Beruflich Dokumente
Kultur Dokumente
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
5 Conclusions 25
List of Attachments
Attachment A Curricula Vitae
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Scientific Review NIOH Endosulfan Study
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
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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.
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Scientific Review NIOH Endosulfan Study
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.
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.
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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:
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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.
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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.
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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.
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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
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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.
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
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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.
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,
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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.
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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.
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.
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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
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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
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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.
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.
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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:
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
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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.
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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.
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
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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
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Scientific Review NIOH Endosulfan Study
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.
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
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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.
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.
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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
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.
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Scientific Review NIOH Endosulfan Study
findings of the study in these terms is inconsistent with both the results obtained and the
generally accepted meaning of these terms.
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%.
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
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Scientific Review NIOH Endosulfan Study
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.
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Scientific Review NIOH Endosulfan Study
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.
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.
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Scientific Review NIOH Endosulfan Study
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.
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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.
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). 2010. September 24 Letter Report from P.C.
Yadav (NIOH) to B. Mallesham re: Information Provided under the RTI Act, 2005.
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Scientific Review NIOH Endosulfan Study
Attachment A:
Curricula Vitae
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
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.
Chemicals/Agents
2
Robert P. DeMott, Ph.D., D.A.B.T.
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
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.
public health threat to recreational swimmers. Provided technical comments regarding citys
consideration of ban on pavement sealers for controlling PAHs in waterways.
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
Robert P. DeMott, Ph.D., D.A.B.T.
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
Robert P. DeMott, Ph.D., D.A.B.T.
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.
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.
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
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
Robert P. DeMott, Ph.D., D.A.B.T.
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
Robert P. DeMott, Ph.D., D.A.B.T.
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
Toxicology and Chemistry, November 2010.
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
Robert P. DeMott, Ph.D., D.A.B.T.
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
Toxicology and Chemistry, November 2008.
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
Toxicology and Chemistry, November 2006.
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
Toxicology and Chemistry, November 2006.
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
Environmental Toxicology and Chemistry, November 2006.
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
Robert P. DeMott, Ph.D., D.A.B.T.
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
Environmental Toxicology and Chemistry, November 1998.
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
Robert P. DeMott, Ph.D., D.A.B.T.
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.
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
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.
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).
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.
Hudson River PCBs. Evaluated the hypothesis that anaerobic dechlorination of PCBs
was naturally occurring in Hudson River sediments by examining PCB congener profiles
2
Thomas D. Gauthier, Ph.D.
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.
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.
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
Thomas D. Gauthier, Ph.D.
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.
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.
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.
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.
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.
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.
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.
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
Thomas D. Gauthier, Ph.D.
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.
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.
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.
Vapor Emissions. Modeled historical vapor emissions from a wood treating facility
based on pentachlorophenol and creosote usage rates.
6
Thomas D. Gauthier, Ph.D.
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.
Analysis of Filtered Wood Smoke. Project manager for a patent litigation case involving
the analysis of filtered wood smoke in fish.
Employment History
1999 - 2001 Sciences International Inc., Bradenton, FL, Senior Project Manager
1995 - 1999 Gradient Corporation (an IT Company), Sarasota, FL, Senior Project Manager
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
Thomas D. Gauthier, Ph.D.
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., 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
Thomas D. Gauthier, Ph.D.
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.
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.
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Thomas D. Gauthier, Ph.D.
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., 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
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:
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:
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.
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
PROFESSIONAL ACTIVITIES
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.
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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
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.