27-1. Ex. 1 - Lemly Decl.

Case: 5:17-cv-00292-DCR Doc #: 27-1 Filed: 10/17/17 Page: 1 of 44 - Page ID#: 1040
Exhibit 1
UNITED STATES DISTRICT COURT

EASTERN DISTRICT OF KENTUCKY
CENTRAL DIVISION
AT LEXINGTON
KENTUCKY WATERWAYS ALLIANCE and

SIERRA CLUB, No. 5:17-cv-00292-DCR
Plaintiffs, ELECTRONICALLY FILED

v.
KENTUCKY UTILITIES COMPANY,
Defendant.
DECLARATION OF DR. A. DENNIS LEMLY
I, DR. A. DENNIS LEMLY, declare under penalty of perjury that the following is true and
correct and within my personal knowledge.
1. I submit this declaration in support of Kentucky Waterway Alliance and Sierra Clubs
motion for summary judgment in this case. I am over the age of 18 and am competent to testify
about the following matters. I have personal knowledge of the matters stated herein and, if
called as a witness, would and could competently testify thereto.
I. Introduction
A. Overview
2. I have been retained by Plaintiffs counsel to conduct studies, review information, and
provide my expert opinion and testimony regarding the aquatic ecological hazard and toxic
impact on aquatic life of selenium and other toxins present in Herrington Lake in the vicinity of
Kentucky Utilities E.W. Brown plant as a result of coal ash contamination from the E.W. Brown
site.
1
3. I am qualified as an expert by education, training, and experience in the field of aquatic
pollution related to coal ash and its impacts on living organisms.
4. I specialize in the ecotoxicology of selenium. I have conducted and published numerous
investigations of selenium pollution and its impacts on aquatic ecosystems. Moreover, I am one
of the creators of the established, peer-reviewed protocols for conducting such investigations.
The investigation I conducted for this case is similar to the many I have conducted in the past
and follows the same peer-reviewed protocols that I have used in previous investigations.
5. My professional experience is in fisheries biology. Until my retirement in April 2016, I
held dual appointments as Research Associate Professor of Biology at Wake Forest University
and Research Fisheries Biologist in the United States Forest Service. My position at Wake
Forest University commenced in 2008. My position in the United States Forest Service
commenced in 1991. I also served for six years with the United States Fish and Wildlife Service,
where I held the position of Research Fisheries Biologist.
6. My academic training is in biology. I have a Ph.D. in biology from Wake Forest
University in Winston-Salem, North Carolina.
7. My curriculum vitae and professional qualifications and a list of my publications are
attached to my testimony as Exhibit A.
8. My work for this case consists of two principle components, which I describe in greater
detail in the sections below. First, I conducted an aquatic hazard assessment of Herrington Lake
in the vicinity of the E.W. Brown site, including a review of data from the E.W. Brown site
itself. The purpose of the aquatic hazard assessment was to determine the magnitude of the risk
of poisoning by coal ash pollutants to aquatic life in the vicinity of the E.W. Brown plant.
Second, I conducted a selenium toxicity impact analysis for Herrington Lake in the vicinity of
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the E.W. Brown plant. The purpose of the toxicity impact analysis was to determine the
incidence of population-level impacts of selenium poisoning in fish in the vicinity of the E.W.
Brown site. I conducted these analyses in accordance with published protocols.
9. My findings consist of two principal conclusions. First, the levels of selenium pollution
found in Herrington Lake water, sediments, and benthic organisms, as well as in groundwater at
the E.W. Brown site, exceed the toxic thresholds for fish reproduction and survival. Moreover,
several other toxins, including arsenic, are also present at levels exceeding the high-hazard
threshold for biological effects in fish and wildlife. Second, population-level impacts of
selenium poisoning are occurring in Herrington Lake fish, as confirmed by the incidence of
morphological deformities in juvenile fish. The deformity rate in Herrington Lake is 25 times
greater than the reference condition and was expressed almost exclusively (97% of specimens) as
spinal and craniofacial defects.
10. I have submitted my study of Herrington Lake and E.W. Brown for publication in a
professional journal. It is currently undergoing peer review.
11. In addition to my investigations into aquatic hazard and toxicity impact, I also conducted
reviews of (1) the groundwater monitoring practices and remedial action plans currently in place
at the E.W. Brown site, and (2) the Corrective Action Plan for selenium contamination in
Herrington Lake that has been proposed by Kentucky Utilities. I found significant deficiencies
in both, as further described below.
12. In the remainder of my testimony, I will first discuss selenium and its toxic effects on fish
and aquatic and aquatic-dependent wildlife in general. I will next discuss the results of my
