the computed means and variances and ascertain
how non-detected values were included.
The survey approach used to document health conditions is subject to substantial sources of
potential bias and did not include steps to either eliminate or specifically recognize the impact of
biases. Tests for confounding factors were not included and the simple summary statistics
compared are not sufficient to determine the potential interactions among various factors
affecting health. The conditions were grouped and categorized such that the seriousness and
prevalence of conditions was overplayed. Endpoints that are highly subjective, such as
arrogance or aggressiveness reported by a teacher, were represented to be neurobehavioral
disorders. Quantitative measurements such as hormone levels were compared using summary
statistics that did not account for the obvious and expected effect of age in pubescent subjects.
25
Congenital conditions reported as male reproductive effects were actually found among the
boys from Padre village at rates below the prevalence expected in the general population.
The reporting of the investigation also failed to meet standards of transparency and clarity
expected in scientific reports. Sample results were excluded and the number of subjects
participating was manipulated between different versions of reporting the same study.
Information presented in a followup publication from the study was selected in ways that inflated
the apparent prevalence of congenital conditions in Padre village. Summary statistics were
computed from varying numbers of subjects without explanation and there were serious
discrepancies in some cases between the raw data obtained through a Right to Information
request and the numbers presented in the report and publication.
In conclusion, the NIOH Report was necessarily limited, as any investigation, by the practical
issues of timing, participation and study design. In addition, however, the uncertainties of the
investigation were not made clear and its lack of suitability, as a brief, preliminary hypothesis-
generating study, for informing regulatory or judicial actions was not acknowledged. In contrast,
the conclusions presented, in particular the finding that endosulfan application is the most
probable causative factor for conditions reported, amount to stretched and selective
interpretations of the results obtained. The study is not a valid means to support such a
conclusion. The report is not an appropriate or complete scientific representation of the study
conduct and findings. Substantive corrections, expanded disclosures and further analyses are
necessary before the report would meet the expected standards for scientific reporting.
26
References
Abraham, C.C. 2004. Endosulfans Effects: Omissions and Flawed Data. Environmental
Health Perspectives 112(10): A538.
Arrebola, F.J., J.L. Martinez Vidal and A. Fernandez-Gutierrez. 2001. Analysis of endosulfan
and its metabolites in human serum using gas chromatography-tandem mass spectrometry.
Journal of Chromatographic Science. 39(5): 177-182.
Cerrillo, I., Granada, A., Lopez-Espinosa, M-J., Olmos, B., Jimenez, M., Cano, A., Olea, N., and
M.F. Olea-Serrano. 2005. Endosulfan and its metabolites in fertile women, placenta, cord
blood, and human milk. Environmental Research 98:233-239.
Goyal, R.K. and H.G. Koshia. 2011. Report of the Committee to Evaluate the Safety Aspects of
Endosulfan. Report submitted to Department of Health & Family Welfare, Government of
Gujarat, Gandhinagar, Gujarat, India. March 15.
Gupta, P.K. and R.C. Gupta. 1979. Pharmacology, toxicology and degradation of endosulfan.
A review. Toxicology 13: 115-130.
Indulkar, A.S. 2004. Endosulfans Effects: Inaccurate Data. Environmental Health

Perspectives 112(10): A538-A539.
Mathur, H.B., Agarwal, H.C., Johnson, S., and N. Saikia. 2005. Analysis of Pesticide Residues
in Blood Samples from Villages of Punjab. Report of the Centre for Science and
Environment, Pollution Monitoring Laboratory. New Dehi. March 2005.
National Institute of Occupational Health (NIOH). 2002. Final Report of The Investigation of
Unusual Illnesses Allegedly Produced by Endosulfan Exposure in Padre Village of Kasargod
District (N. Kerala). Report submitted to the Honorable National Human Rights Commission
by Indian Council of Medical Research. Ahmedabad-380016. July 22.
National Institute of Occupational Health (NIOH). Undated. Report of The Investigation of

Unusual Illnesses Allegedly Produced by Endosulfan Exposure in Padre Village of Kasargod
District (N. Kerala) (First Report). Report prepared by Indian Council of Medical Research.
Ahmedabad-380016.
National Institute of Occupational Health (NIOH). 2010. September 24 Letter Report from P.C.
Yadav (NIOH) to B. Mallesham re: Information Provided under the RTI Act, 2005.
Saiyed, H., A. Dewan, V. Bhatnager, U. Shenoy, R. Shenoy, H. Rajmohan, K. Patel, R.

Kashyap, P. Kulkarni, B. Rajan and B. Lakkad. 2003. Effect of endosulfan on male
reproductive development. Environmental Health Perspectives 111(16): 1958-1962.
Saiyed, H.N. 2004. Endosulfans Effects: Saiyeds Response. Environmental Health

Perspectives 112(10): A539-A541.
27
Attachment A:
Curricula Vitae
Project Director and Toxicologist:

Dr. Robert P. DeMott
Project Chemist:
Dr. Thomas D. Gauthier
Project Epidemiologist:
Dr. Diane J. Mundt
28
1
Robert P. DeMott, Ph.D., D.A.B.T.
Education
1993 Ph.D., Physiological Science, University of Florida, Gainesville
1987 B.A., Biology, with Honors, Williams College
Registrations & Affiliations

Board Certified in ToxicologyAmerican Board of Toxicology (Diplomate)
Experience Overview
A board-certified toxicologist who has practiced for more than 15 years in the field of chemical
risk analysis, Dr. DeMott evaluates exposures to chemicals in the workplace and the environment.
His expertise includes reproductive and developmental toxicology and endocrine-related health
effects. He has extensive experience evaluating potential interactions among chemicals and
developing risk-based target levels for environmental cleanup.
Dr. DeMott analyzes exposure concerns regarding specific claims of exposure to various
chemicals. He is experienced using toxicological causation analysis to characterize the potential
for specific health effects to correspond to particular exposure scenarios and providing related
opinions.
Dr. DeMotts experience includes preparing and directing human health and ecological risk
assessments and identifying site-relevant cleanup goals for human and ecological receptors. He
uses these tools in presenting effective risk management strategies for workplace, residential and
other settings.
Dr. DeMott has worked extensively on soil arsenic target levels and incorporating bioavailability
factors as chairman of the Florida Contaminated Soils Forum. Under Dr. DeMotts leadership,
this 50-member stakeholder group chartered to review new scientific findings and recommend
revisions to target cleanup levels also recommended new exposure factors incorporated for the
calculation of risk-based target levels.
Toxicology and Chemical Risk Evaluation Experience

Exposure Analysis and Evaluation
Evaluated claims of environmental exposure. Developed exposure analyses, evaluated potential
toxic effects and rendered expert opinions. Experienced with toxicity issues relating to volatile
and particulate indoor air irritants, solvents, metals, pesticides, asphyxiants and acid gases.
Experienced evaluating acute responses and reproductive, developmental, respiratory,
immunological and neurological endpoints for chronic toxicity. Specific cases included:
Chemicals/Agents
2
PCBs / Dioxins Acid Gases, Chlorine, Phosgene

Carbon Monoxide Pesticides, Herbicides
Ethanol Indoor Air Allergens
Benzene, Xylene, Styrene Paints/Solvents
Arsenic PCE/TCE/Vinyl Chloride
Boron Lead
Radionuclides Silicone Implants
Particulates (PM10/2.5) Ethylene Oxide
Sulfur & Nitrogen Oxides Diisocyanates
Facilities/Settings
Residential Vehicles, rail yards
Golf courses Pesticide plants
Phosphate processing plants Paint manufacturing plants
Superfund waste sites Incinerators
Rubber manufacturing Power generating plants
Chemical Risk Related Property Impacts

Provided consulting support and expert opinions on regulatory and toxicological implications of
emissions and offsite migration and associated health concerns, property damage or cleanup cost
recovery issues. Cases included the following issues:
Concerns over health threats Remedies for indoor air issues

Importation of soil materials Hormonal activity of discharges
Utility worker exposure Regulatory liabilities
Property value damages Remedial cost recovery
Superfund waste sites Superfund listing
Dioxin Profiling -- Wingate Road Landfill Superfund Site, Ft. Lauderdale, FL

Evaluated soil dioxin results obtained from neighborhood surrounding site and developed dioxin
congener profile analysis to distinguish incinerator ash from typical urban sources and diesel
emissions. Provided risk-based analysis of potential site contributions versus ambient urban
exposures.
Analysis of Potential Health Risks for Proposed Power Plant

Assessed human health risks based on ISCST3 dispersion modeling for proposed gas turbine
peaking power plant in Libertyville, Illinois. Reevaluated manufacturer emissions estimates and
compared to risk-based concentrations for volatile HAPs, dioxins and metals. Addressed city
issues regarding human health and ecological issues using EPA guidance for combustor facilities.
Analysis of Risk Implications for Kalamazoo River Angler Study

Reanalyzed source data and documented statistical inconsistencies in body burdens of PCBs,
DDE, and mercury found in anglers consuming Kalamazoo River fish. Submitted comments for
3
PRP group documenting that body burdens for fish-eaters and non-fish-eaters were not different
than regional background and consumption from river was not significant to overall exposure.
Analysis of Endocrine Disruption Concerns from Livestock Operations

Analyzed and prepared review of current scientific advances in the area of endocrine disruption
for livestock trade association. Presented information on surveys of hormonally active
compounds in water bodies and new publications linking poultry, beef, and hog operations to
endocrine disruption.
Exposures in Waste Disposal Facility Fire, Memphis, Tennessee

Assessed potential for combinations of fire suppressant materials, fire retardant materials, waste
solvents and contaminated soils to produce hepatitis reported by workers present during facility
fire. Characterized lack of acute liver toxicants among relevant chemical interactions.
Review of State Monitoring Study of Estrogens in Streams

Critiqued approach, analytical methods, and toxicity testing of monitoring study directed by
Missouri Department of Natural Resources for estrogenic compounds near a pork producers
facilities. Characterized limitations of study for distinguishing active from inactive hormonal
forms. Developed study design for evaluating regional sources and inputs.
Risk-Based Criteria for Chlorinated and Arsenical Pesticides at Golf Courses

Developed exposure scenarios and corresponding risk-based soil and sediment target
concentrations for recreational and maintenance areas impacted by chlorinated pesticides on the
Robbins Air Force Base golf course. For several private golf courses in Florida, developed site-
relevant cleanup targets for arsenical pesticides and characterized remedial alternatives.
Alternative Cleanup Strategy Development Former Nursery, Osprey, Florida

Obtained state agency concurrence on suitable uses for soils with naturally elevated arsenic
levels. Developed strategy for localizing site-impacted arsenic-containing soils and focusing
remedial actions in specific areas. Negotiated soil reuse strategy for manufacture of soil cement.
Three-Tier Analysis of Potential Arsenic Risks at Indiana Childrens Camp

Analyzed elevated background levels of arsenic and impacts related to prior uses at a site under
development as a camp for children with health problems. Characterized derivation and
applicability of federal and state screening levels, provided quantitative estimation of risks for
campers and staff and comprehensive profile on arsenic toxicology and exposure.
Bioavailability of Arsenic at Pesticide-Impacted Sites

Prepared report for the Florida Department of Environmental Protection on the transport and
bioavailability of arsenic at former livestock dip sites. Evaluated mobility of dip vat sediments,
transformation reactions, and sequestration of arsenic in backfilled dip sites. Characterized
toxicology and exposure differences between varying forms of arsenic and changes over time.
Evaluation of Roadway Drainage Related PAHs Barton Creek, Austin TX

Evaluated City of Austin reports on parking lot related samples and environmental impacts on
urban creek watershed. Characterized routine urban nature of roadway drainage and lack of
4
public health threat to recreational swimmers. Provided technical comments regarding citys
consideration of ban on pavement sealers for controlling PAHs in waterways.
Analysis of Plant Uptake Models for Residential Gardens Runcorn, UK

