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Exhibit 1
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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.

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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
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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).
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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).
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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).
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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).
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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).
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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).
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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


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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.

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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).
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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).
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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.

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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.

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Figure 2. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016


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.

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Figure 3. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016


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.

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Figure 4. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016


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
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Figure 5. 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.

22
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Figure 6. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016


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.

23
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Figure 7. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016


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.

24
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Figure 8. 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.

25
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Figure 9. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016


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.

26
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Figure 10. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

27
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Figure 11. 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.

28
Case: 5:17-cv-00292-DCR Doc #: 27-1 Filed: 10/17/17 Page: 30 of 44 - Page ID#: 1069

Figure 12. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

29
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Figure 13. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

30
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Figure 14. 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.

31
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Figure 15. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

32
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Figure 16. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

33
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Figure 17. 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.

34
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Figure 18. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

35
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Figure 19. Young-of-the-year largemouth bass (Micropterus salmoides) collected in June 2016
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.

36
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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

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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).
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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
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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
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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.

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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
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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