investigations. Finally, I will discuss my reviews of (1) the groundwater monitoring practices
and remedial action plans currently in place at the E.W. Brown site and (2) the Corrective Action
3
Plan for selenium contamination in Herrington Lake that has been proposed by Kentucky
Utilities.
B. Selenium Toxicity
13. Selenium is a well-documented contaminant in coal ash wastewater that is handled,
stored in impoundments, and discharged by coal-fired power plant facilities. 1
14. Although selenium is nutritionally required in small amounts, it is highly toxic in slightly
greater amounts.
15. Selenium stands apart from other coal ash pollutants in that the primary mechanism of
selenium toxicity is through bioaccumulation in the aquatic food chain and dietary uptake by fish
and aquatic life. Bioaccumulation occurs when an organism absorbs a substance at a rate faster
than the rate at which the organism excretes the substance. Once consumed, dietary selenium
readily accumulates in tissues, sometimes to levels several thousand times the ambient
waterborne concentration.
16. Selenium can cause developmental abnormalities and reproductive failure in fish and
wildlife. In fish, this occurs as a result of the transfer of bioaccumulated selenium from parent to
offspring. This transfer occurs in the egg. First, the parent is exposed to selenium through
dietary uptake. The selenium then accumulates in the parents tissue, as well as in the yolk of the
parents eggs. The offspring are exposed to the selenium contained in the yolk, which they
metabolize after hatching.
17. The effects of selenium toxicity in fish offspring are severe. Selenium exposure in the
egg can kill developing embryos before they hatch, or shortly thereafter, and can cause a variety
1
U.S. EPA, Office of Water, Publn No. EPA 822-F-16-005, Aquatic Life Ambient Water Quality Criterion for
Selenium in Freshwater 2016 Fact Sheet (2016).
4
of morphologic deformities in young fish. Once an egg hatches, the yolkand the selenium
contained withinis absorbed into the tissues of the young fish. Once absorbed by the
developing fish, selenium alters the formation of proteins, resulting in distorted and misshaped
bones and other tissues. The skeletal deformities are known as teratogenic deformities. The
toxicity that gives rise to teratogenic deformities is known as teratogenic poisoning.
18. Teratogenic deformities cause increased mortality. Deformities that affect feeding or
respiration can be lethal shortly after hatching. Terata that distort the spine and fins, although
not lethal, can reduce the swimming ability of fish and lead to increased susceptibility to
predation. These two factors generally prevent most deformed individuals from surviving to
adulthood.
19. The toxic potency of selenium is reflected in EPAs recent decision to revise the
freshwater criteria for selenium. In July 2016, EPA revised its freshwater criteria for selenium to
1.5 micrograms per liter (ug/L) for lentic water (i.e. standing water) and 3.1 ug/L for lotic water
(i.e. flowing water). 2 These criteria are much lower 70% lower for lentic water and 38% lower
for lotic water than the agencys previous criterion of 5 ug/L, which the agency issued in 1987.
20. The findings from my research contributed to EPAs revision of the selenium criteria.
Specifically, I conducted coal ash pollution studies in North Carolina demonstrating that
waterborne selenium in concentrations of less than 5 ug/L bioaccumulates in lakes and poisons
fish. 3 Moreover, the bioaccumulation and associated selenium toxicity continued after the
source of coal ash pollution ceased discharging into the lake.
2
Recommended Aquatic Life Ambient Water Quality Criterion for Selenium in Freshwater, 81 Fed. Reg. 45285
(Jul. 13, 2016).
3
A.D. Lemly, Teratogenic effects and monetary cost of selenium poisoning of fish in Lake Sutton, NC, 104
Ecotoxicology and Environmental Safety 160-67 (2014).
5
21. EPAs newly revised criteria point to the fact that selenium is more toxic to aquatic life,
and presents a more serious environmental hazard related to coal ash wastewater, than EPA
previously recognized. More specifically, this means that selenium toxicity in aquatic life occurs
at lower concentrations than EPA previously acknowledged. By the same token, the toxic hazard
to aquatic life that results from very low concentrations of waterborne selenium is substantially
greater than EPA previously acknowledged.
22. Selenium poisoning in fish can be invisible, even as it has a massive impact on the
ecology of a lake. Because the primary point of impact is the egg, adult fish can survive and
appear healthy despite the fact that reproductive failure is occurring. Consequently, fish
populations can decline or even disappear over the course of a few years for no apparent reason.
For example, in Belews Lake, located in North Carolina, fish populations disappeared over the
span of just four years. By the time biologists documented the population impacts of selenium
toxicity, it was too late to prevent the fishery from collapsing. Ultimately, selenium toxicity