Reviewed exposure estimation for hexachlorobutadiene (HCBD) based on PLANTX plant uptake
and SNAPS soil-water transport models for consistency with Contaminated Land Exposure
Assessment (CLEA) framework of UK SNIFFER guidance. Compared exposure among various
garden crops using fugacity models. Provided comments on guidance specifying models.
Development of Risk-Based Target Levels for Iron, Manganese, Sulfate

Developed cleanup target levels based on primary toxicology literature for several metals with
esthetic-based, secondary MCLs. Successfully negotiated substitution of risk-based values and
application of Florida RBCA approach for metalworking site in Jacksonville, FL. Applied risk-
based sulfate value at Georgia HSRA site.
Analysis of Sulfate Risks to Infants and Transient Adults

Reviewed proposed EPA standard and primary literature related to sulfate in drinking water.
Provided critique of the available laboratory and epidemiology studies. Provided comparisons
between proposed regulatory limits and documented no-adverse-effects levels for diarrhea in
infants and non-acclimated adults.
Human Health and Ecological Risk Assessment Experience
Risk Assessment Strategy for Hazardous Waste Incinerator Permitting

Prepared report on human health and ecological risk assessment issues relevant to permitting a
hazardous waste incinerator and presented to state legislators and regulatory officials. Principal
chemicals assessed included dioxins, mercury, PAHs, and chromium. Developed strategy for
incorporating reproductive risk concerns.
Site/Facility Risk Assessments

Managed risk assessment projects, completed risk assessments and developed risk-based cleanup
target levels for regulatory submission and strategic evaluations. Worked under CERCLA,
RCRA and RBCA guidance for submissions to EPA and state agencies. Representative projects
include:
Lockheed Tallevast Site, Sarasota, Florida Directed probabilistic human health risk
assessment and evaluated potential health effects for community surrounding chlorinated solvent
and 1,4-dioxane groundwater plume from metal working facility. Designed soil gas and indoor air
risk analysis strategies.
Hardeman County Landfill Superfund Site, Toone, Tennessee Directed human health and
ecological risk assessments completed for 5-year review of CERCLA remedy at pesticide
manufacturing waste landfill. Evaluated potential risks to residents, anglers, hunters, game, fish,
livestock and sediment communities. Designed fish sampling and indoor air sampling strategies.
Characterized remedy failures via risk increases and developed trigger levels to implement indoor
air mitigation for carbon tetrachloride and chloroform.
5
Univ. of Miami, South Campus, Miami, Florida Designed and conducted first radionuclide
background study accepted under the Florida Global RBCA program (62-780, F.A.C.).
Demonstrated that radionuclide levels in soil on campus property matched expected background
levels for corresponding area of Miami-Dade County.
Raytheon St. Petersburg Facility, Florida Directed human health risk assessment for
residential and recreational areas surrounding electronic equipment assembly plant with
groundwater impacts from chlorinated solvents, 1,4-dioxane and BTEX compounds. Developed
site-specific exposure model to address volatilization from irrigation and vapor intrusion into
single-story and multi-story residences.
Savannah River Site, Aiken, South Carolina Developed area-specific multi-level
screening/risk assessment process and used to achieve closure without further action on site
where South Carolina regulatory agency rejected previous risk assessment. Managed assessments
for dioxins at burn pits and disposal sites and chemical and radionuclide risks at additional sites.
Fike Chemical Superfund Site, Nitro, West Virginia Managed human health and ecological
risk assessments for site involving dioxins, arsenic, chlorinated solvents, petroleum products, and
chlorinated pesticides/herbicides (DDT, aldrin, dieldrin).
Eglin Air Force Base, Florida Submitted human health risk assessments and achieved site
closure for sites involving petroleum impacts alongside a runway and BTEX compounds and
PCB/dioxin impacts in a lake using RBCA-type approach.
Gas Pipeline Compressor Station, Bay St. Louis, Mississippi Directed ecological risk
assessment (USEPA Step 4-8 process) and biota/sediment sampling study in creek and bayou
system impacted by PCBs. Addressed state agency and Natural Resource Damage trustee
requests and inconsistencies with USEPA direction on the site. Directed earthworm
bioaccumulation study and shrimp toxicity testing.
LCP Chemicals Superfund Site, Brunswick, Georgia Directed ecological risk assessment for
terrestrial uplands to demonstrate post-remedial risk reduction at mercury and PCB-impacted site.
Negotiated approach and sampling plan for extending estuarine risk assessment to comprehensive
analysis of biota (Step 4-8 USEPA process).
GE Power Delivery Systems, Rome, Georgia Developed expedited human health and
ecological risk assessment approaches and methodology consistent with Georgia RCRA guidance
for calculating remedial target levels accounting for multi-pathway risks from PCBs.
Moundsville Superfund Site, Moundsville, Ohio Developed risk-based alternative cleanup
levels for PAHs, mercury, and PCBs and prepared risk-benefit analysis during the EE/CA to
identify accelerated removal options minimizing the likelihood of subsequent removals.
Kennedy Space Center and Cape Canaveral Air Station, Florida Managed human health
and ecological risk assessments for sites involving chlorinated solvents, petroleum products, and
pesticides/herbicides. Prepared standard risk assessment procedures manual adopted by NASA
for all contractors. Developed ecological risk-based screening levels for chlorinated pesticides
(DDTs, chlordane, heptachlor, aldrin/dieldrin), metals, PAHs, and PCBs. Directed study of PAH
background levels in roadway drainage ditches.
Honeywell Facility Redevelopment, Brighton, Massachusetts Directed Method 3 Risk
Assessment for site with differential exposure pathways/plume profiles on different levels
(basement and slab-on-grade) and multiple solvent and metal constituents. Assessed soil, water
and indoor air.
6
Former Transformer Maintenance Facility, West Lynn, Massachusetts Developed risk-

based air concentrations for chlorinated solvents in basement of facility. Applied site-specific
values for risk assessment and substantial hazard evaluation.
Gillette Manufacturing Facility, Boston, Massachusetts Evaluated potential risks for tunnel
construction workers associated with chlorinated solvent plume intersecting the Central Artery
tunnel component of Bostons Big Dig transportation upgrades. Developed model to predict
potential flux, concentrations and potential risks at the tunnel excavation face.
Cypress Creek/Vollentine-Evergreen Neighborhood, Memphis, Tennessee Directed human
health risk assessment for area downstream from chlorinated pesticide plant. Developed receptor
scenarios and risk estimates for various areas and uses of creek. Key chemicals included
aldrin/dieldin, endrin, chlordane, DDTs. Developed risk communication approaches addressing
environmental justice concerns and presented findings to community and agencies.
North Fork Holsten River, Saltville, Virginia Directed ecological risk assessment approach
for evaluating over 100 miles of river system downstream from mercury-impacted Superfund site.
Developed strategy for addressing Natural Resource Damage Assessment activities and
negotiating scope of supplemental assessment requested by trustees.
Duda Farms Ecological Risk Assessment, Orange County, Florida Developed approach and
completed ecological risk assessment for proposed flooding of agricultural land for wetlands
restoration. Developed toxicity values and derived and validated site-specific sediment-to-biota
transfer factors for toxaphene and DDT. Reviewed acute toxicity for various chlorinated pesticides
and analyzed environmental and tissue residue results. Evaluated analytical criteria and
toxicological relevance of detection limits for toxaphene analyses.
Robbins Air Force Base, Warner Robbins, Georgia Directed human health and ecological
risk assessments for RCRA Facility Investigation at disposal area used for pasture and stables.
Developed cleanup levels for lead slag waste materials based on potential toxicity to horses.
Developed risk-based target levels for chlorinated and current-use pesticides at maintenance area
and adjacent base golf course.
Hitachi Magnetics Site, Michigan Reviewed proposed alternate cleanup levels for different
forms/valence states of mercury in sediments. Determined that toxicology and risk-related
differences to both human and ecological receptors supported form-specific cleanup levels.
Cascade Park Manufactured Gas Plant Site, Tallahassee, Florida Developed site-specific
approach for addressing USEPA Region IV multi-step ecological risk assessment process.
Managed ecological risk assessment for this urban park site impacted by coal tar and combustion
product residues, evaluating receptors in a creek/drainage system and intermittent wetland area.
United Technologies Corp./Pratt & Whitney, West Palm Beach, Florida Prepared RCRA
Corrective Measures Study for risk-based cleanup of PCBs in sediment. Evaluated mercury levels
in pond sediments and compared to South Florida and Everglades background levels. Developed
risk-based justification for natural attenuation strategy at engine test stands and SWMUs adjacent to
runways.
Marine Corps Air Station El Toro, Orange County California Reviewed base risk
assessments for facilities being turned over to the county and represented Orange County in
negotiating land use restrictions consistent with the remedy selected for particular areas.
Developed risk-based target concentrations for site-relevant receptor scenarios.
Santa Barbara Metropolitan Transportation District Depot, Santa Barbara, California
Completed human health risk assessment based on site-specific receptor scenarios for electric bus
7
charging depot at former manufactured gas plant site. Established cleanup target levels for PAHs,
BTEX and provided risk-benefit analysis for removal and capping options proposed.
PCB Manufacturing Facility, Anniston, Alabama Reviewed onsite worker risks from PCBs
and developed ecological risk assessment approach for evaluating Snow Creek-Choccoloco
Creek-Lake Logan Martin system. Identified exposure estimates for stream and floodplain
sediments and characterized habitat zones for ecological and human angler exposures.
Peak Oil/Bay Drums Site, Tampa, Florida Developed and recommended alternative cleanup
levels based on site-specific risk considerations at this Superfund site. Approval of alternative
value proposed for lead reduced areal extent requiring active remediation.
Sikorsky Manufacturing Facility Site on Housatonic River, Stratford, Connecticut
Developed ecological risk screening protocol for aquatic and estuarine receptors relating to solvents
and metals acceptable to USEPA Region 1 and delineated areas of concern for primary focus under
RCRA cleanup.
Rhone-Poulenc Phosphate Processing Site, Mt. Pleasant, Tennessee Completed human health
risk assessment demonstrating efficacy of proposed containment strategy for precluding risks from
waste pile and settling pond.
Methodology Revisions/Updates for Florida Soil Cleanup Approaches

Chairman of Florida Contaminated Soils Forum
This 50-member stakeholder group makes presentations and recommendations to Florida
Department of Environmental Protection regarding updates to policy, science, and applications
issues pertaining to soil cleanup. Activities include reviews of inputs used to develop default soil
cleanup targets and recommendations for revisions.
Radon Risk Assessment Methods Review

Prepared report for National Association of Home Builders and U.S. Department of Housing and
Urban Development on risk assessment methodology used in developing indoor radon standards
and the implications of new studies regarding the protectiveness of existing standards.
Development of Multi-Tier Risk Assessment Protocol for U.S. Air Force

Designed RBCA-type multi-tier approach including probabilistic risk elements specifically for
the needs of U.S. Air Force Environmental Services Branch. Completed protocol and technical
directive for carrying out screening level assessments. Initiated pilot program at Cape Canaveral
and demonstrated risk reduction achieved through prioritizing exposure sub-areas.
Preparation of Risk Impact Statements for Florida Brownfields Cleanup Criteria

and Petroleum Contamination Site Cleanup Criteria
Prepared reports on potential risk associated with implementation of Florida Brownfields
Program (62-785, F.A.C.) and revisions to Petroleum Contamination, Site Cleanup (62-770,
F.A.C.). Analyzed human health risks associated with brownfields and petroleum-related sites
and how risks would change implementing Florida's RBCA initiative.
Review of Superfund Scoring Packages

