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COMMONWEALTH OF MASSACHUSETTS

EXECUTIVE OFFICE OF ENERGY AND ENVIRONMENTAL AFFAIRS


MASSACHUSETTS DEPARTMENT OF ENVIRONMENTAL PROTECTION

THE OFFICE OF APPEALS AND DISPUTE RESOLUTION

____________________________________
)
In the Matter of ) OADR Docket Nos. 2019-008, 2019-009,
) 2019-010, 2019-011, 2019-012 and 2019-013
) DEP File No.: Application No. SE-15-27
) No. X266786 Air Quality Plan Approval
) Weymouth, MA
Algonquin Gas Transmission, LLC )
____________________________________)

PRE-FILED TESTIMONY OF PETER A. VALBERG

Health Risk Assessment Qualifications

I, Peter A. Valberg, hereby state as follows:

1. My name is Peter Valberg, and I am a public health professional specializing in

inhalation toxicology, health risk assessment, and evaluation of relative risks. For 23 years I was

a faculty member in the Department of Environmental Health of the Harvard School of Public

Health (HSPH) in Boston, Massachusetts. I am currently a Principal and Health Scientist at

Gradient, an environmental consulting firm based in Cambridge, Massachusetts.

2. I am the author of over 100 articles in peer-reviewed journals, plus many

additional reports and abstracts dealing with lung biology, inhalation toxicology, and risk

assessment.

3. My curriculum vitae (CV) is attached to this testimony as Exhibit A, and it

describes more fully my credentials and lists my publications.


4. I have a Ph.D. degree in physics and a M.S. degree in human physiology, both

from Harvard University. In addition, I received postdoctoral training in alveolar macrophage

function (National Heart, Lung, and Blood Institute), pulmonary pathology (University of

Vermont Lung Center), analytical and quantitative microscopy (Woods Hole Marine Biological

Laboratory), and advanced quantitative health risk assessment (University of Cincinnati).

5. I have held the following academic research and training awards: Atomic Energy

Commission Fellow, Cottrell Research Corporation Science Grant, National Science Foundation

Fellow, National Institutes of Health New Investigator Pulmonary Research Award, and Andrew

W. Mellon Foundation Faculty Award.

6. I was appointed to the HSPH faculty in 1977 and promoted to Associate Professor

of Physiology in 1985. I directed and participated in research programs funded by the National

Institutes of Health. My research topics included: studies of lung function and dysfunction; the

reaction of lung cells to inhaled materials; and the deposition, clearance, and retention of

aerosols inhaled into the lungs. As a faculty member in the Department of Environmental

Health, I participated in the teaching of courses not only at Harvard’s School of Public Health,

but also at Harvard College, Harvard Medical School, Massachusetts Institute of Technology,

and Tufts University. I participated in and taught graduate and undergraduate courses on human

physiology, cell biology, airborne particles, and inhalation toxicology.

7. During the time I was a faculty member at HSPH, I was invited to be a visiting

scientist on two occasions at other institutions. In 1982, I was a Visiting Scientist at the

Inhalation Toxicology Research Institute (ITRI) in Albuquerque, NM. At ITRI, I designed and

coordinated animal research that tracked the fate of substances inhaled into the lungs. In 1989, I

was a Visiting Researcher at the Institute of Occupational Medicine in Helsinki, Finland. There,

2
I participated in research on human subjects that examined the condition of their lung cells, as

recovered by a lung lavage procedure. Throughout my research, teaching, and consulting career,

I have been engaged in studying the mechanisms by which and the doses at which chemicals in

our environment affect human health.

8. I have served in an advisory capacity to a wide variety of governmental

organizations concerned with health. These include the National Institutes of Health (NIH), the

Office of Health and Environmental Research (Department of Energy), the National Academy of

Sciences, the US Navy Office of Occupational Health and Preventive Medicine, the US

Department of Transportation, the US Environmental Protection Agency (US EPA), the NIH

Division of Research Grants, and the World Health Organization (WHO). I also have been an

advisor to the Health Effects Institute (HEI) and the American Conference of Governmental

Industrial Hygienists (ACGIH).

9. In my consulting work at Gradient, I have provided health risk analyses to a

variety of parties, including government and industry. Health risk analyses that I’ve completed

have focused on the health effects of environmental chemicals, air toxics, volatile organic

compounds (VOCs), and inhaled particulate matter (PM). I am an expert in human health risk

assessment, toxicology, and public health. Examples of completed projects include serving as an

expert for the USDOJ Environmental Enforcement Section in air quality cases, preparing toxicity

profiles for US EPA for the noncancer health effects of the 189 Hazardous Air Pollutants

(HAPs), analyzing diesel-exhaust health-risk data, and investigating mechanisms of action for

environmental exposures to ozone, particulates, and electromagnetic radiation.

PURPOSE OF MY TESTIMONY

10. I am testifying on behalf of Algonquin Gas Transmission (AGT), and I have been

asked to support the Air Quality Plan Approval (AQPA) by explaining the scientific basis for

3
health-protective air quality guidelines developed by public health agencies, and specifically

point out the margin of safety built into MassDEP’s AALs and TELs.

PRINCIPLES OF AND PERSPECTIVES ON HUMAN HEALTH RISK ASSESSMENT

11. The term “risk” is susceptible to different interpretations, and it is important to

define what it means in the context of the multitude of factors that affect our health. Our life and

health are constantly at risk. Risks to life and health are never zero and our lives cannot be made

risk-free. As described in Exhibit B, background risks to life and health are ever present.

12. Our bodies, everyday objects, and the food we eat are made up of chemicals.

Because our ability to analyze for tiny quantities of chemicals has vastly improved over time,

virtually all of the chemicals considered to be environmental contaminants can be detected in

environmental media. However, for quantifying potential disease risk, mere detection of a

chemical is not sufficient, but rather the dose delivered to individuals must be calculated. Dose

depends on demonstrating the pathways of exposure and quantifying the intensity, frequency,

duration, and extent of contact with the chemicals of interest. Identifying peoples’ potential dose

is the first step in assessing health risks.

13. The majority of human cancers arise from (a) unavoidable conditions in the world

around us (e.g., our genes, viruses, sunlight, background ionizing radiation), (b) processes

inherent to life itself (e.g., errors in DNA duplication, creation of free radical molecules by

metabolism, production of reactive chemicals for defense against germs), and (c) lifestyle factors

(e.g., smoking, drugs, alcohol intake, poor nutrition, obesity, lack of exercise). The process of

human health risk assessment can be used to estimate the relative magnitude of risks from the

exposures of interest to other sources of cancer risk. US EPA generally considers calculated

residual lifetime cancer risks in the range from 1-in-ten-thousand to 1-in-a-million to be

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acceptable. These target (hypothetical) cancer risks are much smaller than the combined risk

from the factors (a) through (c) noted in this paragraph.

14. The (sometimes) narrow focus on risks from one source may prevent appreciation

of the broader scope of risks we all face daily throughout our lives, and this may lead to

considerable misapprehension of the actual risks we all face. The hypothetical health risks

calculated for low-level exposures to environmental chemicals must be examined relative to

those contributions from unavoidable background risks and alternative causes of disease.

15. Guidelines and regulations have been developed for chemicals in the environment

as to permissible concentrations. Such guidelines rely on extrapolation from health risks studied

at different levels of exposure. Quantitative risk estimates are derived either from (a) actual

human experience (for example, from death certificates, hospital admissions, insurance claims),

or by (b) extrapolating correlations between “exposure” and “effect” based on analyses of

occupational, laboratory-animal, clinical, or population data. The former (a) are called

“actuarial” because they derive from actual counts tabulated by the National Center for Health

Statistics and insurance company actuaries. The latter risk estimates (b) are called

“hypothetical” because they are extrapolated from high-level concentrations, indirect exposure

estimates, correlative statistics, or laboratory-animal data. The hypothetical risks may be

assumed to exist for precautionary, public-health purposes, but, at low exposure levels typically

encountered in the ambient environment, the risks are neither clearly established nor clearly

evident in human populations. For example, if high-dose studies show health effects, the results

may be put into mathematical models that extrapolate to estimated human risk at much lower

doses. Such a risk number is hypothetical, because the risk at low doses cannot be demonstrated.