resulting from coal ash contamination caused the total elimination of 19 species of fish from
Belews Lake. The species that survived suffered selenium impacts, including teratogenic
deformities.
23. The presence of skeletal deformities in post-swim-up fish, in combination with the
presence of elevated levels of selenium in tissue, is a reliable indicator of selenium toxicity.
Post-swim-up is a distinct life stage. A post-swim-up fish is a fish that has absorbed most or all
of its yolk sac and has begun to swim upwards to emerge from the gravels where it lived during
the period of time immediately after hatching. In post-swim-up fish, teratogenic deformities are
among the most conspicuous and diagnostic symptoms of chronic selenium poisoning. For this
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reason, the established protocols for measuring selenium impacts in fish populations call for
surveying the incidence of teratogenic deformities in young fish.
24. Studies that fail to survey teratogenic deformities in young fish inevitably undercount the
incidence and impact of selenium toxicity. Because the primary impacts of selenium toxicity
occur in embryonic and young fish, any study that focuses on mature fish overlooks the
population impacts of chronic selenium exposure. Moreover, outside factors may contribute to
the replenishment of adult populations, further obscuring the incidence of reproductive failure.
Specifically, fish stocking programs and the migration of fish through open aquatic systems can
bolster populations of mature fish, thereby concealing the effects of selenium toxicity even as
mortality among young fish may be rising.
II. Research Findings at E.W. Brown
A. Aquatic Hazard Assessment
25. I analyzed the aquatic hazard related to the presence of coal ash pollutants in Herrington
Lake in the vicinity of the E.W. Brown plant and at the E.W. Brown site itself. Contamination of
water bodies by coal ash pollutants creates a toxic hazard to fish and other aquatic life. The
purpose of the aquatic hazard assessment was to determine the magnitude of the risk to aquatic
life of poisoning by coal ash pollutants. My analysis followed published protocols for aquatic
hazard assessment. 4
26. My conclusions are based upon my review of pollutant concentration data for 15 primary
coal ash pollutants measured in Herrington Lake surface water, sediments, and benthic
organisms, as well as in groundwater collected from the E.W. Brown site. The pollutants
4
A.D. Lemly, A protocol for aquatic hazard assessment of selenium, 32 Ecotoxicology and Environmental Safety
280-88 (1995).
7
reviewed here were arsenic, barium, cadmium, chromium, cobalt, copper, lead, manganese,
mercury, nickel, selenium, silver, thallium, vanadium, and zinc.
27. Data for Herrington Lake came from laboratory analysis of surface water, sediment, and
benthic macroinvertebrate samples. Sample collection was performed by a contractor retained
by Plaintiffs counsel. Samples were collected from Herrington Lake in the vicinity of the E.W.
Brown plant according to a protocol that I designed in collaboration with the contractor, and
which I ultimately approved. Groundwater data for the E.W. Brown site came from laboratory
analysis reported to the Kentucky Division of Waste Management by Kentucky Utilities. These
data are found in the Sitewide Groundwater Remedial Action Plan 5 and the Groundwater
Assessment Report Update. 6
28. I evaluated the aquatic ecological hazard of coal ash pollutants by comparing measured
concentrations to toxic threshold values and biological effects criteria for aquatic life and aquatic
dependent wildlife. Toxic threshold values are the lowest concentrations of a pollutant that
cause physiological damage or mortality of an aquatic organism. Biological effects criteria are
guidelines and standards used to protect aquatic life from potential harm, and are generally in
close agreement with toxic threshold values. Because EPA and states have not established
effects criteria for wildlife, I relied on peer-reviewed scientific literature for wildlife toxicity
information and guidance. For aquatic life, I used either EPA surface water quality criteria,
values provided in the peer-reviewed scientific literature, or criteria for surface water,
groundwater, or sediment adopted by the State of Kentucky or the State of Washington. In
5
Amec Foster Wheeler Envt & Infrastructure, Inc., Sitewide Groundwater Remedial Action Plan (2015). This
report was filed with the Court by Kentucky Utilities Company as Exhibit 1 to the Companys motion to dismiss.
6
Amec Foster Wheeler Envt & Infrastructure, Inc., Groundwater Assessment Report Update (2015).
8
instances where multiple standards exist, I chose to use the most restrictive standard. The toxic
threshold values appear in Table 1.
Table 1. Chemical concentrations used as toxicity criteria to establish hazard ratings.
Element Concentrationa Required for Hazard Level Rating
and Source Highb Moderate Low Minimal None Data Sourcec
Arsenic, waterd 150 75 37 18 <18 USEPA 2014 7