Reviewed consistency of Superfund scoring with guidance requirements for uranium rod
processing facility and metal ore processing/smelting facility. Completed shadow scoring
8
using PRESCREEN to determine most significant factors and potential alternative scores.
Documented outdated toxicity values used in one scoring package and use of an incorrect
exposure pathway in another scoring package.
Review of Assessment Strategies/Costs for Liability Transfer

Reviewed ecological risk assessments, feasibility studies, Natural Resource Damage mitigation
plans and remedial cost estimates for risk reduction for riverine/estuarine sites in Wisconsin and
Michigan on behalf of institution proposing to assume site liabilities. Advised client on
uncertainties in regulatory status and potential third-party toxic exposure claims.
Environmental Toxicology Experience

Development of Ecological Toxicity Reference Values for NASA Kennedy
Space Center
Analyzed primary and regulatory literature and determined toxicity testing values to be used in
ecological risk screening approach for aquatic and terrestrial species KSC. Derived toxicity
values optimized for KSC fish, bird and mammal species for over 100 chemicals and presented to
contractor/regulator/NASA team for adoption in all KSC RCRA assessments.
Direction of Ecological Toxicity Management for Phosphate Processing

Facility Discharge, Hillsborough County, FL
Designed and directed toxicity testing program required in conjunction with ordered water
releases from holding ponds. Directed pre-discharge biological reconnaissance of Alafia River
tributary. Developed anticipated toxicity thresholds for process-related metals, pH, and
conductivity. Provided what-if analyses in conjunction with evaluation of treatment options
and implementation of emergency contingencies during storm events.
Evaluation of Aquatic Impacts from Process Water Release to Polk County, FL

Lake
Provided expert support regarding the extent of impacts and approaches for re-stocking associated
with an acid water discharge during a major storm event that reached a nearby lake. The spatial
characteristics pertaining to where toxic levels could have occurred and the duration of a fish kill
were determined and alternative strategies for restocking were prioritized based on time to return
to baseline and cost.
Development of Terrestrial Toxicity Screening Values for Idaho National

Engineering Laboratory
Analyzed primary literature and selected toxicity testing values used in ecological risk screening
approach for INEL. Identified and derived toxicity values specifically pertaining to soil contact
for terrestrial mammals and birds for 212 chemicals without previous regulatory values.
Development of Toxicity Screening Values for DDT & Toxaphene in Wetlands

Ecosystem
Analyzed primary literature and industry toxicology testing results and derived toxicity values
specifically relevant to benthic invertebrates, fish and piscivorous birds exposed to chlorinated
pesticides in a managed wetland. For DDT and toxaphene, developed locally relevant
representations of bioaccumulation and bioavailability from sediment using field data.
9
Mercury and PCB Sediment Bioavailability via Food Chain Exposures

Provided toxicological analysis of mercury and PCB uptake through local food chains in Georgia
estuary using measured, site-specific bioavailability factors and current modeling approaches.
Compared measured to modeled results documenting optimal risk estimation approach.
Tampa Bay National Estuaries Program, Tampa, Florida

Derived toxicity values for chlorinated pesticides and metals relevant to estuarine receptors and
site-specific food web. Developed ecological risk assessment approach for bay sediments and
local receptor species used to support sediment quality triad approach and leading to prioritization
of chemicals (PAHs, pesticides, copper, mercury) for particular drainage basins.
Research Experience
Postdoctoral Fellowship Research:
Effects of adrenergic stimulation on the developmental and hepatotoxicity of various
environmental contaminants and pharmacological agents.
Doctoral Research:
Examined sperm cell biology in the female reproductive tract and chemical interactions/signaling
relating to sperm cell binding. Characterized sperm motility pattern changes in the mammalian
oviduct and cell surface changes.
Professional Activities
American Board of Toxicology
Society of Toxicology
Society for Risk Analysis
Society for Environmental Toxicology and Chemistry
Professional Honors/Awards
Graduate Research Merit Award, American Society of Andrology
Publications
Freeman, G.B., DeMott, R.P., Gauthier, T., Stevenson, M., and J. Hubbard. 2011. Continued
Corrosion After Removal of Corrosive Drywall. Journal of Failure Analysis and Prevention
11:265273.
DeMott, R.P., Gauthier, T.D., Wiersema, J.M., and G. Crenson. 2010. Polycyclic Aromatic
Hydrocarbons (PAHs) in Austin Sediments After a Ban on Pavement Sealers. Environmental
Forensics 11: 372-382.
10
DeMott, R.P. and T.D. Gauthier. 2006. Comment on Parking Lot Sealcoat: An Unrecognized
Source of Urban Polycyclic Aromatic Hydrocarbons. Environmental Science & Technology 40:
3657-3658.
DeMott, R.P., Balaraman, A. and M.T. Sorensen. 2004. The Future Direction of Ecological Risk
Assessment in the United States: Reflecting on U.S. EPAs Examination of Risk Assessment
Practices and Principles. Integrated Environmental Assessment and Management 1: 77-82.
Margolin, J. and R.P. DeMott. 2004. Emerging Issues in Human and Ecological Health. State
Bar of Georgia Environmental Law Section. Summer 2004, p. 5.
DeMott, R.P. and J.C. Alonso. 2002. The role of the environmental consultant in risk assessment
and risk-based corrective actions. In: Florida Environmental and Land Use Law. DeMeo, R.A.,
Lotspeich, R. and T. Zinn (eds.), pp. 3.2-1--3.2-4. REGfiles, Inc., Tallahassee, FL.
DeMott, R.P. and C.J. Borgert. 2000. Reproductive and Developmental Toxicology. In:
Principles of Toxicology: Environmental and Industrial Applications, 2nd ed. Williams, P.L.,
James, R.C. and S.M. Roberts (eds.). John Wiley & Sons, New York.
Budinsky, R.A., R.P. DeMott, M.W. Wernke, and J.D. Schell. 1999. An evaluation of modeled
benzene exposure and dose estimates published in the Chinese-National Cancer Institute
collaborative epidemiology studies. Regulatory Toxicology and Pharmacology 30:244-258.
DeMott, R.P. 1998. Ecological Risk Assessment Issues for Hazardous Waste Incineration. In:
Hazardous Waste Incineration: Evaluating the Human Heath and Environmental Risks. Roberts,
S.M., CM. Teaf, and J.A. Bean (eds.). CRC Press, Boca Raton, FL.
Harbison, R.D. and R.P. DeMott. 1997. Cocaine Hepatotoxicity. In: Comprehensive Toxicology.
Sipes, I.G, C.A. McQueen, and A.J. Gandolfi (eds.). Elsevier SciencesPergamon Press, New
York.
Roberts, S.M., R.P. DeMott, and R.C. James. 1997. Adrenergic modulation of hepatotoxicity.
Drug Metabolism Reviews 29:329-353.
ATRA, Inc. 1997. Environmental risk assessment at a Lake Apopka Muck Farm Wetlands
Restoration. Special Publication SJ98-SP7St. Johns River Water Management District, Palatka,
FL.
McConnell, R.G., R.P. DeMott, and J.A. Schulten. 1996. Toxic contamination sources
assessmentrisk assessment for chemicals of potential concern and methods for identification of
specific sources. Tampa Bay National Estuary Program Technical Publication #09-96. Tampa
Bay National Estuary Program, St. Petersburg, FL (peer reviewed agency publication).
DeMott, R.P., R. Lefebvre, and S.S. Suarez. 1995. Carbohydrates mediate the adherence of
hamster sperm to the oviductal epithelium. Biology of Reproduction 52:1395-1403.
Lefebvre, R., R.P. DeMott, S.S. Suarez, and J.C. Samper. 1995. Specific inhibition of equine
sperm binding to oviductal epithelium. Biology of Reproduction Monographs 1:689-696.
11
DeMott, R.P. and S.M. Roberts. 1994. A review of available methodologies for
evaluating the potential human, health and environmental impacts of a hazardous, waste
incinerator. A Report to the Florida Department of Environmental Protection. The
Florida Center for Solid and Hazardous Waste Management, Gainesville, FL; pp 1-143.
DeMott, R.P. 1993. Factors affecting sperm transport in the mammalian oviduct. Ph.D.
Dissertation, University of Florida, Gainesville, FL.
DeMott, R.P. and S.S. Suarez. 1992. Hyperactivated sperm progress in the mouse oviduct.
Biology of Reproduction 46:779-785.
Suarez, S.S., X.B. Dai, R.P. DeMott, K. Redfern, and M.A. Mirando. 1992. Movement
characteristics of boar sperm obtained from the oviduct or hyperactivated in vitro. Journal of
Andrology 13:75-80.
Suarez, S.S. and R.P. DeMott. 1991. Functions of hyperactivated motility of sperm in the
oviduct. Archivos de Biologia y Medicina Experimentales 24:331-337.
DeMott, R.P. 1987. The adaptive significance of swimming and feeding morphology in anuran
larvae. B.A. Thesis, Williams College, Williamstown, MA.
Abstracts
DeMott, R.P. and Gauthier, T.D. 2010. A new risk characterization metric to present potential
change compared to background for human health risk assessment. Society for Environmental
Toxicology and Chemistry, November 2010.
Torres, C.W., Sower, G.J., DeMott, R.P. and Thompson, G.P. 2010. Simulation and exposure
estimation from products containing polymeric flame retardant. Society for Environmental
DeMott, R.P., Gauthier, T.D., Alessandroni, M.A., and Poole, J.L. 2010. Abiotic production of
sulfide gases from elemental sulfur in gypsum wallboard from certain Chinese sources. Abstract
10-SR-981-AIHA. American Industrial Hygiene Conference and Exposition, May 2010.
Krause, D. and DeMott, R.P. 2010. Causes of transient sensory irritation reported by occupants in
homes with imported corrosive drywall. American Industrial Hygiene Conference and
Exposition, May 2010.
Poole, J.L., Gauthier, T.D., DeMott, R.P. and Shinn N. 2010. Occupational exposure evaluations
in conjunction with repair of homes containing Chinese wallboard. American Industrial Hygiene
Conference and Exposition, May 2010.
DeMott, R.P., Alessandroni, M.A., Hayes, H., Freeman, G. and Gauthier, T.D. 2009. Elemental
sulfur and trace metal content in Chinese and domestic brands of gypsum wallboard. U.S. EPA
and Florida Dept. of Health Technical Symposium on Corrosive Imported Drywall, November
2009.
Freeman, G.B., Gauthier, T.D. and DeMott, R.P. 2009. Chinese wallboard: the corrosion
challenges. U.S. EPA and Florida Dept. of Health Technical Symposium on Corrosive Imported
Drywall, November 2009.
12
Lebeau, A.L., Gauthier, T.D., Poole, J.L. and DeMott, R.P. 2009. Determination of reduced sulfur
gases in construction materials. U.S. EPA and Florida Dept. of Health Technical Symposium on
Corrosive Imported Drywall, November 2009.
Gauthier, T.D. and DeMott, R.P. 2008. Analysis of PAH concentrations detected in Austin, Texas
stream sediments following a ban on the use of coal tar sealers. Society for Environmental
Williams, H.I., Tufariello, E., Santamaria, A.B. and DeMott, R.P., 2008. An in utero human health
risk assessment approach for pharmaceuticals discharged with wastewater. Society for
Environmental Toxicology and Chemistry, November 2008.
DeMott, R.P., Begemann, P., Williams, H.I. and Santamaria, A.B. 2007. Environmental risk
assessment for pharmaceuticals: establishing a methodology to evaluate population-derived
pollutants. 2007 Northeast Water Science Forum, August 2007.
DeMott, R.P., Williams, H.I., Begemann, P. and Santamaria, A.B. 2007. Use of pharmaceutical
testing data to derive receptor activity equivalence factors for application in aquatic toxicity
characterization. Abstract 3861-1252, International Congress of Toxicology, July 2007.
DeMott, R.P., Williams, H.I. and Santamaria, A.B. 2006. Population Pollution: Establishing a
framework for characterizing surface water risks from pharmaceuticals and population-derived
constituents. Abstract T2-G1, Society for Risk Analysis, December 2006.
DeMott, R.P., Gauthier, T.D., Wiersema, J.M. and Crenson, G. 2006. Characterization of urban
PAH distributions in sediments from Austin, Texas. Abstract 567, Society for Environmental
DeMott, R.P. and Crenson, G. 2006. Using environmental assessment tools to evaluate a product-
based sediment management strategy for urban PAHs. Abstract 511, Society for Environmental
Gauthier, T.D., DeMott, R.P. and Crenson, G. 2006. Evaluation of polycyclic aromatic
hydrocarbon sources in Austin, Texas stream sediments. Abstract P743, Society for
DeMott, R.P. 2003. In vivo arsenic bioavailability results used for refinement of risk-based soil
cleanup target levels in Florida. Abstract No. T18.4, Society for Risk Analysis, December 2003.
DeMott, R.P., Duffy, J.S., Edwards, M., Mann, P. and Sauvage, R.X. 2003. Multiple reproductive
endpoint testing with grass shrimp refines ecological risk characterization for PCBs in estuarine
sediment. Abstract No. PH1072, Society of Environmental Toxicology and Chemistry, November
2003.
Mackay, C.E., DeMott, R.P., Habig, C., Gard, N.W. and Pastorok, R.A. 2003. Integrating
temporal changes in receptor sensitivity in the development of TMDLs for non-persistent
chemicals. Abstract No. 187, Society of Environmental Toxicology and Chemistry, November
2003.
Saranko, C.J., E.M. Tufariello, E.K. Block, K.H. Kertesz, J. Duffy, R.P. DeMott, M. Kershner,
and H. Williams. 2001. Compilation of toxicity data and exposure factors for southeastern
mammalian and avian wildlife. Abstract No. 1092, Society for Toxicology, March 2001.
13
Caesar, K.G., C.J. Saranko, H. Williams, T.A. Peel, and R.P. DeMott. 2000. Adaptation of
preliminary risk evaluation (PRE) approach to accelerate soil risk assessments. Abstract No. P1.11,
Society for Risk Analysis, December 2000.
DeMott, R.P., K.H. Kertesz, R.G. McConnell, T.A. Peel, and H. Williams. 2000. Supplemental
ecological risk screening improves 8-step process for multi-site facility. Abstract No. 361, Society
for Environmental Toxicology and Chemistry, November 2000.
Wernke, M.J., J.D. Schell, R.A. Budinsky, R.P. DeMott, and H.D. Jones. 1999. A human health
and ecological assessment of volatile components of PM10 emissions. Abstract No. 1861,
Toxicological Sciences, 48:Supp. 1.
DeMott, R.P., H.D. Jones, and J.D. Schell. 1998. Prospective ecological risk assessment for
risk/benefit and risk management evaluation of proposed wetlands restoration. Society for
DeMott, R.P. 1997. Paradoxical conservatism in risk assessment assumptions related to lower
surrogate values for analytical data. Abstract 840, Fundamental and Applied Toxicology (Supp.),
38(1).
Schulten, J.A., R.G. McConnell, and R.P. DeMott. 1996. Development of a risk-based approach
for management of an estuarine watershed. Society for Environmental Toxicology and
Chemistry, November 1996.
DeMott, R.P. and S.E. Noren. 1996. Utilizing site-specific risk-based remediation goals to
improve the defensibility and efficiency of remedial actions. In: 11th Annual Conference on
Contaminated Soils, University of Massachusetts at Amherst.
McConnell, R.G., R.P. DeMott, and J.A. Schulten. 1996. Application of a risk-based approach for
guiding management of an estuarine resource, Florida Water Resources Conference.
DeMott, R.P., J.A. Schulten, R.D. Harbison, and S.E. Noren. 1996. Prioritization scheme for
evaluating risk assessment issues. Abstract 13, Fundamental and Applied Toxicology (suppl.)
30(1).
Harbison, R.D., J. Gill, S.M. Roberts, and R.P. DeMott. 1996. Reevaluation of adrenoreceptor
mediated hepatoprotection from bromobenzene, Abstract 1486, Fundamental and Applied
Toxicology (suppl.), 30(1):
DeMott, R.P., R.C. James, R.A. Westhouse, S.M. Roberts, and R.D. Harbison. 1995.
Nephrotoxicity of 2-bromohydroquinone can be reduced by the adrenergic antagonist
phentolamine. Abstract 1605, The Toxicologist, 15.
DeMott, R.P., R.C. James, S.M. Roberts, and R.D. Harbison. 1994. Antagonism of
bromobenzene-induced hepatotoxcity following delayed administration of phentolamine.
Abstract 699, The Toxicologist, 14.
DeMott, R.P. and S.S. Suarez. 1993. Fetuin labeling of hamster sperm is related to binding in
the oviduct. Abstract 1441, Molecular Biology of the Cell 4 (supplement).
Lefebvre, R., R.P. DeMott, J.C. Samper, and S.S. Suarez. 1993. Specific inhibition of equine
sperm binding to oviductal epithelium. Abstract H68, American Society for Cell Biology.
DeMott, R.P., R. Lefebvre, J.C. Samper, and S.S. Suarez. 1993. Specific inhibition of hamster
sperm binding to oviductal epithelium. Abstract 90, Journal of Andrology (supplement).
14
DeMott, R.P. and S.S. Suarez. 1992. Production of monoclonal antibodies to stage-specific
hamster sperm surface antigens. Abstract 50, Molecular Biology of the Cell 3 (supplement).
DeMott, R.P. and S.S. Suarez. 1992. Oviductal mucus appears to be in the path of mouse sperm
during transport. Abstract 111, Biology of Reproduction 46 (supplement 1).
DeMott, R.P. and S.S. Suarez. 1991. Evidence for an advantage of hyperactivated mouse sperm
in remaining free the oviductal wall. Abstract 258, Biology of Reproduction 44 (supplement 1).
DeMott, R.P. and S.S. Suarez. 1990. The progress of hyperactivated sperm in the mouse oviduct
is intermittent. Abstract 2035, Journal of Cell Biology 111, 5:Part 2.
Invited Seminars and Presentations