The potential for human health effects is sometimes assumed to exist solely because of model

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extrapolations from observations at high levels of exposure, or because of other kinds of indirect

evidence.

AIR QUALITY GUIDELINES ARE DEVELOPED TO IDENTIFY ACCEPTABLE AIR


QUALITY IMPACTS

16. In her pre-filed direct testimony (Baird, 2019), Dr. Sandra J.S. Baird of MassDEP

testified that, “[T]he AALs and TELs, including those for benzene, formaldehyde and acrolein,

were derived using the best available toxicity information, set at levels where no adverse effects,

cancer and noncancer, are expected in sensitive populations over a lifetime of exposure, account

for exposure to the same chemical from sources in addition to outdoor air and limit the potential

for concentration excursions.” She further concluded, “Given the elements taken into account

during the derivation process, AALs and TELs are considered protective of public health.”1

17. In her testimony about the AALs and TELs, Dr. Baird referred to the 2011

MassDEP guidance document “Methodology for Updating Air Guidelines: Allowable Ambient

Limits (AALs) and Threshold Effects Exposure Limits (TELs)” (MassDEP, 2011)2. This

document outlines the process developed by MassDEP for updating the AALs and TELs and

demonstrates the conservative (i.e., health-protective) nature of the AALs and TELs. In this

document, MassDEP stated, “The AAL is considered to be protective of public health for both

threshold and non-threshold effects over many years of exposure and compared to annual

average concentrations for compliance determination.” MassDEP has defined the TEL as a

1
Baird, SJS. [Massachusetts Dept. of Environmental Protection (MassDEP)]. March 26, 2019. "Pre-filed direct
testimony of Sandra J.S. Baird, Ph.D. [In the matter of Algonquin Gas Transmission, LLC]." Submitted to
Massachusetts Dept. of Environmental Protection (MassDEP), Office of Appeals and Dispute Resolution. OADR
Docket Nos. 2019-008 through 2019-013 Weymouth. 84p.
2
Massachusetts Dept. of Environmental Protection (MassDEP), Office of Research and Standards. December 21,
2011. "Methodology for Updating Air Guidelines: Allowable Ambient Limits (AALs) and Threshold Effects
Exposure Limits (TELS) (Final)." 67p.

6
value “intended to protect the general population, including sensitive members and children,

from adverse health effects over a life-time of exposure to ambient air” (MassDEP, 2011).

Through its requirement that the TEL be compared to chemical concentrations averaged over a

24-hour period, MassDEP described the TEL as providing “additional protection from threshold-

type effects in that it represents a cap on potential concentration excursions within a 24-hour

time period (i.e., chemical concentrations in air averaged over a 24-hour period should not

exceed the TEL, even if the concentration in air is below the AAL when averaged over a longer

time period)” (MassDEP, 2011).

18. As discussed in the MassDEP guidance document, the foundations of the non-

cancer TELs and AALs are US EPA Reference Concentrations (RfCs) or equivalent toxicity

values (e.g., Agency for Toxic Substances and Disease Registry [ATSDR] chronic inhalation

Minimal Risk Levels [MRLs], California Office of Environmental Health Hazard Assessment

[CalOEHHA] chronic Reference Exposure Levels [RELs]) that typically specify exposure levels

that are from several-hundred-fold to several-thousand-fold lower than the exposure levels at

which an actual adverse effect was observed in people or laboratory animals. This is typically

the case because, in order to conservatively estimate human risk at much lower doses, agency

guidelines are commonly extrapolated downward from high-dose studies (in workers or in

animal studies) where adverse health effects have been observed. Multiple “safety factors” are

typically used that allow for factors such as human variability in sensitivity, resulting in

guidelines that are protective of the general population and sensitive subpopulations including

children and the elderly. Such health-protective guidelines envision hypothetical risks, because

actual adverse health effects at these low doses are not observed. Consequently, agency

7
guidelines for safe exposure are typically many orders of magnitude (many factors of 10) below

the concentrations where actual adverse health outcomes might be expected.

19. MassDEP’s TELs incorporate a Relative Source Contribution (RSC) factor to take

into account potential exposures to chemicals from other sources, such as indoor air, food, water,

and soil. The 2011 AAL and TEL guidance document discussed MassDEP’s decision to retain

the usage of a RSC factor in the development of TELs, which was done despite MassDEP’s

recognition that other states do not typically include such a factor in their ambient air guideline

values (MassDEP, 2011). As discussed in MassDEP (2011), “The inclusion of an RSC in the

derivation of the TEL represents a science policy decision that air guidance values should

consider other sources of exposure to chemicals in addition to ambient air.” Most TELs,

including those for benzene, formaldehyde, and acrolein as discussed below, incorporate a

default RSC factor of 0.2, meaning that they are reduced by a factor of 5 to take into account the

potential for cumulative exposure via other exposure pathways.

20. As demonstrated by the series of points below in more detail, for benzene,

formaldehyde, and acrolein, non-cancer TELs and cancer-protective AALs are multiple orders of

magnitude (i.e., several factors of 10) lower than the lowest concentrations at which either non-

cancer or cancer health effects were observed or would be expected to occur in humans.

BENZENE TEL AND AAL (AS BASED PRIMARILY ON MASSDEP


DOCUMENTATION3)

21. Both the benzene TEL and AAL have been updated according to the 2011

MassDEP updated methodology for development of AALs and TELs (MassDEP, 2011).

3
https://www.mass.gov/eea/docs/dep/toxics/stypes/benzene.doc

8
22. TEL: US EPA, ATSDR, and CalOEHHA used an occupational study of workers

exposed to low levels of benzene and identified the potentially adverse effect most sensitive to

chronic benzene exposure as being “decreased levels of B cells in the blood.” As documented by

MassDEP, these agencies identified the lowest chronic-exposure benzene level at which this

effect was detected (the lowest-observed-adverse-effect-level, or LOAEL) to be 1,860 µg/m3.

23. From a dose-response analysis of the worker study, the no-observed-adverse-

effect-level (NOAEL), which is defined as the exposure level at which there is no statistically or

biologically significant increase in the critical adverse effect, was determined to be a chronic

exposure level of about 3-fold lower, at 665 µg/m3.

24. To allow for within-population variability in sensitivity, for possible repeated

exposures, and for possible data incompleteness, this no-effect concentration was reduced further

by a factor ranging from 25 to about 200, depending on the specific conservatisms used by each

public health agency.

25. The final results, for chronic inhalation exposure guidelines, yielded three, health-

protective, screening values available to MassDEP:

US EPA, Reference Concentration = RfC = 30 µg/m3


CalOEHHA, Reference Exposure Level = REL = 3 µg/m3
ATSDR, Minimum Risk Level = MRL = 10 µg/m3

All three of these agency derivations are based on being protective of health, including for

sensitive sub-groups such as children.

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26. Studies of indoor air have shown that people are exposed to indoor concentrations

of benzene at median levels of about 4.2 µg/m3.4,5 Air concentrations of benzene due to common

exposure situations are given on the tables in Exhibit C.

27. MassDEP selected the lowest of these health-protective concentrations, namely

the CalOEHHA REL (3 µg/m3), and reduced it further by a relative source contribution (RSC)

factor of 5, to arrive at a benzene TEL of 0.6 µg/m3.

28. The benzene TEL is thus a factor of 3,100-fold below the LOAEL concentration

where a “most sensitive” potential health effect was demonstrated to occur in humans.