sediment 14 7 3.5 1 <1 WDE 2014 8
Cadmium, water 0.25 0.125 0.0625 0.03 <0.03 USEPA 2014
sediment 2.1 1.05 0.525 0.2 <0.2 WDE 2014
Chromium, water 11 5.5 2.75 1 <1 USEPA 2014
sediment 72 36 18 4 <4 WDE 2014
Cobalt, sediment 50 25 12.5 6.25 <6.25 USEPA 2015a9
Copper, water 1.45 0.725 0.3625 0.25 <0.25 USEPA 2014
sediment 32 USEPA 2015a
Lead, water 2.5 1.25 0.625 0.2 <0.2 USEPA 2014
sediment 36 USEPA 2015a
Manganese, sediment 920 460 230 115 <115 USEPA 2015a
Mercury, water 0.77 0.385 0.1925 0.05 <0.05 USEPA 2014
sediment 0.41 0.205 0.1025 0.05 <0.05 WDE 2014
Nickel, water 8.2 4.1 2.05 1 <1 USEPA 2014
sediment 26 13 6.5 1 <1 WDE 2014
7
U.S. EPA, National Recommended Water Quality Criteria (2014).
8
Washington Dept of Ecology, Sediment Benthic Marine Chemical Criteria (2014).
9
U.S. EPA, Region 4, Region 4 Ecological Risk Assessment Supplemental Guidance Interim Draft (2015).
9
Selenium, water 2 1 0..5 0.25 <0.25 USEPA 2016 10
sediment 2 1 0.5 0.2 <0.2 Lemly 1993, 2002a 11
tissue* 3 1.5 0.75 0.37 <0.37 Lemly 1993, 2002a
Silver, water 3.2 1.6 0.8 0.4 <0.4 USEPA 2014
sediment 0.57 0.285 0.1425 0.07 <0.07 WDE 2014
Thallium, water 20 10 5 1 <1 USEPA 1980 12
sediment NC
Zinc, water 120 60 30 15 <15 USEPA 2014
sediment 410 205 102.5 50 <50 WDE 2014
aConcentrations in ug/L (parts-per-billion) for water, ug/g dw (parts per million, dry weight) for
sediments.
bWater numbers for high hazard level are freshwater aquatic life acute and chronic toxicity values and
maximum acceptable criterion levels given by USEPA 2014, 2016, derived from W.A. Hopkins wildlife
toxicology laboratory studies and publications, or taken from other scientific literature sources cited in
the references. Sediment numbers for high hazard use values from State of Washington 2014, USEPA
2015a, and Lemly 1993, 2002a.
cData sources are given in references.
dAll water concentration values refer to surface water.
eNo criterion for sediments has been established for this element by either USEPA or WDE; no sediment
toxicity value is available from other scientific literature sources.
*Tissue concentrations are for food items of fish and wildlife, for example, benthic invertebrates.
29. I assigned hazard ratings to each pollutant. The hazard rating is a measure of toxic risk
associated with a given pollutant. Ratings are based on the relationship between measured
10
U.S. EPA, Office of Water, Publn No. EPA 822-F-16-005, Aquatic Life Ambient Water Quality Criterion for
Selenium in Freshwater 2016 Fact Sheet (2016).
11
A.D. Lemly, Guidelines for evaluating selenium data from aquatic monitoring and assessment studies, 28
Environmental Monitoring and Assessment 83-100 (1993); A.D. Lemly, Symptoms and implications of selenium
toxicity in fish: The Belews Lake case example, 57 Aquatic Toxicology 39-49 (2002).
12
U.S. EPA, Office of Water, Publn No. EPA-440/5-80-074, Ambient Water Quality Criteria for Thallium (1980).
10
chemical concentrations and demonstrated toxic effects in fish and other aquatic life, and
aquatic-dependent wildlife such as crayfish, frogs, toads, salamanders, turtles, waterfowl,
insectivorous and fish-eating birds. The measured chemical concentrations used in this protocol
are the maximum concentrations observed in the dataas opposed to average concentrations.
This is consistent with the real-world exposure scenarios of fish and wildlife in coal ash polluted
ecosystems. The ratings are reflective of both waterborne and dietary exposure, and of both
acute and chronic duration.
30. Five degrees of hazard are possible: high, moderate, low, minimal, and none. High
hazard indicates that pollutant concentrations equal or exceed acute or chronic toxic levels.
Moderate hazard indicates that pollutant concentrations equal or exceed one-half of the chronic
toxic levels. Minimal hazard indicates that pollutant concentrations are elevated above
background or reference conditions in unpolluted habitats but do not reach one-fourth of the
chronic toxic levels. No hazard indicates that concentrations are not elevated above background
or reference water quality conditions. The hazard ratings appear in Table 2.
Table 2. Maximum concentrationa of contaminants measured in surface water (S), groundwater (G),
and sediments at E.W Brown Generating Station and/or receiving waters (Herrington Lake), and
corresponding hazard ratings.
Element and Measured Hazard Rating Data Sourceb
Source Concentration High Moderate Low Minimal None
Arsenic, S-water 340 X L
G-water >150 X KU
sediment 180 X L
Cadmium, S-water <0.03 X L
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G-water <5 X KU
sediment 5 X L
Chromium, S-water 2.5 X KU
G-water 2.5 X KU
sediment 36 X L
Cobalt, sediment 21 X L
Copper, S-water 42 X KU
G-water >42 X KU
sediment 37 X L
Lead, S-water 15 X KU
G-water 2 X KU
sediment 38 X L
Manganese, sediment 3,500 X L
Mercury, S-water <0.2 X KU
G-water <0.2 X KU
sediment NM
Nickel, S-water 20 X L
G-water NM
sediment 22 X L
Selenium, S-water 50 X KU
G-water >50 X KU
sediment 15 X L
tissued 28 X L
Silver, S-water <.01 X L
G-water NM
sediment 0.05 X L
Thallium, S-water 2.3 X KU