DeMott, R.P. Sulfide Gas: Sources and Exposures. American Bar Association Tort Trial &
Insurance Practice Section Spring CLE Meeting, Amelia Island, FL, May 20, 2011.
DeMott, R.P. Human Responses to Sulfide Gases and Irritants: easy concepts, complex details.
U.S. EPA and Florida Dept. of Health Technical Symposium on Corrosive Imported Drywall,
Tampa, Florida, November 2009.
DeMott, R.P. Corrosive Imported Wallboard: investigating emissions. U.S. EPA and Florida
Dept. of Health Technical Symposium on Corrosive Imported Drywall, Tampa, Florida,
November 2009.
DeMott, R.P. Endocrine Disruption: Emerging Pressures and Liabilities. Environmental Law
Summer Seminar, Institute for Continuing Legal Education in Georgia, August 5, 2005.
DeMott, R.P. and Rodricks, J. Pharmaceuticals and Consumer Products in the Environment: New
Challenges in Risk Assessment and Management. 33rd Annual Conference on Environmental
Law, Keystone, Colorado, March 11, 2004.
DeMott, R.P. Global RBCA Realizations upon grasping the ring. Florida Remediation
Conference, Orlando, FL, November, 2003.
DeMott, R.P. Critical Toxicology Concepts for Environmental Concerns --
Current Topics Arsenic and Mold. Hillsborough County Bar Association, April, 2003.
DeMott, R.P. Methodology updates for Florida soil cleanup target levels. Recurrent report for
public meetings as chairman of Methodology Focus Group and Florida Contaminated Soils Forum,
1997-2003.
Cline, P.V. and DeMott, R.P. Vitellogenin gene expression and protein production: Potential
predictors of exposures to xenoestrogens, adverse reproductive effects in fish. 18th Annual
International Conference on Contaminated Soils, Sediments, and Water, University of
Massachusetts at Amherst, October, 2002.
Paustenbach, D.J., DeMott, R.P. and Madl, A.K. Recent improvements in the practice of risk
assessment as illustrated through case studies. 18th Annual International Conference on
Contaminated Soils, Sediments, and Water, University of Massachusetts at Amherst, October,
2002.
DeMott, R.P. Emerging Trends in Ecological Risk Assessment for Product Registration.
Syngenta Crop Protection Conference, May, 2002.
15
DeMott, R.P. The arsenic playing field major moves affecting cleanup goals and decisions.
Florida Brownfields 2001 Conference, November, 2001.
DeMott, R.P. DEP regulatory and policy update. Florida Chamber of Commerce, Environmental
Permitting Summer School, July, 20002001.
DeMott, R.P. Florida approaches to brownfields. Panelist for American Bar Association, Region
IV SONREEL Conference, Brownfields Break-Out Session, November, 1998.
DeMott, R.P. Risk-based decision making: its not just for humans anymore. Florida Bar
Environmental and Land Use SectionEvolution or Revolution in Florida Cleanup, January, 1998.
DeMott, R.P. Uncertainty and variability in risk assessment. Florida Association of Environmental
Assessors, September, 1997.
DeMott, R.P. Dealing with uncertainty in dose reconstruction for risk assessment. American
College of Occupational and Environmental Medicine Annual Meeting, May, 1997.
DeMott, R.P. Incorporating contemporary technical approaches into risk-based decision making.
AlliedSignal, Inc, Technical Training Workshops, 1996.
DeMott, R.P. Risk analysis in the environmental decision-making of the '90s. Hillsborough County
Bar Association Environmental Section, 1996.
DeMott, R.P. Application of risk assessment within the remediation process. The Princeton
Remediation Course, 1996.
DeMott, R.P. Improving dose extrapolation through basic research. Risk Assessment Symposium,
ecology and environment, 1995.
DeMott, R.P. Adrenergic modulation of halogenated hydrocarbon toxicity. Texaco, Environmental
Health and Safety Division, 1995.
DeMott, R.P. Functional significance of sperm/oviductal binding: considerations for male
reproductive toxicology. U.S. EPA - Health Effects Research Laboratory, 1993.
1
Thomas D. Gauthier, Ph.D.
Education
1986 Ph.D., Analytical Chemistry, University of New Hampshire
1982 B.S., Chemistry, Merrimack College
Registrations & Affiliations