29. The benzene TEL is about 1,000-fold below the no-effect level (NOAEL). This is

more than for criteria pollutants, where the “significant impact level” or SIL is only about 30-

fold below the respective NAAQS no-effect guideline. Being below the SIL “shows that the

proposed source will not have a significant or meaningful impact on air quality” [footnote 12 in

Dr. Dockery’s pre-filed testimony].

30. AAL: For chemicals such as benzene with both cancer and non-cancer health

effects, MassDEP AALs are the lower of either the TEL or a Non-threshold Effects Exposure

Limit (NTEL) based on extrapolating down to the concentration that, during a lifetime of

exposure to that level, leads to a hypothetical 1-in-a-million risk of developing cancer over a

lifetime. This requires analyzing studies where cancer was caused in an exposed cohort of

people and extrapolating to what cancer risk would be expected from a lifetime exposure to 1

µg/m3, which is called the “unit risk.”

4
http://publications.jrc.ec.europa.eu/repository/bitstream/JRC31622/1622%20-
%20INDEX%20%20EUR%2021590%20EN%20report[1].pdf
5
Loh, MM; Houseman, EA; Gray, GM; Levy, JI; Spengler, JD; Bennett, DH. 2006. "Measured concentrations of
VOCs in several non-residential microenvironments in the United States." Environ. Sci. Technol. 40 (22): 6903-911.
doi: 10.1021/es060197g.

10
31. Several agencies have used the so-called “Pliofilm cohort” of rubber

hydrochloride workers to estimate the inhalation unit risk for benzene. The lowest exposure

group experienced benzene concentrations of about 16,300 to 32,600 μg/m3 over their working

lifetimes, and compared to workers with no exposure to benzene, this group of benzene-exposed

workers experienced a 120% greater risk of developing cancer (i.e., a relative risk for developing

cancer of 2.2).

32. Estimates of unit risk by US EPA, CalOEHHA, and the World Health

Organization (WHO) have been derived for these benzene workers. The dimensions of unit risk

can be expressed as “how many units of 1-in-a-million lifetime risk” per “µg/m3” air

concentrations of benzene. The estimates of unit risk are

US EPA, unit risk = 2.2 - 7.8 10-6 (lifetime risk) per µg/m3
CalOEHHA, unit risk estimates = 16 and 29 10-6 (lifetime risk) per µg/m3
WHO, unit risk = 6 10-6 (lifetime risk) per µg/m3

The benzene unit risk values derived by the three agencies for developing air guidelines

considered the same set of studies as the basis for the unit risk. Differences in their results had to

do with different dose metrics and different dose-response analyses.

33. MassDEP used the cancer unit risk factor at the high end of the US EPA unit risk

range (i.e., the more stringent end of the range), and calculated that AAL = NTEL = 1 x 10-6

(lifetime exposure risk) / 7.8 x 10-6 per µg/m3 (high end of US EPA range) = 0.128 µg/m3,

rounded to 0.1 µg/m3.

34. The AAL is thus a factor of 163,000 to 326,000-fold below the lowest benzene

concentration where an elevation of cancer risk was demonstrated to occur in humans.

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FORMALDEHYDE TEL AND AAL (AS BASED PRIMARILY ON MASSDEP
DOCUMENTATION6)

35. Both the formaldehyde TEL and AAL have been updated according to the 2011

MassDEP updated methodology for development of AALs and TELs (MassDEP, 2011).

36. TEL: Based on the same occupational study population, the European

Commission (EC), CalOEHHA, and ATSDR identified the potentially adverse effects most

sensitive to chronic formaldehyde exposure to be irritation of the eyes, nose, and respiratory

tract.

37. Based on the nasal obstruction, nasal discomfort, lower airway discomfort, and

eye irritation observed in the occupational study of formaldehyde exposure, the LOAEL for

chronic exposures was 260 - 300 µg/m3, and the chronic-exposure NOAEL was 90 µg/m3.

38. The results of three analyses, for safe levels of chronic inhalation exposure,

yielded the following three, health-protective screening values available to MassDEP:

EC, Exposure Limit = EL = 1 µg/m3


CalOEHHA, Reference Exposure Level = REL = 9 µg/m3
ATSDR, Minimum Risk Level = MRL = 10 µg/m3

39. All three of these derivations are based on being protective of health, including

for the most sensitive groups such as children.

40. Studies of indoor air have shown that people are exposed to indoor concentrations

of formaldehyde at median levels of about 26 µg/m3.7,8 Air concentrations of formaldehyde due

to common exposure situations are given on the tables in Exhibit C.

6
https://www.mass.gov/eea/docs/dep/toxics/stypes/formaldehyde-aaltel.doc
7
http://publications.jrc.ec.europa.eu/repository/bitstream/JRC31622/1622%20-
%20INDEX%20%20EUR%2021590%20EN%20report[1].pdf
8
Loh, MM; Houseman, EA; Gray, GM; Levy, JI; Spengler, JD; Bennett, DH. 2006. "Measured concentrations of
VOCs in several non-residential microenvironments in the United States." Environ. Sci. Technol. 40 (22)6903-911.
doi: 10.1021/es060197g

12
41. The World Health Organization guideline for indoor air quality for formaldehyde

is 100 µg/m3, a concentration that WHO deems protective against health effects from both short-

term and long-term exposures.9

42. MassDEP selected the CalOEHHA chronic REL (9 µg/m3) health-protective

concentration, and reduced it further by a relative source contribution (RSC) factor of 5, to arrive

at the formaldehyde TEL of 2 µg/m3.

43. The TEL is thus a factor of 1,000 to 1,500-fold below the LOAEL concentration

where a “most sensitive” potential health effect was demonstrated to occur in humans.

44. The formaldehyde TEL is about 450-fold below the no-effect level (NOAEL).

This is more than for criteria pollutants, where the “significant impact level” or SIL is only about

30-fold below the respective NAAQS no-effect guideline. Being below the SIL “shows that the

proposed source will not have a significant or meaningful impact on air quality” [footnote 12 in

Dr. Dockery’s pre-filed testimony].

45. AAL: For chemicals such as formaldehyde with both cancer and non-cancer

health effects, MassDEP AALs are the lower of either the TEL or a Non-threshold Effects

Exposure Limit (NTEL) based on extrapolating to the concentration that, during a lifetime of

exposure to that level, leads to a hypothetical 1-in-a-million risk of developing cancer over a

lifetime.

46. For formaldehyde, the studies of carcinogenicity in humans have not been able to

derive dose-response relationships, and thus, unit risk is based on a laboratory animal study.

9
"WHO Guidelines for Indoor Air Quality" (2010)
http://www.euro.who.int/__data/assets/pdf_file/0009/128169/e94535.pdf

13
47. In the animal studies that are the basis for the formaldehyde unit risk, the lowest

exposure group with any tumors was exposed to 5.6 ppm formaldehyde, which is 5,600 ppb, or

6,900 µg/m3.

48. MassDEP had available three estimates of cancer potency, which differ over three

orders of magnitude from each other, but which are based on the same laboratory-animal tumor

data. The dimensions of unit risk can be expressed as “how many units of 1-in-a-million risk”

per “µg/m3” air concentrations. The three estimates of unit risk are

US EPA, unit risk = 13 10-6 (lifetime risk) per µg/m3


CalOEHHA, unit risk estimates = 6 10-6 (lifetime risk) per µg/m3
CIIT, unit risk = 0.0055 10-6 (lifetime risk) per µg/m3

49. MassDEP used the highest (most stringent) cancer unit risk factor (US EPA UR =

13), and calculated the AAL = NTEL = 1 x 10-6 (lifetime exposure risk) / 13 x 10-6 per µg/m3

(highest, US EPA UR) = 0.077 µg/m3, rounded up to 0.08 µg/m3.

50. The MassDEP formaldehyde AAL is nearly 100,000-fold (86,250-fold) below the

lowest concentration where an elevation of tumors was demonstrated to occur in laboratory

animals.