12
G-water NM
sediment NM L
Zinc, S-water 7 X L
G-water NM
sediment 41 X L
aConcentrations in ug/L for water, ug/g dw (dry weight) for sediments.
bL = data collected for Lemly studies by Plaintiffs contractor; KU = data collected for Kentucky Utilities
studies by Kentucky Utilities contractor.
cNot measured. dBenthic macroinvertebrates.
31. First, I will discuss the results of the hazard rating as applied to surface water. The high
hazard pollutants in Herrington Lake surface water are arsenic, copper, lead, nickel, and
selenium. These pollutants were measured at concentrations four to fifty times greater than the
toxic threshold. At such levels, direct waterborne exposure to these pollutants would be
expected to cause poisoning in a wide range of animals including fish, amphibians, crustaceans,
mollusks, insects, and worms. Many of these animals have been shown to be present in the
discharge areas and downstream receiving waters, or would be expected to be present according
to species distribution data. Consequently, waterborne chemical poisoning of aquatic life is
highly probable.
32. Next, I will discuss the results of the hazard rating as applied to groundwater data from
the E.W. Brown site. The high hazard elements found in groundwater collected at the E.W.
Brown site are arsenic, copper, and selenium. Direct waterborne exposure to these pollutants
would occur once the groundwater discharges to surface waters. Selenium was measured at
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levels greater than 25 times the toxic threshold for bioaccumulation in aquatic food chains and
tissue. Moreover, exposure to copper in the concentration observed here (> 42 ug/L) is known to
be fatal to a wide variety of aquatic organisms within only 48 to 96 hours. Consequently, the
polluted groundwater at the E.W. Brown site poses a significant threat to aquatic life when it
contacts surface waters.
33. Next, I will discuss the results of the hazard rating as applied to Herrington Lake
sediment data. The high hazard pollutants in Herrington Lake sediments are arsenic, nickel, and
selenium. Sediments are an important route by which fish and wildlife are exposed to coal ash
pollutants. Coal ash pollutants tend to become concentrated in sediments and the interstitial pore
water and overlying boundary layer. As a result, benthic organisms, which reside in the
sediment, are exposed to levels of pollutants that are much greater than in the open water column
above. Moreover, the coal ash pollutants are known to persist in sediments. As a result, benthic
organisms may experience prolonged exposure. These organisms typically include certain fish,
such as suckers, catfish, and darters; amphibians, such as frogs, toads, and salamanders;
crustaceans, such amphipods and crayfish; mollusks, such as clams, mussels, and snails; and
insects and worms.
34. Selenium levels in the sediment are especially concerning. Selenium was measured at
concentrations 15 times greater than the threshold for toxic bioaccumulation in aquatic life. This
is an extremely high level of contamination and it conveys an extremely high level of biological
hazard. I have observed significant biological effects resulting from exposure to selenium at
similar sediment concentrations at several other field sites in the southeastern United States.
Those effects ranged from subtle morphological abnormalities to complete population collapse.
14
35. Next, I will discuss the results of the hazard rating as applied to tissue data for benthic
organisms collected from Herrington Lake. The high hazard pollutants found in Herrington Lake
biological tissues are arsenic and selenium. Arsenic, in the concentration measured here (162
ug/g), is known to cause chronic poisoning in fish. Selenium, in the concentration measured here
(28 ug/g), is known to cause fish mortality and reproductive failure. Because benthic organisms
constitute an element in the aquatic food chain, they are a source of dietary uptake of selenium
for fish. Given the levels of sediment and aquatic food chain selenium reported in Herrington
Lake, concentration data alone strongly suggest that Herrington Lake fish are undergoing
chemical poisoning as the result of coal ash pollution.
36. In sum, my aquatic hazard assessment demonstrates that coal ash contaminants from
E.W. Brown are present in Herrington Lake surface waters, sediments, and benthic organisms, as
well as in groundwater at the E.W. Brown site, at levels sufficient to poison fish and wildlife.
Moreover, selenium levels in benthic organisms are sufficiently high to cause dietary toxicity
and reproductive impairment in fish.
B. Selenium Toxicity Impact Analysis
37. I conducted a selenium toxicity impact analysis for Herrington Lake fish in the vicinity of
the E.W. Brown plant. The research described in the preceding section established that selenium
concentrations in surface water, sediments, benthic organisms, and groundwater exceed
diagnostic toxic levels for fish. The purpose of the toxicity impact analysis was to determine if
selenium impacts are actually occurring. My analysis followed published protocols for selenium
toxicity impact analysis. 13
13
A.D. Lemly, A teratogenic deformity index for evaluating impacts of selenium on fish populations, 37
Ecotoxicology and Environmental Safety 259-266 (1997); A.D. Lemly, Teratogenic effects of selenium in natural
populations of freshwater fish, 26 Ecotoxicology and Environmental Safety 181-204 (1993).
15
38. My conclusions are based on my examination of specimens of young fish for the
presence of morphological abnormalities that are diagnostic indicators of selenium poisoning.
The specimens examined were young-of-the-year largemouth bass (Micropterus salmoides,
family Centrarchidae) within the range of 2.5 to 5 centimeters in length. Specimens did not
include other ecologically and recreationally important species, such as bluegill, crappie, carp,
catfish, white bass, and striped bass. Specimen collection was performed by a contractor
retained by Plaintiffs counsel. Specimens were collected from Herrington Lake in the vicinity
of the E.W. Brown plant according to a protocol that I designed in collaboration with the
contractor, and which I ultimately approved. Specimens were preserved in denatured alcohol.
39. I examined a total of 548 specimens under magnification. I noted and recorded physical
abnormalities, and I photographed individual specimens exhibiting representative abnormalities.
Further, I compared the observed rate of deformity with published reference values for young-of-
the-year largemouth bass and other Centrarchidae obtained from High Rock Lake, located in
Davidson County, North Carolina. High Rock Lake does not have elevated selenium levels. In
addition, I sent a subset of specimens (six composite samples of three to five individual fish per
sample) to a certified commercial analytical chemistry laboratory for measurement of whole-
body selenium concentration in order to compare body burdens to known toxic levels and
determine if selenium levels were commensurate with the incidence of terata. Finally, I cross-
referenced observed deformity rates with a Teratogenic Deformity Index, per published protocols
in order to estimate mortality and population-level impacts. 14
14
See A.D. Lemly, Teratogenic effects and monetary cost of selenium poisoning of fish in Lake Sutton, North
Carolina, 104 Ecotoxicology and Environmental Safety 160-167 (2014).
16
40. The results of my examination are as follows. Of 548 fish, 67 (12.2%) exhibited
abnormalities. The abnormalities observed were spinal deformities (49), craniofacial deformities
(16), and fin deformities (2). Eight fish exhibited multiple deformities. Photographs of
representative specimens appear in Figures 1 through 19.
17
Figure 1. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016