Member, American Chemical Society
Experience
Dr. Thomas Gauthier is a senior environmental chemist with more than 25 years of experience in
analytical and environmental chemistry focusing on the transport and fate of chemicals in the
environment, historical dose reconstruction, source identification and the statistical analysis of
environmental chemistry data. He has considerable experience addressing issues related to PAH
contamination at former MGP sites, metals in soils, chlorinated solvents in groundwater and
volatile organic chemicals in indoor air; and he has worked on numerous environmental forensic
investigations concerning a wide variety of contaminants, including dioxins/furans, lead,
petroleum, PCBs, metals, pesticides, and PCE. He is the author of more than 25 publications and
presentations including the chapter on Statistical Methods found in Introduction to Environmental
Forensics published by Academic Press. Dr. Gauthier received his BS in Chemistry from
Merrimack College and PhD in Analytical Chemistry from the University of New Hampshire.
Key project experience includes:
Environmental Forensics
Chinese Drywall. Investigated the source of corrosion and odors in homes containing
Chinese drywall. Identified elemental sulfur in mined gypsum as the cause of the
corrosion; developed a laboratory method for analysis of elemental sulfur in drywall; and
developed a non-destructive technique for identifying corrosive drywall in the home
(patent pending).
PAH Fingerprinting. Examined PAH fingerprinting analysis of tar samples unearthed

during building construction and offered deposition testimony related to the source of the
tar material. (Merco Group vs. Tampa Electric Company; Case No. 04-22909 CA 09).
PCE in Ground Water. Analyzed ratios of concentrations of PCE and its biodegradation
products (TCE and DCE) to determine the relative contribution to a large PCE plume
from a small release at a dry cleaning facility located down gradient from the primary
source.
PAH Fingerprinting. Used Cluster Analysis and Principal Components Analysis to

distinguish sources of PAHs in sediments located adjacent to a former manufactured gas
plant and former coal tar distillation facility.
Hudson River PCBs. Evaluated the hypothesis that anaerobic dechlorination of PCBs
was naturally occurring in Hudson River sediments by examining PCB congener profiles
2
as a function of depth in sediment cores and comparing these data to PCB congener
profiles for commercial Aroclor mixtures using multiple linear regression techniques.
Source of PAHs in Stream Sediments. Investigated coal-tar based parking lot sealants as
a potential source of PAHs in Austin, Texas stream sediments. Prepared double ratio
plots and used principal components analysis to compare PAH profiles in stream
sediments with coal-tar sealed parking lot runoff samples.
Dioxins/Furans. Examined congener profiles using principal component analysis to

distinguish sources of dioxins and furans at a wood treating facility.
Lead in Soil. Performed a statistical analysis of lead in surface soils at residential

properties surrounding a former dump in order to assess the potential contributions from
urban background, house paint, and contaminated soils originating from the dump.
Petroleum Contamination. Examined the results of advanced hydrocarbon

fingerprinting analyses to determine the source of an oil sheen appearing on the
Allegheny River.
Manufactured Gas Plant Wastes. Reviewed historical operating practices in relation to

the nature and extent of contamination at MGP sites in Massachusetts and New York to
establish whether the contamination was the result of accidental releases or intentional
disposal.
Metals in Dust. Compared X-ray Fluorescence and Atomic Absorption methods for
analysis of lead, cadmium, and zinc in soils and dust at the Palmerton Zinc Pile
Superfund Site. Assessed quality of the data and performed statistical analysis to
determine sources of elevated metal concentrations.
BTEX Chemicals in Indoor Air. Performed a statistical analysis of indoor air samples
collected in homes built over a former refinery site. Compared relative concentrations of
contaminants in indoor air with relative concentrations detected in soil gas samples
collected beneath the site and determined that indoor air contaminants were unrelated to
former refinery operations.
Pesticide Contamination. Examined the spatial distribution of pesticides in soil and

ground water at a former pesticide formulation plant in California in order to determine
the impact of historical waste disposal practices.
Leaking Underground Storage Tanks. Investigated the source and timing of gasoline
storage tank releases using a variety of environmental forensic techniques at convenience
stores located in Berkeley, CA; Houston, TX; and Windham, ME.
Dioxins in Soil. Examined dioxin fingerprint in boiler ash generated from combustion of
solvent waste and compared it to the fingerprints associated with background levels in
sediments and soils to determine contributions from the boiler.
3
Risk Assessment/Exposure Assessment
Chlorinated Solvent Release. Performed a multi-pathway risk assessment and calculated

risk-based cleanup levels for residential exposures to chlorinated solvents in groundwater
used for irrigation purposes.
Manufactured Gas Plant. Estimated risks from exposure to volatile organic compounds
and polycyclic aromatic hydrocarbons at a former manufactured gas plant site in central
Florida.
Monte Carlo Risk Assessment. Developed a probabilistic risk model in Excel using
Crystal Ball software for the local population surrounding a former beryllium metal
manufacturing facility.
Chlorinated Solvents. Estimated risks from exposure to chlorinated solvents in ground

water via the soil vapor intrusion pathway using the Johnson & Ettinger Model.
Vinyl Chloride. At a west coast Superfund Site, estimated the range of vinyl chloride
concentrations in air that would result in an unacceptable cancer risk for an off-site
receptor using Monte Carlo simulation techniques.
Explosives Manufacturer. Calculated risk-based clean up levels for explosive

compounds in ground water at a site in Utah. Prepared a comprehensive literature review
on the uptake and bioconcentration of RDX by plants.
Circuit Board Manufacturer. Assessed the risks to nearby workers from potential
exposures to chlorinated solvents in ground water at a former circuit board manufacturing
site located in central Florida.
Arsenic in Soil. Developed alternative Soil Cleanup Target Levels (SCTLs) for arsenic
and PAHs in soil under a recreational exposure scenario in support of a remedial action
plan for a redevelopment project in Florida.
DCE in Indoor Air. Estimated the health risks from exposure to 1,1-DCE in indoor air at
residences located above a ground water contamination plume.
Battery Breaking Site. Performed a statistical analysis of lead concentrations measured

in soils collected from a former battery breaking site. These data were used to perform a
health risk assessment for the site.
Monte Carlo Simulation. Developed a Monte Carlo simulation model to predict blood
lead concentrations in children exposed to lead in soil, dust, water and food. Model is
based upon the EPA LEAD model.
Blood Lead Analysis. Performed a sensitivity analysis on an empirical model designed

to predict soil lead clean-up levels based on blood lead levels. Interpreted the results of
an electron microprobe and selective extraction study designed to assess the
bioavailability of lead in soils. Prepared a review on the bioavailability of lead in mining
waste for submission to the CDC.
4
Copper Smelter, Arsenic. Determined the health risk of cancer from inhalation of
arsenic containing particulates at a primary copper smelter located in southwest United
States. Estimated fugitive particulate emissions from the facility, directed air dispersion
modeling, and conducted a probabilistic risk assessment using Monte Carlo simulation
techniques.
Drinking Water. Estimated household exposures to residents with drinking water wells
installed in an aquifer containing low levels of 1,1,1-TCA, 1,1-DCE, and chloroform.
Exposures to ground water contaminants were compared with exposures to contaminants
in chlorinated drinking water and naturally occurring radon levels.
Automotive Parts Manufacturer. Modeled chemical emissions from three automotive

parts manufacturing plants in Matamoros, Mexico. Estimated potential exposures to
residents in nearby Brownsville, TX as part of a toxic tort anencephaly case.
Fate & Transport Analyses/Model Development
PAH Mass Balance. Estimated PAH contributions from coal tar-based pavement sealers
on a city-wide scale. Used U.S. Census data coupled with literature-sourced PAH
emission rates in a Monte Carlo analysis to generate a probability distribution of PAH
mass loadings from various sources.
Vapor Emissions. Modeled potential vapor emissions released during proposed soil and
groundwater remediation scenarios at a chlorinated solvent release site located in central
Florida.
Lead-Sheathed Power Cable. Prepared a report summarizing the environmental impacts

of lead released from paper-insulated lead-covered power cables. Examined corrosion
processes, environmental chemistry, bioavailability, and transport and fate of lead in soil.
Iron Cyanide. Prepared a comprehensive review of the transport and fate of iron cyanide
complexes in manufactured gas plant wastes. Reviewed the chemistry of formation,
chemical and biological transformation processes, transport properties, and methods of
analysis of ferric ferrocyanide and related cyanide species.
Soil Vapor Intrusion. Used the Johnson & Ettinger Model to estimate concentrations of
chlorinated solvents in indoor air at residential locations situated above a groundwater
plume.
VOC Infiltration. Modeled infiltration of volatile organic chemicals into basements of

homes surrounding the Roxy Cleaners Site and estimated resulting indoor air
concentrations for incorporation into a baseline risk assessment.
Vapor Emissions. Modeled chemical vapor emissions at the Tar Lake (MI) wood-tar
contamination site for Paramount Inc.
Soil Flushing. Project manager for a subcontract to design, oversee, and evaluate soil
flushing as a remedial alternative for a Superfund Site in the midwest. Involved in
experimental design, collection of field samples, experiment oversight, and report
preparation.
5
Bioremediation Alternatives. Evaluated the potential for bioremediation of organic

constituents in tars produced during production of manufactured gas. Reviewed recent
literature on this topic and the results of a treatability study conducted at a former
manufactured gas plant site owned by the utility.
Model Development. Developed an equilibrium fugacity based model to predict the

transport and fate of organic contaminants emitted from municipal waste combustors as
part of an evaluation of alternative monitoring and assessment strategies.
Landfill Vapors. Modeled chemical vapor emissions from the 102nd Street Landfill Site
in Niagara Falls, NY as part of a risk assessment evaluating potential remedial
alternatives for the Site.
Transport of VOCs. Investigated the effects of organic cosolvents and surfactants on the
transport of volatile organic chemicals in groundwater. Considered effects on the
dissolution of Non Aqueous Phase Liquids (NAPL) and effects on contaminant
retardation factors.
Air Quality Studies
Indoor Air Sampling. Conducted indoor air sampling at an elementary school to

evaluate the potential for soil vapor intrusion associated with a nearby chlorinated solvent
plume.
Community Air Monitoring Program. Project manager for a large multi-year

community air monitoring project located in Tallevast, Florida. Analyzed results from
SUMMA canister samples and real-time monitoring data to evaluate potential offsite
impacts from remediation activities. Prepared a statistical analysis of over 20 months of
monitoring data using cluster analysis techniques to identify trends in the data.
Landfill Study. Investigated air quality related issues associated with the expansion of an
existing landfill. Examined leachate collection system, landfill gas extraction system,
and gas flare design in relation to potential air emissions.
Ambient Sampling. Designed an air sampling program to determine the emission of

chemicals from the present landfill cover. Estimated emissions from the proposed
landfill expansion based on existing data and air monitoring results.
PCBs, Dioxins. Estimated vapor emissions from PCB contaminated soils at a General
Motors facility in Region II. Estimated the potential for dioxin formation from the
incineration of PCB contaminated soils.
Engineering Estimate of Emissions. Estimated volatile organic emissions from three

automobile parts manufacturing facilities located in Mexico. Emission estimates were
based on mass balance calculations involving purchasing records, waste disposal
quantities, material safety data sheet information, and production quantities.
Vapor Emissions. Modeled historical vapor emissions from a wood treating facility
based on pentachlorophenol and creosote usage rates.
6
Miscellaneous Experience
Lignite Energy Council. Critiqued the State Department of Healths rationale for
maintaining State Ambient Air Quality Standards more stringent than federal standards.
Analyzed ambient air monitoring data, air dispersion modeling results, and insurance
claims data for the treatment of asthma to support our opinions.
RCRA Facility Investigation. Project manager for a RCRA Facility Investigation at a

former specialty metals manufacturing facility contaminated with radionuclides, metals
and chlorinated solvents. Responsible for overall project oversight and report
preparation, including human health and ecological risk assessments.
Analysis of Filtered Wood Smoke. Project manager for a patent litigation case involving
the analysis of filtered wood smoke in fish.
Employment History
2004 present ENVIRON, Tampa, FL, Senior Science Advisor
2002 2004 Exponent, Inc., Tampa, FL, Managing Chemist
1999 - 2001 Sciences International Inc., Bradenton, FL, Senior Project Manager
1995 - 1999 Gradient Corporation (an IT Company), Sarasota, FL, Senior Project Manager
1989 - 1994 Gradient Corporation, Cambridge, MA, Senior Project Manager
1988 - 1989 Roy F. Weston, Inc., Burlington, MA, consultant to EPA
1986 - 1988 Boston University, Boston, MA, Postdoctoral Research Associate

Professional Activities
Reviewer for Environmental Science and Technology and Environmental Forensics
Completed ASTM training course on Risk Based Corrective Action, 1996
Completed "Environmental Project Management" course at Tufts University, 1993
Selected Publications & Presentations