ACROLEIN TEL AND AAL (AS BASED PRIMARILY ON MASSDEP


DOCUMENTATION10)

51. Both the acrolein TEL and AAL have been updated according to the 2011

MassDEP updated methodology for development of AALs and TELs (MassDEP, 2011).

52. TEL and AAL: For acrolein, these two values are the same, because acrolein

health effects data are inadequate for assessment of human carcinogenic potential. For non-

10
https://www.mass.gov/eea/docs/dep/toxics/stypes/acrolein.doc

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cancer effects, the most sensitive health effect from chronic acrolein exposure is development of

nasal lesions.

53. MassDEP had available the results of three analyses providing safe levels of

chronic inhalation exposure, which are the following three, health-protective, screening values:

US EPA RfC = 0.02 µg/m3


CalOEHHA REL = 0.35 µg/m3
Health Canada TC (Tolerable Concentration) = 0.4 µg/m3

54. MassDEP selected the CalOEHHA REL as the basis for the TEL, because it is

based on a newer animal bioassay with greater ability to detect adverse effects, and it used a

chemical-specific animal-to-human extrapolation method.

55. The concentration- response for the most sensitive effect (nasal lesions) in the

underlying study provided a LOAEL = 1,380 µg/m3, and a NOAEL = 460 µg/m3.

56. After adjustment to continuous exposure and extrapolation to human equivalent

concentrations, the NOAEL was reduced about 6.6-fold, to 70 µg/m3.

57. A further composite uncertainty factor of 200 was applied to adjust for human

variability in sensitivity, and for chronic, lifetime exposure, to yield a REL of 0.35 µg/m3.

58. Studies of indoor air have shown that schoolrooms have indoor concentrations of

acrolein of about 1.2 µg/m3.11 Air concentrations of acrolein due to common exposure situations

are given on the tables in Exhibit C.

59. MassDEP selected the CalOEHHA REL (0.35 µg/m3) health-protective

concentration, and reduced it further by a relative source contribution (RSC) factor of 5, to arrive

at the acrolein TEL of 0.07 µg/m3.

11
Health Effects Institute (HEI). 2007. "Mobile-Source Air Toxics: A Critical Review of the Literature on Exposure
and Health Effects." Air Toxics Review Committee. HEI Special Report 16. 240p.

15
60. The chronic-exposure acrolein TEL is thus a factor of nearly 20,000 below the

LOAEL concentration where a “most sensitive” potential health effect was demonstrated to

occur in laboratory animals.

61. The acrolein TEL is about 6,500-fold below the no-effect level (NOAEL). This is

more than for criteria pollutants, where the “significant impact level” or SIL is only about 30-

fold below the respective NAAQS no-effect guideline. Being below the SIL “shows that the

proposed source will not have a significant or meaningful impact on air quality” [footnote 12 in

Dr. Dockery’s prefiled testimony].

62. AAL: Acrolein is not classifiable as to its carcinogenicity (IARC Group 3) due to

inadequate evidence in both humans and experimental animals for its carcinogenicity. As a

result, MassDEP designated the AAL to be the same as the TEL, namely, AAL = 0.07 µg/m3.

THE MASSDEP TELS AND AALS ARE USED AS SCREENING LEVELS

63. In its responses to public comments on the “Proposed Plan Approval” for the

Weymouth compressor station project (MassDEP, 2019)12, MassDEP described the AALs and

TELs as “screening-level guidelines that indicate the maximum ambient air concentration of a

toxic pollutant that may be contributed by a single source or facility.” They are appropriate for

comparison with incremental ambient concentrations of air toxics caused solely by a specific

source’s emissions, because they represent very conservative exposure levels, purposely set

many orders of magnitude (many factors of 10) below levels where health effects have been

reported.

12
Massachusetts Dept. of Environmental Protection (MassDEP). January 11, 2019. "MassDEP Response to Public
Comments on the "Proposed Plan Approval" - January 2019 [concerning Algonquin Gas Transmission, LLC
Weymouth natural gas compressor station]." 57p.

16
64. The air dispersion modeling conducted for the proposed compressor station was

conservatively based on the emission sources’ potential to emit (PTE), which is the maximum

possible emissions from each source, rather than actual expected emissions (Goodrich, 2019, p.

8, point 2813; Fickas, 2019, p. 15, point 3614). Therefore, the modeled air toxics concentrations

being compared to the AALs and TELs are very conservative (i.e., health protective).

65. The nature of the TELs as screening-level guidelines is enhanced even further

through the MassDEP requirement that they be compared to modeled 24-hour air concentrations

associated with facility air emissions. This is required despite the fact that the TELs are intended

to be protective of the general population, including sensitive subpopulations such as children

and the elderly, from non-cancer health effects over a lifetime of continuous exposure. There is

thus a substantial amount of health protection afforded by the TELs when they are compared to

24-hour air concentrations, meaning that the exceedance of TELs by 24-hour air concentrations

should not be assumed to result in actual adverse non-cancer health effects. For example, there

would generally be no expectation of actual adverse health effects for 24-hour air concentrations

exceeding TELs by around an order of magnitude (~10 fold) or more, and in general, further

assessment is needed to identify whether a TEL exceedance may result in exposures with the

potential for actual adverse health effects.

66. Other health-based exposure guidelines are available that are more appropriate

than the MassDEP TELs for comparison with 24-hour ambient air concentrations to evaluate

whether the measured 24-hour air concentrations are at levels of potential health risk. In

13
Goodrich, LB. [Enbridge, Inc.]. March 19, 2019. "Pre-filed direct testimony of L. Barry Goodrich [In the matter
of Algonquin Gas Transmission, LLC]." Submitted to Massachusetts Dept. of Environmental Protection
(MassDEP), Office of Appeals and Dispute Resolution. OADR Docket Nos. 2019-008 - 2019-013. 13p.
14
Fickas, J. [Trinity Consultants, Inc.]. March 19, 2019. "Pre-filed direct testimony of Justin Fickas [In the matter of
Algonquin Gas Transmission, LLC]." Submitted to Massachusetts Dept. of Environmental Protection (MassDEP),
Office of Appeals and Dispute Resolution. OADR Docket Nos. 2019-008, 2019-009, 2019-010, 2019-011, 2019-
012, 2019-013. 15p.

17
particular, the Agency for Toxic Substances and Disease Registry (ATSDR) has developed acute

inhalation Minimal Risk Levels (MRLs) that are specifically developed to be protective of 24-

hour exposure durations according to a well-documented, conservative (i.e., health-protective)

process. They are generally based on the most sensitive substance-induced end point considered

to be of relevance to humans.15 ATSDR further defines MRLs as being set “below levels that,

based on current information, might cause adverse health effects in the people most sensitive to

such substance-induced effects”.16 ATSDR acute inhalation MRLs are derived for 1-14 day

exposure durations; therefore, because adverse health effects are generally observed at lower

concentrations only over longer exposure durations, comparison of the MRL with 24-hour air

concentrations is conservative.

67. As compared to the MassDEP TEL of 0.6 µg/m3, the ATSDR acute inhalation

MRL is 29 µg/m3 for benzene.17

68. As compared to the MassDEP TEL of 2 µg/m3, the ATSDR acute inhalation MRL

is 49 µg/m3 for formaldehyde.18

69. As compared to the MassDEP TEL of 0.07 µg/m3, the ATSDR acute inhalation

MRL is 7 µg/m3 for acrolein.19

70. As stated in the Baird testimony regarding the AALs for benzene and

formaldehyde (which are based on 1-in-a-million excess lifetime cancer risks over a lifetime of

continuous exposure), the cancer toxicity values (unit risks) underlying the AALs for benzene

15
https://www.atsdr.cdc.gov/mrls/index.asp
16
https://www.atsdr.cdc.gov/mrls/index.asp
17
https://www.atsdr.cdc.gov/mrls/index.asp
18
https://www.atsdr.cdc.gov/mrls/index.asp
19
https://www.atsdr.cdc.gov/mrls/index.asp

18
and formaldehyde are based on upper-bound estimates of the cancer risk; in other words, they are

expected to overestimate than to underestimate cancer risk. It should be noted that US EPA’s

acceptable cancer risk ranges from 1-in-ten-thousand per lifetime down to 1-in-a-million per

lifetime, which is the lower, most restrictive bound.