from Herrington Lake. The top individual exhibits a condition known as lordosis, or concave
curvature of the lumbar region of the spine. This condition is a common teratogenic deformity
caused by selenium poisoning. The bottom individual is normal.
18

from Herrington Lake. The top individual has a compressed, shortened head and deformed gill
cover. It also exhibits a condition known as pugnose, which is a deformity of the jaws and
anterior portion of the skull. These conditions are common teratogenic deformities caused by
selenium poisoning. The bottom individual is normal.
19

from Herrington Lake. The top individual exhibits lateral curvature of the spine, a condition
known as scoliosis. This condition is a common teratogenic deformity caused by selenium
poisoning. The bottom individual is normal.
20

from Herrington Lake. The top individual has multiple abnormalities. It has a deformed caudal
(tail) fin and also has a compressed, shortened head and deformed gill cover. These conditions
are common teratogenic deformities caused by selenium poisoning. Eight of the 67 abnormal
fish identified in Herrington Lake samples exhibited multiple malformations. The bottom
individual is normal.
21

22

23

24

25

26
27
28
29
30
31
32
33
34
35
36
41. The morphological defects observed are strikingly distinct from reference values, both in
frequency and type. The observed rate of morphological abnormality in Herrington Lake
specimens was 25 times greater than reference value. Further, whereas the abnormalities present
in the reference case are only minor fin deformities, the deformities observed in the Herrington
Lake specimens were almost exclusively (97%) spinal and craniofacial defects.
42. Fish tissue concentrations of selenium provide additional confirmation of selenium
toxicity. Measured concentrations uniformly exceeded the toxic threshold for fish mortality and
reproductive failure.
43. Finally, applying the Teratogenic Deformity Index method yielded a conservatively
estimated rate of teratogenic mortality of 3.05%. This value represents the percentage of all
juvenile largemouth bass that are likely to express a lethal teratogenic deformity. These are
generally severe deformities of the spine and craniofacial structure that endanger fish by
impairing swimming and feeding. Other, less severe deformities, such as slight skeletal and fin
abnormalities, may be sublethal. A teratogenic mortality rate of 3.05% is categorized as a Level
1 Teratogenic Deformity Index rating, meaning that population collapse and elimination of bass
due to terata alone would not be expected.
44. However, pre-swim-up mortality would be expected to far exceed estimated teratogenic
mortality. Estimated teratogenic mortality does not take into account embryo mortality and pre-
swim-up mortality. These two values can collectively range from 25% to 100% for individual
spawns when the selenium concentration in the spawning habitat is at levels similar to the
maximum selenium concentrations reported in Herrington Lake. A conservatively estimated
mortality rate that takes into account teratogenic mortality, embryo mortality, and pre-swim-up
37
mortality would be in the range of 25% of the total largemouth bass population. It is likely that
site-specific mortality rates could far exceed that.
45. In sum, the selenium toxicity impact assessment confirms that selenium poisoning is
taking place in Herrington Lake in the vicinity of the E.W. Brown plant. This conclusion is
supported both by the occurrence of morphological abnormalities that are indicators of selenium
toxicity and the measurement of selenium concentrations in fish tissue in excess of the biological
effects threshold. Because selenium is closely associated with coal ash, it appears highly likely
that the selenium poisoning documented here is the result of coal ash contamination emanating
from E.W. Brown.
III. Flaws in Kentucky Utilities Groundwater Assessment and Remedial Action Plan
46. In the course of my work on this case, I identified a significant deficiency in the analyses
relied upon by Kentucky Utilities in its Sitewide Groundwater Remedial Action Plan 15 and
Groundwater Assessment Report Update. 16 Specifically, the analyses rely upon toxicity
thresholds that are too high to protect against environmental impacts. This technical flaw
invalidates the reports conclusions about pollutant concentrations and associated environmental
hazard.
47. The toxicity thresholds used in the Kentucky Utilities studies are problematic because
they are not protective of fish and wildlife. The toxicity thresholds used in the studies are
Maximum Concentration Limit (MCL) and Action Level (AL), which are designated by EPA.
The purpose of EPAs thresholds is to protect human health from exposure to contaminants in
drinking water. However, this mechanism of toxicity to humans is quite different from those
15
Amec Foster Wheeler Envt & Infrastructure, Inc., Sitewide Groundwater Remedial Action Plan (2015). This
report was filed with the Court by Kentucky Utilities Company as Exhibit 1 to the Companys motion to dismiss.
16
Amec Foster Wheeler Envt & Infrastructure, Inc., Groundwater Assessment Report Update (2015).
38
contemplated in my studies. My studies, which focus on impacts on fish and wildlife, take into
account the distinct sensitivities of fish and wildlife, as well as additional exposure routesboth
dietary and waterborne. Thus, for example, while the water quality criterion for human
consumption of waterborne selenium is 50 ug/L, my studies rely upon the toxic threshold for
wildlife, which is only 2 ug/L.
48. The harm in relying on these inflated thresholds is that the studies underreport toxicity
risks and set inappropriate standards for measuring corrective action. In short, the water quality
criteria employed in the Kentucky Utilities studies are too high to protect aquatic life and
wildlife from toxic impacts.
IV. Flaws in Kentucky Utilities Corrective Action Plan for Selenium in Herrington
Lake
49. I reviewed the Corrective Action Plan for selenium in Herrington Lake that was proposed
by Kentucky Utilities. 17 Based on my review, the studies proposed in the Corrective Action Plan
are unnecessary because available information already answers the questions posed in the
Corrective Action Plan. More specifically, available information already demonstrates the
ecological risk and actual toxic impacts of selenium contamination in Herrington Lake. Thus,
the appropriate step at this juncture would be to proceed to determining and implementing
remedial actions. Further, even if further studies of the extent of contamination are necessary
(which I do not believe they are), Kentucky Utilities proposed studies are incorrectly designed
because they fail to take into account selenium bioaccumulation.
50. At the outset, although I generally welcome any endeavor to collect additional data on
selenium contamination in Herrington Lake, the Corrective Action Plan represents a misplaced