DeMott, R.P., S.J. Roberts and T.D. Gauthier. 2011. Use of Mass Balance Bounding Estimates
and Sensitivity Analysis to Prioritize PAH Inputs in Urban Systems. Paper presented at
the Society of Environmental Toxicology and Chemistry 32nd Annual Meeting, Boston,
Massachusetts, November 13-17.
Freeman, G., R. DeMott, T. Gauthier, M. Stevenson and J. Hubbard. 2011. Continued Corrosion
After Removal of Corrosive Drywall. Journal of Failure Analysis and Prevention
11:265-273.
7
DeMott, R.P., T.D. Gauthier, J.M. Wiersma and G. Crenson. 2010. Polycyclic Aromatic
Hydrocarbons (PAHs) in Austin Sediments after a Ban on Pavement Sealers.
Environmental Forensics 11(4): 372 382.
Gauthier, T.D., M.C. Masonjones, M.A. Alessandroni, and R. DeMott. 2009. Proposed
Mechanism for the Release of reduced Sulfur Compounds from Corrosive Imported
Drywall. Paper presented at the Technical Symposium on Corrosive Imported Drywall,
Tampa, Florida, November 5-6.
Gauthier, T.D. and R.P. DeMott. 2008. Analysis of PAH Concentrations Detected in Austin
Texas Stream Sediments Following a Ban on the Use of Coal Tar Sealers. Paper
presented at the Society of Environmental Toxicology and Chemistry 29th Annual
Meeting, Tampa, Florida, November 16-20.
Gauthier, T.D. and M. Hawley. 2007. Statistical Methods. In: Introduction to Environmental
Forensics, 2nd Edition. B.L. Murphy and R.M. Morrison, Eds. Elsevier/Academic Press,
London.
Gauthier, T.D., R.P. DeMott and G. Crenson. 2006. Evaluation of Polycyclic Aromatic
Hydrocarbon Sources in Austin Texas Stream Sediments. Poster presented at the Society
of Environmental Toxicology and Chemistry 27th Annual Meeting, Montreal Canada,
November 5-9.
Gauthier, T.D. 2005. Deriving Florida-Specific Attenuation Factors Using Radon Data. Paper
presented at the Florida Air & Waste Management Association 2005 Annual Conference,
St. Pete Beach, FL. November 22.
Gauthier, T.D. 2005. Deriving Florida-Specific Attenuation Factors Using Radon Data. Paper
presented at the 2005 Florida Brownfields Conference, Jacksonville, FL. October 11.
Gauthier, T.D. 2004. Environmental Impacts of Lead from Paper-Insulated Lead-Covered

Cable. EPRI Technical Update Report No. 1009513. April.
Gauthier, T.D., and B.L. Murphy. 2003. Age dating groundwater plumes based on the ratio of
1,1-dichloroethylene to 1,1,1-trichloroethane: an uncertainty analysis. Environmental
Forensics 4: 205-213.
Gauthier, T.D., and B.L. Murphy. 2003. Uncertainties in age dating groundwater plumes using
1,1-DCE/1,1,1-TCA ratios. Poster presented at the Battelle In Situ and On-Site
Bioremediation Symposium, Orlando, FL. June 2- 5.
Bigham, G., C. Mackay, B. Henry, and T.D. Gauthier. 2002. Fate of mercury deposited in the
Everglades. Paper presented at the Air and Waste Management Association Florida
Section 2002 Annual Conference, Jupiter, FL. September 15 17.
Gauthier, T.D. 2001. Detecting trends using Spearmans rank correlation coefficient.
Environmental Forensics. 2(4):359-362.
Gauthier, T.D. 2001. Statistical Methods. In: Introduction to Environmental Forensics, B.L.
Murphy and R.M. Morrison, Eds. Academic Press, London.
8
Gauthier, T.D., and B.L. Murphy. 2001. Recent Developments in Environmental Forensics:
Statistical analysis techniques. Environmental Claims Journal. 13(2): 83-102.
Gauthier, T.D., and B.L. Murphy. 2000. Edible plant bioconcentration factors for RDX. Paper
presented at the 2000 Annual Meeting, Society for Risk Analysis, Arlington, VA.
December 3-6.
Murphy, B.L., and T.D. Gauthier. 2000. Current Developments in Environmental Forensics: A
Survey of Environmental Forensics Topics Presented at Seven Recent Conferences.
Environmental Claims Journal. 12(4):113-125.
Murphy, B.L., and T.D. Gauthier. 2000. Dose reconstruction for toxic torts. Environmental
Claims Journal. 12(3):161-171.
Murphy, B.L., and T.D. Gauthier. 1999. Forensic analysis of chlorinated solvent contamination
data. Environmental Claims Journal. 11(4):81-96.
Murphy, B.L., and T.D. Gauthier. 1999. Determining air emission source contributions to soil
concentrations. Environmental Claims Journal. 11(2):143-155.
Gauthier, T. D. and B. L. Murphy. 1998. "Avoiding Sick Buildings at Brownfield Sites,"

Brownfield News, August.
Butcher, J.B., T.D. Gauthier, and E.A. Garvey. 1997. Use of historical PCB Aroclor
measurements: Hudson River fish data. Environmental Toxicology and Chemistry
16(8):1618-1623.
Slayton, T.M., B.D. Beck, K.A. Reynolds, S.D. Chapnick, P.A. Valberg, L.J. Yost, R.A. Schoof,
T.D. Gauthier, and L. Jones. 1997. Issues in arsenic cancer risk assessment.
Environmental Health Perspectives 104(10): 1012-1014.
Gauthier, T.D. 1996. Application of risk-based corrective action to sites contaminated with
chlorinated solvents. Paper presented at the Florida Environmental Expo, Tampa, FL.
October.
Shifrin, N.S., B.D. Beck, T.D. Gauthier, S.D. Chapnick, and G. Goodman. 1996. Chemistry,
toxicology and human health risk of cyanide compounds in soils at former manufactured
gas plant sites. Reg. Tox. Pharm. 23: 106-116.
Bowers, T.S. and T.D. Gauthier. 1995. Use of the output of a lead risk assessment model to
establish soil lead cleanup levels. Environmental Geochemistry and Health 16(3): 191-
196.
Butcher, J.B. and T.D. Gauthier. 1994. Estimation of residual dense NAPL mass by inverse
modeling. Ground Water 32(1): 71-78.
Beck, B.D., G. Goodman, and T.D. Gauthier. 1994. Risk assessment for cyanides in soil at
manufactured gas plant (MGP) sites. Paper presented at 1994 Annual Meeting, Society of
Toxicology.
9
Drivas, P.J., P.A. Valberg, and T.D. Gauthier. 1991. Health assessment of air toxics emissions
from alternative fuels. Presented at 84th Annual Meeting, Air and Waste Management
Association, Vancouver, BC, June.
Clarke, R.H., J.M. Isner, T.D. Gauthier, K. Nakagawa, F. Cerio, E. Hanlon, H. Brody, E.
Gaffney, E. Rouse, and S. DeJesus. 1988. Spectroscopic characterization of
cardiovascular tissue. Lasers in Surgery and Medicine 8:45-59.
Gauthier, T.D., R.H. Clarke, and J.M. Isner. 1988. Time resolved plasma photoemission of
myocardium with excimer laser excitation. Journal of Applied Physics 64:2736-2741.
Gauthier, T.D., W.R. Seitz, and C.L. Grant. 1987. Effects of structural and compositional
variations of dissolved humic materials on pyrene Koc values. Environmental Science &
Technology 21 :243-248.
Gauthier, T.D. 1986. "Partitioning of Polyaromatic Hydrocarbons in Natural Waters: Dissolved

Organic Matter Effects." Paper #496. Presented at Pittsburgh Conference, Atlantic City,
NJ, March.
Gauthier, T.D., E.C. Shane, W.F. Guerin, W.R. Seitz, and C.L. Grant. 1986. Fluorescence
quenching method for determining equilibrium constants for polycyclic aromatic
hydrocarbons binding to dissolved humic materials. Environmental Science &
Technology 20:1162-1166.
Gauthier, T.D. 1985. "A Novel Method for Determining Polyaromatic Hydrocarbon Binding to
Dissolved Humic Material." NERM 15. Presented at American Chemical Society, June.
Gauthier, T.D. 1984. "A Fluorescence Quenching Study of the Interaction of Polyaromatic
Hydrocarbons with Natural Organics." Presented at Pittsburgh Conference, Atlantic City,
NJ, March.
Testimony Experience
Merco Group vs. Tampa Electric Company; Case No. 04-22909 CA 09. Offered
deposition testimony related to the source of the tar material unearthed during building
construction. October 4, 2005.
BASF Catalysts LLC (f/k/a Engelhard Corp) v. Allstate Insurance Co., et al. No. MID-L-
2061-05. Offered three days of deposition testimony as a fact witness in an insurance
litigation case. November 9-10, 2009; January 13, 2010.
Patents
DBR. No. P2399US. Process and Apparatus for Detecting Sulfur Gases Emitted from Defective
Chinese Drywall (patent pending).
1
Diane J. Mundt, PhD
EDUCATION
1991 Post Doctoral Fellowship, Musculoskeletal Epidemiology, Columbia University

1990 PhD, Epidemiology, University of Massachusetts at Amherst
1979 MS, Epidemiology, Harvard University
1977 BS, Biology & English, Valparaiso University
EXPERIENCE
Dr. Diane J. Mundt is a Principal Consultant of ENVIRON with over 25 years of experience in the
application of epidemiological methods in the areas of occupational and environmental health,
specializing in research and policy applications. She has particular expertise in the systematic
evaluation of health effects of chemical compounds and an extensive background in the critical review
and interpretation of epidemiological studies. Prior to joining ENVIRON, Diane served as Director of
Public Health Policy for Applied Epidemiology, Inc. She also spent several years managing and
providing scientific input to numerous Institute of Medicine, National Academies committees. She
began her career as an epidemiologist in the Environmental Epidemiology Branch of the National
Cancer Institute. Dianes recent work at ENVIRON includes the following:
Heading ENVIRONs team of experts on epidemiology, toxicology, industrial hygiene, and

environmental fate and transport of nanomaterials.
Membership on the Industry Advisory Board to Northeastern University Collaborative
Nanoscale Science & Engineering Center for High Rate Nanomanufacturing.
Directed an epidemiological study of perflourinated surfactant exposure and possible clinical
health outcomes.
Directed a critical review and evaluation of confounding in the occupational asphalt
epidemiological literature and a field assessment of historical process changes for a trade
organization.
Directed two reviews in the refining and hot mix paving sectors to evaluate and document
materials added historically to asphalt in each of these sectors.
Provided technical and editorial oversight of reviews of the epidemiological and toxicological
literature regarding the health effects of dioxin exposure for the Air Force 2002 Ranch Hands
Health Study.
At the request of the Institute of Medicine, comprehensively reviewed and summarized
occupational and environmental epidemiology studies of associations between solvent exposure
(including benzene, trichloroethylene, perchloroethylene, methelyne chloride) and risk of
disease in humans.
Providing technical and editorial oversight of reviews of the epidemiological literature for
various chemical compounds in support of various litigation matters.
1998-2000 - Staff Scientist, Health Effects Institute