71. To put the calculated, hypothetical cancer risks from ambient air exposures into

perspective, it is helpful to consider how these risks compare to overall health risks faced by the

general public (see also Exhibit B). Of the US population (currently over 328 million people

[US Census Bureau, 2018]20), about 0.8% die every year (2.6 million people). Of the annual US

deaths (Siegel et al., 2018)21:

 Heart disease is responsible for about one-quarter of all deaths, and

 Cancer deaths are responsible for about another one-quarter.

72. Thus, for the population generally, our lifetime risk of dying from heart disease is

about 1-in-4, and for dying from cancer is about 1-in-4, that is, far above 1-in-a-million. These

proportions of deaths from heart disease and cancer are roughly stable over time and from place

to place in the US.

73. Only a proportion of the individuals who develop cancer die of the disease. In the

US, the baseline chances of developing invasive cancer (cancer incidence) sometime during

one’s life are as follows (from Siegel et al., 2018).

 40% for men


 38% for women

20
https://www.census.gov/popclock/
21
Siegel, RL; Miller, KD; Jemal, A. 2018. "Cancer statistics, 2018." CA Cancer J. Clin. 68 (1): 7-30. doi:
10.3322/caac.21442.

19
Or, 39% as an average for both sexes, which can be expressed as a lifetime odds of nearly 1-in-

2.5. By comparison, a 1-in-a-million lifetime cancer risk is about 400,000-fold lower than

everyone’s baseline risk of developing cancer.

74. Suppose a particular set of assumptions about benzene or formaldehyde exposure

resulted in a calculated 1-in-100,000 lifetime hypothetical cancer risk. How can this numerical

value be given context? The lifetime risk estimate of 1-in-100,000 can be expressed in a variety

of ways that can help give perspective to its meaning:

(a) If 100,000 people were continuously exposed (each day, 24 hrs/day) over

a lifetime to the required average benzene or formaldehyde concentrations,

then, out of those 100,000 lifetimes, one individual might develop an

formaldehyde- or benzene-related tumor. Meanwhile, 40,000 people in

this group would develop cancer from other causes.

(b) The probability for any one person of being diagnosed with a

formaldehyde- or benzene-related tumor over a lifetime of exposure to the

assumed necessary dose would be, at most, one chance in 100,000.

(c) If human lifetime were not limited, an exposed individual might expect

that the likelihood of being diagnosed with an formaldehyde- or benzene-

related tumor would approach near 100% after 7,000,000 years of

exposure (i.e., after 100,000 sequential 70-year lifetimes).

75. The conclusion to be drawn from these perspectives is that people living in

today’s society would not be expected to spend significant time, energy, and resources to reduce

such incrementally small lifetime risks, which would correspond to daily risks of about 1-in-

2,500,000,000.

20
76. Given that they are highly conservative screening guidelines, the exceedance of

either a TEL or an AAL cannot be interpreted as indicating either the presence of unacceptable

risks or the likelihood that an actual adverse health effect will occur. This is recognized by

MassDEP in its responses to public comments on the “Proposed Plan Approval” for the

Weymouth compressor station project where they note that “exposure above an AAL or TEL

does not automatically mean an individual will develop cancer or experience non-cancer health

effects” (MassDEP, 2019)22.

REBUTTAL TO DR. DOCKERY

77. Dr. Dockery makes statements that are not correct, for example:

(a) p. 10, point 25: “The evaluation of the impact of emissions of compressor

and associated facilities as a single source without consideration of other

sources or background ambient air concentrations is not consistent with

the stated MassDEP policies to protect the public health.” But, this is

consistent with MassDEP policy for air toxics.

(b) p. 10, point 26: “Thus, the TELs for ambient air limit total chemical

exposures, and not incremental chemical exposure from any specific

sources.” This is not consistent with MassDEP policy.

(c) p. 11, point 29: MassDEP’s protocol for assessing air toxics impacts

caused solely from a facility’s emissions “is not consistent with the

MassDEP use of a relative source contribution factor in defining TELs,

which accounts for cumulative risk of chemical exposures from multiple,

22
Massachusetts Dept. of Environmental Protection (MassDEP). January 11, 2019. "MassDEP Response to Public
Comments on the "Proposed Plan Approval" - January 2019 [concerning Algonquin Gas Transmission, LLC
Weymouth natural gas compressor station]." 57p.

21
independent pathways (outdoor air, indoor air, water, soil and food).”

MassDEP’s air toxics protocol is consistent with MassDEP’s TEL

methodology and use of a RSC factor.

78. MassDEP has granted a substantial number of air permits over the years, in which

modeled facility-only air toxics concentrations have been compared to MassDEP TELs and

AALs in the air permit applications. Dr. Dockery did not provide any example where TELs and

AALs have been applied to “total ambient air chemical concentrations.” Gradient has been a

consultant on at least three gas-fired power plant projects where, to my knowledge, air modeling

results for facility-only air toxics concentrations were compared to TELs and AALs.

79. In response to Dr. Dockery’s point 29, MassDEP documented its long-standing

practice of requiring only incremental ambient concentrations of air toxics caused solely by a

specific source’s emissions to be compared with the AALs and TELs in a 1989 “Air Toxics

Implementation Update”: “DAQC requires new or modified sources of air contaminants to

demonstrate the application of Best Available Control Technology (BACT), and assess, through

computer modeling, the ambient concentrations caused solely by that source’s emissions. These

modelled concentrations are then compared to the AALs to determine whether there may be

potentially unacceptable risks associated with that particular source.”23 US EPA documents have

also recognized the generally accepted practice of assessing incremental air toxics risks posed by

emissions from specific facilities without consideration of background concentrations.24,25, This

23
Massachusetts Dept. of Environmental Protection (MassDEP), Division of Air Quality Control. August 1989.
"Air Toxics Implementation Update." 7p.
24
US EPA, Office of Air Quality, Planning and Standards (Research Triangle Park, NC) March 1999. "Residual
Risk: Report to Congress." EPA-453/R-99-001. 225p. (see p. 90-94).
25
US Environmental Protection Agency (US EPA). April 2004. "Air Toxics Risk Assessment Reference Library,
Volume 1: Technical Resources Manual." Office of Air Quality Planning and Standards. EPA-453-K-04-001A.
899p. (see p. 13-12 to 13-13).

22
practice also applies to risks posed by sites and facilities via other media aside from air, e.g.,

risks from water or soil contamination are evaluated on a source-specific basis by comparison of

intake from that source to reference doses (RfDs).

80. On p. 13, points 36-38, Dr. Dockery would appear to agree that TELs and AALs

could be used as source-specific screening levels, similar to the SILs used in the case of

NAAQS. As presented in the earlier points of my testimony, the TELs and AALs are indeed

smaller fractions of the “effect levels” than the SILs are of NAAQS levels, and hence, by Dr.

Dockery’s argument, are appropriate to serve as screening levels. Dr. Dockery, as well as other

Petitioners' experts, appear to disregard the fact that MassDEP, as well as the agencies

(MassDEP, MADPH, Metropolitan Area Planning Council [MAPC]) involved in the preparation

of the Health Impact Assessment (HIA) report, considered existing air quality in the Fore River

Basin area in their determinations that the Project would not pose an unacceptable risk to public

health.26,27

81. P. 15, point 42 is based on erroneous information, because none of the MassDEP

24-hour benzene measurements for the Fore River Basin monitoring sites are in excess of the

TELs. In fact, in point 44, Dr. Dockery reverses himself and acknowledges “there were not any

24 hour average benzene concentrations observed above the TEL.”