17
Ramboll Environ, Herrington Lake Corrective Action Plan, Mercer County, Kentucky (Aug. 2017).
39
investment of time and resources, and one that unnecessarily puts off, to the detriment of the
ecological health of the Lake, remedial action that is needed now. Sufficient data already exist to
definitively state that (1) Herrington Lake in the vicinity of E.W. Brown is contaminated with
selenium at levels exceeding the toxic thresholds for fish reproduction and survival, and (2) fish
populations are already experiencing toxic impacts of selenium poisoning, as evidenced by the
occurrence of teratogenic deformity associated with exposure to selenium from coal ash. The
studies proposed in the Corrective Action Plan would serve only to waste time while collecting
redundant data. Therefore, the appropriate next step is to evaluate options for the remediation of
Herrington Lake and the E.W. Brown site. Presently, this step is scheduled to take place in late-
2019, after the conclusion of the studies proposed in the Corrective Action Plan. Given that
those studies are not needed, it would be appropriate to advance directly to determining and
implementing remedial actions without additional (and harmful) delay.
51. Further, I have serious concerns about the methods proposed in the Corrective Action
Plan. Specifically, the methods fail to take into account selenium bioaccumulation as a pathway
of selenium toxicity, even though it is well established that bioaccumulation is the principal
pathway of selenium toxicity in fish and wildlife. Instead, the Corrective Action Plan appears to
regard selenium as equivalent to other coal ash pollutants, whose toxicity occurs primarily
through waterborne exposure. As a result, the ecological risk assessment proposed in the
Corrective Action Plan is ill-equipped to accurately assess ecological risk. Below, I briefly list
several, non-exhaustive specific examples in which the Corrective Action Plan fails to account
for selenium bioaccumulation.
52. First, the Corrective Action Plan fails to propose examination of young fish specimens
for evidence of teratogenic deformity. In post-swim-up fish, teratogenic deformities are among
40
the most conspicuous and diagnostic symptoms of chronic selenium poisoning. The presence of
skeletal deformities in post-swim-up fish, in combination with the presence of elevated levels of
selenium in tissue, is a reliable indicator of selenium toxicity. Therefore, the failure to propose a
study of teratogenic deformity seriously compromises the Corrective Action Plans ability to
accurately assess the ecological impact of selenium toxicity.
53. Second, the Corrective Action Plan fails to explain the method for determining
Ecological Screening Values. The Corrective Action Plan calls for the use of Ecological
Screening Values in order to characterize risk of ecological effects of exposure to pollutants, but
does not specify how those values will be determined. This lack of information leaves
considerable uncertainty as to whether the values will accurately take into account the
sensitivities and exposure pathways that are relevant for fish and wildlife. More specifically, it
leaves open the critical question of whether the values will take into account selenium
bioaccumulation. It is well established that toxic threshold values for bioaccumulated selenium
differ considerably from toxic threshold values for waterborne selenium. The Corrective Action
Plans failure to address this point raises serious doubts as to whether it accounts for selenium
bioaccumulation.
54. Third, the Corrective Action Plan misguidedly relies on hazard quotients that fail to take
into account bioaccumulation. The hazard quotients are intended for use when evaluating food
web exposures. However, they are an inaccurate indicator for selenium because they are
calculated on the basis of pollutant concentrations in water. Because selenium bioaccumulates in
the food chain, calculations based on concentrations in water do not fully depict ecological
exposure.
41
55. Fourth, the proposed scheme for sample collection leaves out critical information that
bears upon the diagnostic value of the samples collected. More specifically, the Corrective
Action Plan fails to specify the timing of ovary sample collection. The timing of sample
collection is important because selenium levels are greater in mature eggs than in immature eggs.
Thus, a sampling of immature eggs will undercount actual levels of selenium loading.
56. Fifth, the proposed scheme for sample collection fails to adequately monitor the
downstream effects of coal ash pollution from the E.W. Brown site. The downstream proximity
of the Dix River to the E.W. Brown site makes it a likely destination for selenium and other coal
ash pollutants that are discharged from the E.W. Brown site. Yet, sample collection on the Dix
River is proposed at only a single transect, fairly close to the Dix Dam. This is inadequate for
purposes of measuring the downstream reach of selenium contamination. Moreover, this
proposal stands in stark contrast with the proposed sample collection program for Herrington
Lake, which contemplates collecting samples as far as 28 miles upstream of the E.W. Brown site.
This asymmetry requires correction.
57. Sixth, the Corrective Action Plan fails to reduce the harmful ongoing selenium loading in
Herrington Lake. The Corrective Action Plan asserts that remedial actions already in place at the
E.W. Brown site will limit selenium and other metal loading to Herrington Lake. But this
claim is not supported by the descriptions of remedial measures, none of which reduce the actual
mass of selenium that is present in the ash pond contamination that enters Herrington Lake.
58. In sum, in light of the foregoing significant deficiencies, I have serious reservations about
the Corrective Action Plan. The studies proposed in the Corrective Action Plan are not needed
because available information already establishes that Herrington Lake is contaminated with
selenium from the E.W. Brown site and fish populations are already experiencing toxic impacts
42
of selenium poisoning. Moreover, every additional week and month of delay continues to hann
and to pose further risks to the ecological health of the Lake. Therefore, instead of pursuing the
proposed studies and unnecessarily delaying much-needed action, it is appropriate to proceed
directly to identification and implementation of remedial actions. Further, assuming the studies
proposed in the Corrective Action Plan are needed, they are ineffectively des igned because,
among other reasons, they fail to take into account the well-established fact that the primary
pathway of selenium toxicity is through bioaccumulation.
I declare under penalty of perjury that the foregoing is true and correct to the best of my
knowledge and that this declaration was executed under the laws of the United States.
Dated this~ day of October, 2017.
43