Managed the Health Effects Institute (HEI) Review Committee to peer-review and publish investigator
reports. Responsibilities included, but were not limited to, synthesizing information from the Committee,
drafting the HEI Commentary that accompanies all HEI investigator reports, and assisting in editorial
preparations for publication of the following:
2
Diane J. Mundt, PhD
The National Morbidity, Mortality, and Air Pollution Study: Methods and Methodologic Issues
Part I. Investigators: Samet JM, Zeger S, Dominici F, et al. May 2000.
The National Morbidity, Mortality, and Air Pollution Study: Morbidity and Mortality from Air
Pollution in the United States Part II. Investigators: Samet JM, Zeger S, Dominici F, et al. June
2000.
Identifying Subgroups of the General Population that may be Susceptible to Short-term
Increases in Particulate Air Pollution: A Time Series Study in Montreal, Quebec. Investigators
Goldberg MS, Bailar JC, Burnett RT et al. November 2000.
A Case-Crossover Analysis of Fine Particulate Matter Air Pollution and Out-of-Hospital Sudden
Cardiac Arrest. Investigators: Checkoway H, Levy D, Sheppard L et al. December 2000.
Worked with a specially designated Diesel Epidemiology Expert Panel to assemble work from
investigators, synthesizing information, responding to peer review, writing and editing the Panel report:
Diesel Emissions and Lung Cancer: Epidemiology and Quantitative Risk Assessment. A
Special Report of the Institutes Diesel Epidemiology Expert Panel. June, 1999.
Co-coordinator for: Diesel Workshop: Building a Research Strategy to Improve Risk Assessment.
March 7-9, 1999, Stone Mountain, Georgia. Summarized workshop proceedings, and compiled
presentations for publication in:
Diesel Workshop: Building a Research Strategy to Improve Risk Assessment. HEI

Communications, Number 7. October/November, 1999.
Additional diesel publications:
Research on Diesel Exhaust. A Program Summary. December, 1999.
At the request of the US Environmental Protection Agency, coordinated the work of a formal expert panel
to peer-review a draft EPA document, Reconstruction of Teamsters Union Exposures 1950-1990.
Coordinated peer-review of applications responding to Request for Proposals to conduct feasibility

studies of diesel exposure methods and identifying cohorts for epidemiologic study. Acted as project
officer for the six studies funded by the Institute.
1992-1996 - Senior Program Officer, National Academy of Sciences, Institute of Medicine

Senior staff officer primarily responsible for directing work of a committee of experts to result in the
publications listed below. Responsibilities included, but were not limited to: working directly with all
committee members; interacting with sponsors, extensive information gathering, synthesizing, and
disseminating to committee; writing and editing final reports; responding to and coordinating extensive
peer review of reports:
Institute of Medicine. Health Consequences of Service during the Persian Gulf War:
Recommendations for Research and Information Systems. National Academy Press, 1996.
Institute of Medicine. Health Consequences of Service during the Persian Gulf War: Initial
Findings and Recommendations for Immediate Action. National Academy Press, 1995.
3
Diane J. Mundt, PhD
Final progress report to the US Army Medical Research and Materiel Command, Fort Detrick,
Maryland. Study of Post-Separation HIV-Positive Service Members Lost to Follow-up. October
1995.
Additionally responsible for drafting or editing selected sections or chapters in the following
publications.
Institute of Medicine. Veterans and Agent Orange. National Academy Press, 1994.
National Research Council. Toxicological Assessment of the Armys Zinc Cadmium Sulfide
Dispersion Tests. National Academy Press, 1997.
National Research Council. Toxicological Assessment of the Armys Zinc Cadmium Sulfide
Dispersion Tests. Answers to Commonly Asked Questions. National Academy Press, 1997.
Staff consultant:
Institute of Medicine. Veterans and Agent Orange. Update 1996. National Academy
Press, 1996.
PROFESSIONAL AFFILIATIONS
American College of Epidemiology

ASTM International Committee E56, Nanotechnology
International Society for Environmental Epidemiology
International Commission on Occupational Health ICOH
Medichem Occupational & Environmental Health in the Production & Use of Chemicals
Society for Epidemiologic Research
PROFESSIONAL ACTIVITIES
Secretary, Medichem Boards Executive Committee, 2008-present

Member of the Advisory Editorial Board of Archives of Industrial Hygiene and Toxicology
Member, Industry Advisory Board, National Science Foundation Nanoscale Science and Engineering
Center for High-rate Nanomanufacturing. Northeastern University, Boston, MA 2002-present
Member, InterNano Advisory Board, National Science Foundation Center for Hierarchical
Manufacturing, University of Massachusetts, Amherst, MA, 2007-present
Panel Member, Future of Occupational Exposure Limits, Registries, and Epidemiology, 5th International
Symposium on Nanotechnology, Occupational and Environmental Health, Boston, Massachusetts,
August 9-12, 2011.
Member, Planning Committee for NIOSH sponsored conference Nanomaterials and Worker Health:
Medical surveillance, exposure registries, and epidemiological research, Colorado, July 21-23, 2010.
Session Moderator, Human Health and Environmental Exposure, International Conference on the
Environmental Implications and Applications of Nanotechnology. Co-Hosted by The Environmental
Institute, University of Massachusetts Amherst and the US EPA Office of Superfund Remediation and
Technology Innovation. Amherst, Massachusetts, June 9-11, 2009.
Member, Advisory Committee to the Massachusetts Interagency Committee on Nanotechnology, 2008-
2010
4
Diane J. Mundt, PhD
Co-chair, Nanotechnology Application Program, International Conference on Nanotechnology and

Occupational and Environmental Health & Safety: Research to Practice, 2006
PRIOR EXPERIENCE
Director of Public Health Policy, Applied Epidemiology, Inc., Amherst, MA, 2001-2003
Staff Scientist and Epidemiologist, Health Effects Institute, Cambridge, MA, 1998-2000
Senior Research Professional, University of Chicago, Department of Health Studies, 1997-1998
Instructor, University of Chicago, Department of Health Studies, Chicago, IL, 1997-1998
Consultant and Advisor, Family Practice Residency Program, MacNeal Hospital, Berwyn, IL, 1997-
1998
Senior Program Officer and Study Director, National Academy of Sciences, Institute of Medicine,
Washington, D.C., 1993-1996
Program Officer, National Academy of Sciences, Institute of Medicine, Washington, D.C., 1992-1993
Assistant Research Professor, Division of Biostatistics and Epidemiology, Department of Community and
Family Medicine, School of Medicine, Georgetown University, Washington, D.C., 1991-1992
Post-doctoral Fellow, National Institute of Arthritis, Musculoskeletal and Skin Diseases NIH Training
Grant, Columbia University, New York, NY, 1989-1991
Project Manager, NIH grant: A case-control study of herniated cervical and lumbar disc. Department
of Epidemiology, School of Public Health, University of Massachusetts, 1985-1989
Director, Alumni Relations and Student Activities, Concordia College, Bronxville, NY, 1981-1983
Epidemiologist, Environmental Epidemiology Branch, Radiation Studies Section, National Cancer
Institute, National Institutes of Health, Bethesda, MD, 1979-1981
PRESENTATIONS
Schulte PA, Mundt DJ. Exposure registries: Overview. National Institute for Occupational Safety and
Health (NIOSH) Nanomaterials and Worker Health: Medical Surveillance, Exposure Registries,
and Epidemiologic Research, Keystone, Colorado, July 21-23, 2010.
Mundt DJ, Mundt KA, Bachand A, Carlton LE. Meta-analyses of occupational exposure as a painter
and lung and bladder cancer morbidity and mortality 1950-2008. EPICOHMEDICHEM 2010
Occupational Health under Globalization and New Technology. Taipei, Taiwan, April 2125,
2010
Mundt KA, Mundt DJ, Montgomery R. Meta-Analysis of risk associated with occupational formaldehyde
exposure. Society of Risk Analysis Annual Meeting; Risk Analysis: The Evolution of a Science,
Baltimore, MD, December 6-9, 2009.
Mundt DJ, Mundt KA, Montgomery R., Bachand A. Meta-analysis of formaldehyde exposure and risk of
Leukemia and nasopharyngeal cancer. MEDICHEM Workshop: Risk Assessment and Human
Exposure to Hazardous Materials, Thessaloniki, Greece, October 21-24, 2009.
Praolini F, Guilhem M, Mundt DJ, Mundt KA, Santamaria A. Preparing for the future: proposal for an
International Nanomaterial Exposure Registry (INER). Nanosafe 2008, Grenoble, France
November 3-7, 2008.
5
Diane J. Mundt, PhD
Mundt DJ, Mundt KA, Skinner D, Klapper A, Kosnett MJ. Planning for the future: exposure reqistries for
engineered nanomaterial employees. The 36th Medichem International Congress Innovation in
Occupational Health. Amsterdam, The Netherlands, September 9-11, 2008.
Mundt KA, Mundt DJ. Occupational Health Surveillance: A proactive approach to occupational safety
in the nanotechnology workplace. Nanotechnology: The Future of Environment Health & Safety
Regulatory Policy, Baltimore, MD, March 20, 2008.
Mundt, DJ, Invited Speaker. Next Steps and Concluding Remarks. The Big Picture: Safe Development
of Nanotechnology Workshop. Marlborough, MA, November 15, 2007.
Mundt DJ. From Uncertainty to Practice: Practical Strategies in Nanotechnology. The Big Picture: Safe
Development of Nanotechnology Workshop, Marlborough, MA, November 14, 2007.
Mundt DJ. Nanotechnology and Nanomaterials: Are the Workers Safe? 5th New England
International Nanomanufacturing Workshop, Boston, MA, June 20, 2007.
Adams R, Mundt DJ. What Businesses Should be Doing Now to Prepare for Tomorrow.
Nanotechnology: Waiting for OSHA. Teleconference with Reed Smith, May 2, 2007.
Mundt DJ, Adams R, Daugherty D, Santamaria A, Mundt KA. Managing uncertainty: Practical
approaches to nanoscale materials and occupational health in small workplaces. The 28th
International Congress on Occupational Health (ICOH) Renewing a century of commitment to a
healthy, safe & productive working life, Milan, Italy, June 11-16, 2006.
Mundt DJ, Mundt KA, Luippold R, Schmidt M, Farr C. Clinical epidemiological study of employees
exposed to perfluorononanoic acid (PFNA). The 28th International Congress on Occupational
Health (ICOH) Renewing a century of commitment to a healthy, safe & productive working life,
Milan, Italy, June 11-16, 2006.
Mundt DJ, Adams R, Marano K, Heidenreich M, Nunes A. Historical changes in occupational
exposures in the US asphalt paving industry an investigation of refining and hot mix processes.
BG Academy for Occupational Health and Safety, Health Effects of Occupational Exposure to
Emissions from Asphalt/Bitumen Symposium, Dresden, Germany, June 7-8, 2006.
Mundt DJ, van Wijngaarden E, Mundt KA. An assessment of the possible extent of confounding in
epidemiological studies of lung cancer risk among roofers. BG Academy for Occupational Health
and Safety, Health Effects of Occupational Exposure to Emissions from Asphalt/Bitumen
Symposium, Dresden, Germany, June 7-8, 2006.
Mundt DJ, Mundt KA. Nanotechnology and health: Not a second thought. Nanotechnology from Lab
to Product Seminar, IGERT Program in Nanotechnology Innovation, University of Massachusetts,
Amherst, March 30, 2006.
Santamaria AB, Mundt DJ, Mundt KA. Risk assessment of nanoparticles: Issues and datagaps.
American College of Toxicology Williamsburg, VA, Nov. 6-9, 2005.
Mundt DJ, Mundt KA, Adams RC, Santamaria A, Daugherty D. Health effects of Occupational exposure
to nanoscale materials: Pragmatic approaches to managing occupational health uncertainty. The
2nd International Symposium on Nanotechnology and Occupational Health, National Institute for
Occupational Safety and Health, Minneapolis, MN, October 3-6, 2005.
Mundt DJ, Mundt KA, Smylie M, Brock WJ, Rodricks JV. Nanotechnology a new page in an old
book. Medichems XXXII International Congress Toward Global Sustainable Best Practices in
Chemical Safety and Health Paris, France, September 1-3, 2004.
6
Diane J. Mundt, PhD
PUBLICATIONS
Publications in Peer-Reviewed Journals