82. Dr. Dockery refers to “super-additive” effects (more commonly referred to as

synergistic effects in the risk assessment field). Synergistic interactions between chemicals are

uncommon, however, and when they occur, are typically an elevated-dose phenomenon

26
Massachusetts Dept. of Environmental Protection (MassDEP). January 11, 2019. "MassDEP Response to Public
Comments on the "Proposed Plan Approval" - January 2019 [concerning Algonquin Gas Transmission, LLC
Weymouth natural gas compressor station]." 57p.
27
Metropolitan Area Planning Council (MAPC); Massachusetts Dept. of Public Health (MADPH); Massachusetts
Dept. of Environmental Protection (MassDEP) January 2019. "Health Impact Assessment of the Proposed
Compressor Station, Weymouth, MA." 158p.

23
(Cedergreen, 2014)28. Studies of chemical interactions have shown that effects can be

independent, synergistic, or antagonistic. Synergism is of potential concern only when (1) two

or more chemicals share a common mechanism for a combined action, and (2) exposure levels

for these chemicals are near or above their individual response thresholds (which, for most

chemicals, are orders of magnitude greater than their health-based exposure guidelines, due to

the common usage of multiple safety and uncertainty factors in the development of exposure

guidelines) (Feron and Groten, 200229; Charles et al., 200730). In other words, the combined

impacts of low-level exposures at concentrations below health-based screening levels (and

consequently, far below their individual response thresholds) are not expected to exhibit

synergism.

83. Dr. Dockery, as well as other Petitioners’ witnesses, do not acknowledge in their

testimony that US EPA has endorsed an acceptable cancer risk range from 100-in-a-million (1-

in-ten-thousand) to 1-in-a-million for air toxics risk assessment.31,32 As discussed in these US

EPA documents, this acceptable cancer risk range has its origins in the 1989 benzene National

Emission Standard for Hazardous Air Pollutants (NESHAP) and was endorsed by Congress in

the 1990 Clean Air Amendments as a reasonable approach for protecting public health with “an

28
Cedergreen, N. 2014. "Quantifying synergy: A systematic review of mixture toxicity studies within
environmental toxicology." PLoS ONE 9 (5): e96580. doi: 10.1371/journal.pone.0096580.
29
Feron, VJ; Groten, JP. 2002. "Toxicological evaluation of chemical mixtures." Food Chem. Toxicol. 40 (6): 825-
839.
30
Charles, GD; Gennings, C; Tornesi, B; Kan, HL; Zacharewski, TR; Bhaskar Gollapudi, B; Carney, EW. 2007.
"Analysis of the interaction of phytoestrogens and synthetic chemicals: An in vitro/in vivo comparison." Toxicol.
Appl. Pharmacol. 218 (3): 280-288.
31
US EPA, Office of Air Quality, Planning and Standards (Research Triangle Park, NC). March 1999. "Residual
Risk: Report to Congress." EPA-453/R-99-001. 225p. (see p. 8, 126-128, B-4 to B-6).
32
US Environmental Protection Agency (US EPA). April 2004. "Air Toxics Risk Assessment Reference Library,
Volume 1: Technical Resources Manual." Office of Air Quality Planning and Standards. EPA-453-K-04-001A.
899p. (see pages 27-5 to 27-8).

24
ample margin of safety.” The 1999 US EPA “Residual Risk Report to Congress”33 elaborates on

the use of a benchmark risk of approximately 1-in-ten-thousand serving as the upper-end of the

range of acceptability for maximum individual risk: “The EPA will generally presume that if the

risk to that individual [the Maximum Individual Risk] is no higher than approximately 1-in-10-

thousand, that risk level is considered acceptable and EPA then considers the other health and

risk factors to complete an overall judgment on acceptability. The presumptive level provides a

benchmark for judging the acceptability of maximum individual risk (“MIR”), but does not

constitute a rigid line for making that determination.” US EPA’s stated goal with the use of a

lower benchmark of approximately 1-in-a-million was to protect the greatest number of people

possible to an individual lifetime risk level no higher than approximately 1-in-a-million.

84. Benzene and formaldehyde ambient air concentrations and cancer risks

highlighted by the Petitioners’ pre-filed direct testimony as supporting the health harms posed by

existing air quality in the Fore River Basin area fall within US EPA’s acceptable cancer risk

range, meaning that these hypothetical cancer risks should not be viewed as providing evidence

of unacceptable existing air quality. For example, Dr. Dockery and Dr. Nordgaard point to the 4-

month average formaldehyde concentration of 2.4 µg/m3 from the July to November 2018

measurements made by MassDEP at the Weymouth MWRA Pump Station as supporting

unacceptable cancer risks from existing ambient air. However, if the average formaldehyde

concentration of 2.4 µg/m3 is assumed to represent a continuous lifetime exposure concentration,

a hypothetical excess lifetime cancer risk of 31-in-a-million is calculated based on the US EPA

inhalation unit risk estimate for formaldehyde. This hypothetical cancer risk is well within the

33
US EPA, Office of Air Quality, Planning and Standards (Research Triangle Park, NC). March 1999. "Residual
Risk: Report to Congress." EPA-453/R-99-001. 225p. (see p. 8, 126-128, B-4 to B-6).

25
US EPA acceptable lifetime cancer risk range of 100-in-a-million to 1-in-a-million. Similarly,

Dr. Clapp alleges that a formaldehyde concentration of 0.12 µg/m3 is associated with

“unacceptable” cancer risk, but if this concentration is assumed to represent a continuous,

lifetime of exposure, then a hypothetical excess lifetime cancer risk of 1.6-in-a-million is

obtained, based on the US EPA inhalation unit risk estimate for formaldehyde. This hypothetical

cancer risk is well within the US EPA acceptable cancer risk range.

85. In his concluding point 46, on p. 16, Dr. Dockery asserts that benzene and

formaldehyde have “similar pathways of exposure, update [sic- uptake], metabolism,

detoxification, and pathologies.” This is not correct. In the case of ambient air, benzene and

formaldehyde share the same pathway of exposure (inhalation), but these two chemicals do not

have similar transport, metabolism, detoxification, excretion, or pathology in the body.

Formaldehyde is water soluble and chemically reactive, and is taken up by tissues in the upper

respiratory tract, and does not reach the deeper lung tissues. Also, formaldehyde is naturally

formed within the body as a normal product of metabolism. Benzene is lipid soluble, and less

chemically reactive, meaning it can also be present in exhaled breath and excreted without

chemical alteration. Benzene requires metabolic activation to exert toxic effects, but

formaldehyde becomes oxidized to carbon dioxide. Neither chemical accumulates in the body.

REBUTTAL TO DR. CLAPP

86. In point 13 of his pre-filed testimony, Dr. Clapp selected a limited amount of

2011-2015 cancer incidence data for Weymouth and Quincy, highlighting elevations in

Weymouth of cancer of the urinary bladder for females and cancer of the lung and bronchus for

males, and in Quincy of cancer of the lung and bronchus for both males and females. In his

testimony, Dr. Clapp does not consider information provided in the Health Assessment Report

26
for the proposed compressor station project (MAPC, 2019)34 indicating the community

elevations in several occupational or lifestyle risk factors (e.g., smoking, regular physical

activity, obesity), which are known to play a role in the development of some of the statistically

significantly elevated cancer types, including urinary bladder and lung and bronchus cancer.