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Case: 5:17-cv-00292-DCR Doc #: 27-1 Filed: 10/17/17 Page: 1 of 44 - Page ID#: 1040

UNITED STATES DISTRICT COURT

KENTUCKY WATERWAYS ALLIANCE and

Plaintiffs, ELECTRONICALLY FILED

KENTUCKY UTILITIES COMPANY,

DECLARATION OF DR. A. DENNIS LEMLY

correct and within my personal knowledge.

called as a witness, would and could competently testify thereto.

3. I am qualified as an expert by education, training, and experience in the field of aquatic

pollution related to coal ash and its impacts on living organisms.

4. I specialize in the ecotoxicology of selenium. I have conducted and published numerous

5. My professional experience is in fisheries biology. Until my retirement in April 2016, I

where I held the position of Research Fisheries Biologist.

6. My academic training is in biology. I have a Ph.D. in biology from Wake Forest

University in Winston-Salem, North Carolina.

7. My curriculum vitae and professional qualifications and a list of my publications are

attached to my testimony as Exhibit A.

Brown site. I conducted these analyses in accordance with published protocols.

spinal and craniofacial defects.

professional journal. It is currently undergoing peer review.

in both, as further described below.

13. Selenium is a well-documented contaminant in coal ash wastewater that is handled,

stored in impoundments, and discharged by coal-fired power plant facilities. 1

metabolize after hatching.

toxicity that gives rise to teratogenic deformities is known as teratogenic poisoning.

source of coal ash pollution ceased discharging into the lake.

greater than EPA previously acknowledged.

presence of elevated levels of selenium in tissue, is a reliable indicator of selenium toxicity.

surveying the incidence of teratogenic deformities in young fish.

mortality among young fish may be rising.

II. Research Findings at E.W. Brown

A. Aquatic Hazard Assessment

mercury, nickel, selenium, silver, thallium, vanadium, and zinc.

benthic macroinvertebrate samples. Sample collection was performed by a contractor retained

Assessment Report Update. 6

groundwater, or sediment adopted by the State of Kentucky or the State of Washington. In

threshold values appear in Table 1.

Table 1. Chemical concentrations used as toxicity criteria to establish hazard ratings.

Element Concentrationa Required for Hazard Level Rating

and Source Highb Moderate Low Minimal None Data Sourcec

Arsenic, waterd 150 75 37 18 <18 USEPA 2014 7

sediment 14 7 3.5 1 <1 WDE 2014 8

Cadmium, water 0.25 0.125 0.0625 0.03 <0.03 USEPA 2014

sediment 2.1 1.05 0.525 0.2 <0.2 WDE 2014

Chromium, water 11 5.5 2.75 1 <1 USEPA 2014

sediment 72 36 18 4 <4 WDE 2014

Cobalt, sediment 50 25 12.5 6.25 <6.25 USEPA 2015a9

Copper, water 1.45 0.725 0.3625 0.25 <0.25 USEPA 2014

sediment 32 USEPA 2015a

Lead, water 2.5 1.25 0.625 0.2 <0.2 USEPA 2014

sediment 36 USEPA 2015a

Manganese, sediment 920 460 230 115 <115 USEPA 2015a

Mercury, water 0.77 0.385 0.1925 0.05 <0.05 USEPA 2014

sediment 0.41 0.205 0.1025 0.05 <0.05 WDE 2014

Nickel, water 8.2 4.1 2.05 1 <1 USEPA 2014

sediment 26 13 6.5 1 <1 WDE 2014

Selenium, water 2 1 0..5 0.25 <0.25 USEPA 2016 10

sediment 2 1 0.5 0.2 <0.2 Lemly 1993, 2002a 11

tissue* 3 1.5 0.75 0.37 <0.37 Lemly 1993, 2002a

Silver, water 3.2 1.6 0.8 0.4 <0.4 USEPA 2014

sediment 0.57 0.285 0.1425 0.07 <0.07 WDE 2014

Thallium, water 20 10 5 1 <1 USEPA 1980 12

Zinc, water 120 60 30 15 <15 USEPA 2014

sediment 410 205 102.5 50 <50 WDE 2014