Schulte PA, Mundt DJ, Nasterlack M, Mulloy KB, Mundt KA. Exposure Registries: overview and utility
for nanomaterial workers. Journal of Occupational and Environmental Medicine 2011;53(6
Suppl):S42-7.
Bachand A, Mundt KA, Mundt DJ, Montgomery R. Epidemiological studies of formaldehyde exposure
and risk of leukemia and nasopharyngeal cancer: A Meta-Analysis. Critical Reviews in Toxicology,
2010;40(2)85-100.
Bachand A, Mundt KA, Mundt DJ, Carlton LE. Meta-analyses of occupational exposure as a painter
and lung and bladder cancer morbidity and mortality 1950-2008. Critical Reviews in Toxicology,
2010;40(2):101-125.
Mundt DJ, Marano KM, Nunes AP, Adams RC. A review of changes in composition of hot mix asphalt
in the United States. Journal of Occupational and Environmental Hygiene 2009;6:714-725.
Mundt DJ, Adams RC, Marano KM. A historic review of additives and modifiers used in paving asphalt
refining processes in the United States. Journal of Occupational and Environmental Hygiene
2009;6:705-713.
Schulte PA, Trout D, Zumwalde R, Kuempel E, Geraci C, Castranova V, Mundt DJ, Mundt KA, Halperin
WE. Options for occupational health surveillance of workers potentially exposed to engineered
nanoparticles: State of the science. Journal of Occupational and Environmental Medicine 2008;50
(5):517-526.
Mundt DJ, Marano KM, Nunes AP, Adams RC. A preliminary assessment of historical changes in the
US asphalt paving industry refining and hot mix processes. Journal of Occupational and
Environmental Hygiene 2007 4(S1): 220222
Mundt DJ, Mundt KA, Luippold RS, Schmidt MD, Farr CH. Clinical epidemiological study of employees
exposed to surfactant blend containing perfluorononanoic acid (PFNA). Occupational and
Environmental Medicine 2007;64(9):589-94. Epub 2007 Apr 4.
Mundt DJ, van Wijngaarden E, Mundt KA. An assessment of the possible extent of confounding in
epidemiological studies of lung cancer risk among roofers. Journal of Occupational and
Environmental Hygiene. 2007;4(S1):163-174.
Birk T, Mundt KA, Dell LD, Luippold RS, Miksche L, Steinmann-Steiner-Haldenstaett, Mundt DJ. Lung
cancer mortality in the German chromate industry, 1958-1998. Journal of Occupational and
Environmental Medicine 2006;48(4):426-433.
Mundt DJ, Dell LD, Luippold RS, Sulsky SI, Skillings A, Gross R, Cox KI, Mundt KA. Cause-specific
mortality among Kelly Air Force Base civilian employees, 1981-2001. JOEM 2002;44 (11): 989-
996.
Dell LD, Mundt KA, McDonald, M, Tritschler JP, Mundt DJ. Critical review of the epidemiology literature
on the potential cancer risks of methylene chloride. Int Arch Occup Environ Health 1999;72:429-
442.
Steingrub JS and Mundt DJ. Blood glucose and neurologic outcome in global brain ischemia. Crit
Care Med 1996;24:802-806.
Wolfson M, Mundt DJ, Hawley GG. Recombinant human erythropoietin utilization in Department of
Veterans Affairs Dialysis Units. Am J Kidney Dis 1994;24:184-191.
7
Diane J. Mundt, PhD
Boekeloo BO, Schiavo L, Rabin DL, Conlon R, Jordan C, Mundt DJ. Self-reports of HIV risk factors by
patients at a sexually transmitted disease clinic: audio versus written questionnaires. Am J Public
Health 1994;84:754-760.
Hannallah MS and Mundt DJ. Effect of epidural morphine on sedation requirements during regional
anesthesia. J Clin Anesth 1994;6:10-13.
Howell JM, Stair TO, Howell AW, Mundt DJ, Falcone A, Peters SR. The effect of scrubbing and
irrigation with normal saline, povidone iodine and cefazolin on wound bacterial counts in a guinea
pig model. Am J of Emerg Med 1993;11:134-138.
Hannallah MS, Benumof JL, Bachenheimer LC, Mundt, DJ. The resting volume and compliance
characteristics of the bronchial cuff of left polyvinyl chloride double-lumen endobronchial tubes.
Anesth Analg 1993;77:1222-1226.
Mundt DJ, Kelsey J, Golden A, Panjabi M, Pastides H, Berg A, Sklar J, Hosea T. An epidemiologic
study of sports and weight lifting as possible risk factors for herniated lumbar and cervical discs.
Am J Sports Med 1993;21:854-860.
Love JN, Leasure JA, Mundt DJ. A comparison of combined amrinone and glucagon therapy to
glucagon alone for cardiovascular depression associated with propraninol toxicity in a canine
model. Am J Emerg Med 1993;11:360-363.
DElio MA, Mundt DJ, Bush PJ, Iannotti RJ. Healthful behaviors: Do they protect African-American, urban
preadolescents from abusable substance use? Am J Health Promot 1993;7:354-362.
Mundt DJ, Kelsey J, Golden A, Pastides H, Berg A, Sklar J, Hosea T, Panjabi M. An epidemiologic
study of non-occupational lifting as a risk factor for herniated lumbar intervertebral disc. Spine
1993;18:595-602.
Ginsberg GG, Lewis JH, Gallagher JE, Fleischer DE, al-Kawas FH, Nguyen CC, Mundt DJ, Benjamin
SB. Diazepam versus midazolam for colonoscopy: a prospective evaluation of predicted versus
actual dosing requirements. Gastrointest Endosc 1992;38:651-656.
Love JN, Leasure JA, Mundt DJ, Janz TG. A comparison of amrinone and glucagon therapy for
cardiovascular depression associated with propranolol therapy in a canine model. J Toxicol Clin
Toxicol 1992;30:399-412.
Wrathall JR, Teng YD, Choiniere D, Mundt DJ. Evidence that local non-NMDA receptors contribute to
functional deficits in contusive spinal cord injury. Brain Res 1992;586:140-143.
Howell JM, Stair TO, Howell AW, Mundt DJ. Cefazolin and povidone-iodine as irrigants of
contaminated wounds (abstract). Ann Emerg Med 1992;21:186.
Hauser GJ, Danchak MR, Colvin MP, Myers AK, DiCarlo JV, Hopkins RA, Wocial B, Mundt DJ,
Zukowska-Grojec Z. Circulating neuropeptide Y during open heart surgery: relation to changes in
catecholamine levels and changes in hemodynamics (abstract). Crit Care Med 1992;20:523.
Kelsey JL, Golden AL, Mundt DJ. Low back pain/prolapsed lumbar intervertebral disc. Rheum Dis Clin
of North Am 1990;16:699-716.
McCusker J, Mundt DJ, Stoddard AM, Cole E, Whitbourne SK, Simmons J. Outcomes of a geriatric
rehabilitation program in a long-term care facility. J Aging Health 1989;1:485-506.
Mundt DJ, Gage R, Lemeshow S, Pastides H, Teres D, Avrunin JS. Intensive care unit patient follow-up:
mortality, functional status and return to work at six months. Arch Intern Med 1989;149:68-72.
8
Diane J. Mundt, PhD
Mundt DJ and McCusker J. The use of dead controls in case-control studies (Letter to the editor). Am J
Epidemiol 1985;122:1108.
Other Selected Publications

Mundt DJ. Nanotech: Managing the health risks. Global Investor Focus. Credit Suisse. Issue 02,
October 2006.
Mundt DJ. Book Review: The Particulate Air Pollution Controversy: A Case Study and Lessons Learned.
Applied Occupational and Environmental Hygiene 2003;18(7):1-2.
Kelsey JL, Mundt DJ, Golden AL. Epidemiology of low back pain in: The Lumbar Spine and Back Pain.
ed. Jayson, MIV. Edinburgh: Churchill Livingstone, 4th edition, 1992.

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Review of Scientific Methods

and Findings for

Final Report of The

2 Comments on Analytical Data Quality 5

3 Survey Design Comments 13

4 Comments on Endosulfan Exposure and Effects 18

To confirm the presence of endosulfan residues in environmental and biological samples

1.2 Information Sources

The NIOH Report (NIOH, 2002);

93 pages of Gas Chromatography-Electron Capture Detection (GC-ECD) output

2 Comments on Analytical Data Quality

2.1 Excluded Sample Results

Table 1. Differences Between Summary Statistics Reported in Table 4 of NIOH

Soil Area Mean SD Difference

Top Study -endosulfan 0.274 0.161 0.222 0.133 Yes

Middle Study -endosulfan 0.183 0.076 0.184 0.077 No

2.3 Detection Limits

2.4 Chromatographic Peak Identification

2.5 Random Noise Fluctuations

2.6 Calibration Data

No calibration curve demonstrating linearity of the detector response is presented.

2.7 QA/QC Data

No blank data are presented in the report.

3 Survey Design Comments

3.1 Study Design Considerations

3.2 Confounding Factors and Alternate Interpretations

The presentation of neurobehavioral problems is similarly lacking a discussion of alternative

3.3 Size of Study Groups

Chromosomal analyses presented for 2% of reference group and 5% of study group.

IQ surrogate testing 57% reference group participation compared to 82% participation

In another example, results of chromosomal analyses presented in Table 22 include 8 reference

4 Comments on Endosulfan Exposure and Effects

Observations purportedly associated with neurobehavioral conditions and congenital

4.1 Endosulfan Levels Consistent With Background

4.2 Samples Excluded from Journal Publication

4.3 Obvious Alternate Explanations Not Discussed

SMR scoring involves assigning a categorical value of 1 to 5 based on certain observable

SMR Score 3 Growth of testes and scrotum

4.4 Recorded Observations Not Biologically Relevant

The results apparently categorized to indicate neurobehavioral disorders were 1) differential

Congenital hydrocele is another common condition at birth, occurring in approximately 1-2% of

We recognized serious limitations in the analyses for endosulfan conducted on environmental

Indulkar, A.S. 2004. Endosulfans Effects: Inaccurate Data. Environmental Health

National Institute of Occupational Health (NIOH). Undated. Report of The Investigation of

Saiyed, H., A. Dewan, V. Bhatnager, U. Shenoy, R. Shenoy, H. Rajmohan, K. Patel, R.

Saiyed, H.N. 2004. Endosulfans Effects: Saiyeds Response. Environmental Health

Project Director and Toxicologist:

1987 B.A., Biology, with Honors, Williams College

Registrations & Affiliations

Toxicology and Chemical Risk Evaluation Experience

PCBs / Dioxins Acid Gases, Chlorine, Phosgene

Chemical Risk Related Property Impacts

Concerns over health threats Remedies for indoor air issues

Dioxin Profiling -- Wingate Road Landfill Superfund Site, Ft. Lauderdale, FL

Analysis of Potential Health Risks for Proposed Power Plant

Analysis of Risk Implications for Kalamazoo River Angler Study

Analysis of Endocrine Disruption Concerns from Livestock Operations

Exposures in Waste Disposal Facility Fire, Memphis, Tennessee

Review of State Monitoring Study of Estrogens in Streams

Risk-Based Criteria for Chlorinated and Arsenical Pesticides at Golf Courses

Alternative Cleanup Strategy Development Former Nursery, Osprey, Florida

Three-Tier Analysis of Potential Arsenic Risks at Indiana Childrens Camp

Bioavailability of Arsenic at Pesticide-Impacted Sites