These risk factors, not ambient air chemicals, are most likely to have played a significant role in

the development of cancer in Weymouth and Quincy. Cigarette smoking is well-established as

an important risk factor for several types of cancer, including bladder cancer and lung and

bronchus cancers. Dr. Clapp fails to acknowledge that the communities of Quincy and

Weymouth are among the communities with the highest percentages of adults smoking in the

state. Weymouth and Quincy were in the top quintile within the state for percentage of adult

smoking based on the 2012-2014 Behavioral Risk Factor Surveillance System (BRFSS)

reporting (MAPC, 2019). In Weymouth, the prevalence of adult smoking from 2012-2014 was

20.2%, compared to the state average of less than 14%. In Quincy, the prevalence of adult

smoking from 2012-2014 was 18.2% (MAPC, 2019). An earlier evaluation by MADPH (2002a,

b),35,36 examined the smoking status of individuals diagnosed with lung cancer in Weymouth.

This analysis found that 82% of the individuals diagnosed with lung cancer were current or

former smokers (MADPH, 2002a, b). Both the Fore River HIA and an earlier focused cancer

evaluation conducted by MADPH (MADPH, 2002a, b) thus highlighted tobacco use as a

contributing factor for those diagnosed with lung and bronchus cancer in Weymouth.

34
Metropolitan Area Planning Council (MAPC); Massachusetts Dept. of Public Health (MADPH); Massachusetts
Dept. of Environmental Protection (MassDEP) January 2019. "Health Impact Assessment of the Proposed
Compressor Station, Weymouth, MA." 158p.
35
Massachusetts Dept. of Public Health (MADPH) February 14, 2002. "Assessment of Cancer Incidence in
Weymouth, Abington, Hingham, and Rockland, Massachusetts 1982-1998 (Public Comment Release)."
36
Massachusetts Dept. of Public Health (MADPH) December 2002. "Assessment of Cancer Incidence in
Weymouth, Abington, Hingham, and Rockland, Massachusetts 1982-1998 (Response to Public Comments and
Additional Analyses)."

27
87. In point 14 of his pre-filed testimony, Dr. Clapp fails to use accepted statistical

methods when discussing cancer incidence data for lung and bronchus cancers in two Quincy

Census Tracts (4178.02 and 4179.01) designated as environmental justice areas. Dr. Clapp

grouped all the data together across two time periods (2006 to 2010, and 2011 to 2015), genders

(male and female), and the two census tracts, calculating a “significant 39% excess of this cancer

in this population” based on 125 observed cases compared to 90 expected cases. He then

concluded, “This excess was greater than the excess lung and bronchus cancer for the rest of

Quincy and Weymouth and documents that there is already a greater burden from this cancer in

the residents of the environmental justice areas that will be impacted by the proposed compressor

station.” This is contrary to the data presented in the HIA appendices, which demonstrate no

statistically significant elevations for more than half of the specific comparisons made for lung

and bronchus cancers in these census tracts. It is possible that some of the limited number of

statistically significant elevations are due to chance alone, as MADPH (2017)37 encourages

caution when interpreting the multiple comparisons in cancer incidence reports:

“…when multiple significance tests are performed, some will result in a


significant finding due to chance alone. Based on the number of calculations in
this report, we expect 720 significant findings to be due to chance alone. Half of
these would be significant excesses (360) and half would be significant deficits
(360). There are statistical techniques that can be used to reduce this number,
however use of these techniques leads to the opposite problem - true significant
differences that may be missed. We choose to err on the side of caution and
identify more significant results, knowing that some will be due to chance alone.”

88. Regardless of statistical significance for lung cancer in the two census tracts, the

elevation that Dr. Clapp reports would suggest, in fact, that ambient air is not the basis for this

37
Massachusetts Dept. of Public Health (MADPH), Office of Data Management and Outcomes Assessment. May
2017. "Cancer Incidence in Massachusetts 2009 - 2013: City and Town Supplement."

28
elevation because it is localized to a single census tract and a single gender, and ambient air

effects, if any, would be more broadly distributed.

89. Dr. Clapp makes several unsupported assertions, for example:

(a) p. 6, point 16: Dr. Clapp states that benzene and formaldehyde exceed

AALs and TELs, but the MassDEP air monitoring data for the Fore River

Basin sampling do not show exceedances of either the MassDEP AAL or

TEL for benzene.

(b) p. 6, point 17: “When exposures to known human carcinogens such as

benzene and formaldehyde occur simultaneously, their effects are at least

additive in the exposed population. Furthermore, there is no threshold

exposure level below which no carcinogenic effect would occur.” (Note

that he provides no citation to evidence of “at least additive” or “no

threshold level” or data showing cancer at low exposure levels.) In

fact, Dr. Clapp’s next sentence in point 17 states “The default assumption

is that the exposure-response relationship is linear.” [Emphasis supplied.]

90. In referring to the lack of a “threshold exposure level below which no

carcinogenic effect would occur,” Dr. Clapp infers hypothetical cancer risk from existing

benzene and formaldehyde concentrations in the Fore River Basin area, but provides no

quantitative estimate of the size of the risk. Dr. Clapp disregards the fact that any hypothetical

cancer risk associated with benzene and formaldehyde in ambient air in the Fore River Basin

area is very small compared to the overall background risk of developing cancer in a lifetime.

Overall, Dr. Clapp fails to demonstrate that this hypothetical cancer risk is of public health

significance.

29
91. US EPA’s usage of the linear no-threshold (LNT) model as the default model for

low-dose cancer risk assessment is a policy decision intended to err on the side of increased

protection of public health, and should not be used as scientific evidence that “there is no

threshold exposure level below which no carcinogenic effect would occur” (Dr. Clapp), or that

all dose levels to carcinogens “cause cancer down to the lowest levels measurable in air” (Dr.

Landrigan). As extensively discussed by Calabrese (2019), 38 the LNT model has its origins in

1920s research investigating genetic mutations induced by ionizing radiation. Pushkin (2009)39

discussed the endorsement of the LNT model for assessing risks from ionizing radiation by

various international health and scientific organizations and public health agencies beginning in

the early 1970s, which was followed by US EPA’s policy directive in the mid-1980s to adopt the

LNT model as the default assumption for low-dose cancer risk assessment of chemical

carcinogens.

92. Inherent to the LNT model is the assumption that chemical carcinogens increase

cancer risk down to low dose levels, such as sub-part per billion (ppb) ambient air levels, but no

actual health effects evidence supports the assumption. For example, for benzene and

formaldehyde, the studies linking air exposures of these chemicals with cancer are for

occupational exposure levels and laboratory animal exposure levels, far above typical ambient

air concentrations.

93. There is available mechanistic evidence for a growing number of carcinogens that

directly contradicts the scientific validity of the LNT model as a default assumption to be

38
Calabrese, EJ. 2019. "The linear No-Threshold (LNT) dose response model: A comprehensive assessment of its
historical and scientific foundations." Chem. Biol. Interact. 301: 6-25. doi: 10.1016/j.cbi.2018.11.020.
39
Pushkin, JS. 2009. "Perspective on the use of LNT for radiation protection and risk assessment by the U.S.
Environmental Protection Agency." Dose Response. 7(4): 284-91.

30
universally applied for low-dose risk assessment of chemical carcinogens. First of all, the LNT

model ignores the existence of DNA repair mechanisms. Also, for a number of chemicals

(including formaldehyde), there is evidence that carcinogenicity occurs via a threshold

mechanism. While benzene is considered to be a genotoxic carcinogen (with “genotoxic”

usually assumed to act as if no threshold exists), mechanistic data support formaldehyde being

genotoxic, but having a practical threshold associated with its mechanism of action (Bevan and

Harrison, 2017)40. More specifically, formaldehyde has endogenous sources (i.e., it is present in

all living organisms), such that they can dominate the formation of DNA adducts relative to low

levels of exogenous sources of formaldehyde (Bevan and Harrison, 2017).

94. In its April 2018 proposed rule on “Strengthening Transparency in Regulatory

Science,”41 US EPA raised the possibility of modifying its long-standing policy of defaulting to

the LNT model for low-dose cancer risk, based on the current state of the science indicating the

need to consider alternative dose-response models as well as model uncertainty.

95. In point 18, Dr. Clapp refers to air modeling conducted by John Hinckley of

GeoInsight, Inc. that incorporated emissions from compressor engine start-up events and

identified exceedances of the formaldehyde and benzene AALs and TELs (note that TEL

exceedances were only observed for the Hinckley modeling when a 30-minute start-up event was

assumed, and not for the modeling of 9-minute start-up events). It is my understanding that

another witness (Justin Fickas of Trinity Consultants, Inc.) will testify about inaccuracies in this

air modeling. Putting aside the issue of whether the modeling was done correctly, comparison of

Mr. Hinckley’s maximum modeled formaldehyde and benzene concentrations to the AALs and

40
Bevan, RJ; Harrison, PTC. 2017. "Threshold and non-threshold chemical carcinogens: A survey of the present
regulatory landscape." Regul. Toxicol. Pharmacol. 88: 291-302. doi: 10.1016/j.yrtph.2017.01.003.
41
https://www.epa.gov/osa/strengthening-transparency-regulatory-science

31
TELs is misleading because these concentrations do not represent expected exposures for

residents of the community. It is my understanding that this modeling indicates that small

exceedances of the formaldehyde and benzene AALs and TELs may sometimes occur at

locations to the east within and just outside the facility fence line in the vicinity of the Kings

Cove Conservation Area. These maximum modeled concentrations for locations along and

nearby to the facility fence line are not representative of population exposures across the Fore

River Basin area. Moreover, as has been discussed in this testimony, the modeled exceedances

are far less than an order of magnitude above the pertinent AALs and TELs, which means that

even with a lifetime of exposure at the modeled levels, no adverse effect is expected. For

example, the maximum modeled 24-hour formaldehyde concentrations for these modeling

analyses remain well below the ATSDR acute inhalation MRL of 49 µg/m3, which is a more

appropriate, and properly conservative, benchmark for evaluating the potential for potential

health risks from 24-hour ambient air concentrations than the MassDEP TEL. In addition, the

maximum modeled annual average formaldehyde concentrations are only slightly higher than the

MassDEP AAL and thus well within US EPA’s acceptable cancer risk range of 100-in-a-million

to 1-in-a-million.

96. At the conclusion of his pre-filed testimony on p. 6 (point 19), Dr. Clapp asserts

that “Further exposure of residents to carcinogens such as benzene and formaldehyde from

operations of the proposed Weymouth compressor station will add to an already increased

burden of disease.” However, Dr. Clapp fails to support this assertion with any quantitative

estimation of his claimed “addition” to disease in areas nearby the compressor station. MassDEP

has determined that the projected compressor station air emissions do not pose an unacceptable

health risk, and Dr. Clapp’s testimony does not provide supportable data or analyses to contradict

32
MassDEP's determination. Dr. Clapp erroneously concludes that there are increased rates of

cancer in Weymouth and Quincy because he fails to consider the larger body of cancer incidence

data from MADPH that do not show consistent patterns of statistically significant elevated

cancer types in the four communities. Dr. Clapp fails to present information on lifestyle risk

factors (i.e., smoking) that appear to have a considerable impact on the lung and bronchus

cancers and bladder cancers in Weymouth and Quincy.

REBUTTAL TO DR. LANDRIGAN

97. Dr. Landrigan makes numerous unsupported assertions, for example

(a) p. 6, point 27: “an established body of science that unequivocally links air

pollution (what type, at what levels, for what duration? no citations?)

to elevated (by how much?) risks of multiple chronic diseases (which

diseases?) and premature death (which causes of death?).”

(b) p. 7, point 31: “it is well established that air pollution (what type, at what

levels, for what duration? no citations?) causes (by how much?)

disease and premature deaths (which causes of death?) in other

communities (where?) across the United States.”

Overall, Dr. Landrigan does not provide any specific data to support his claims.

98. In point 30, Dr. Landrigan states that, “Until proven otherwise, it must be

concluded that air pollution and other forms of environmental contamination from past and

current industrial operations as well as from vehicular traffic on the Fore River Bridge are

important contributors to the observed elevated rates of cancer and other chronic diseases in the

communities surrounding the site of the proposed compressor station.” Elevated disease rates

alone do not warrant a conclusion of a possible connection to air pollution or even a conclusion

33
of a public health concern. MADPH cautions that statistical significance alone does not provide

the basis to make conclusions regarding the public health significance of community health

statistics data. The Massachusetts Department of Public Health (MADPH) provides annual

evaluations of cancer incidence for 23 different cancer types in the 351 communities in

Massachusetts. In its reports, MADPH (2017)42 provides extensive qualifying information on

the interpretation of its cancer incidence statistics. For example, with respect to the standardized

incidence ratios (SIRs) that it calculates to compare the cancer incidence of each city or town

with that for the state as a whole, MADPH states:

“The SIR is a useful indication of the disease categories that have relatively high
or low rates for a given community. These statistics, however, should be used
with care. Such statistics provide a starting point for further research and
investigation into a possible health problem, but they do not by themselves
confirm or deny the existence of a particular health problem. Many factors
unrelated to disease causation may contribute to an elevated SIR, including
demographic factors, changes in diagnostic techniques, and changes in data
collection or recording methods over time, as well as the natural variation in
disease occurrence.”

99. In points 60 to 65 of his testimony, Dr. Landrigan provides his general opinions

on how exposure guidelines are based on extrapolations and assumptions, and thus have inherent

limitations. What he fails to mention, and what I’ve previously described, is that extrapolations

and assumptions are purposefully made to be conservative and to err on the side of greater health

protection- i.e., are designed to assure safety. The assumptions always make the conservative

choice (in favor of a more restrictive guideline) even though uncertainty can be in either

direction. As I’ve described previously, the exposure levels typical of studies where actual

adverse health effects have been observed, whether human studies or animal studies, are

extrapolated downward to estimate human risk at much lower doses by using multiple safety or

42
Massachusetts Dept. of Public Health (MADPH), Office of Data Management and Outcomes Assessment. May
2017. "Cancer Incidence in Massachusetts 2009 - 2013: City and Town Supplement."

34
uncertainty factors to reduce the guideline dose to below that at which the actual health-effect

was observed. Such health-protective guidelines envision hypothetical risks, because actual

adverse health effects at low doses are not observed.

100. In point 69 of his testimony, Dr. Landrigan alleges that data shown in the Health

Impact Assessment (HIA) prepared for the proposed compressor station project show 24-hour

and annual average benzene and formaldehyde concentrations exceeding the TELs and AALs.

The specific pages of the HIA that he points to only show benzene and formaldehyde data for the

MassDEP Boston and Lynn air monitoring sites rather than any of the MassDEP air monitoring

conducted specifically within the Fore River Basin area. Notwithstanding the locations of the

benzene and formaldehyde data, the TELs and AALs are screening-level guidelines, such that

their exceedance does not lead to an expectation of significant public health risk. Dr. Landrigan

has not conducted any type of assessment to support his claims that the measured benzene and

formaldehyde concentrations are of human health significance, and the HIA reached contrary

conclusions.

101. In point 70, Dr. Landrigan makes the erroneous statement that there are elevated

rates of leukemia and lymphoma related to background concentrations of benzene and

formaldehyde in the Fore River Basin Area. Dr. Landrigan states that, “In my professional

medical opinion, these existing, elevated, background levels of benzene and formaldehyde

already present a serious risk to public health-specifically elevated risks of leukemia, lymphoma

and other cancers. These risks will be particularly great for vulnerable populations such as

children and the elderly.” However, this statement is not supported by the MADPH cancer

incidence data provided in the Appendix of the MAPC HIA Report. The MADPH data do not

show elevations for either leukemia or lymphoma in Braintree, Weymouth, or Quincy for males

35
or females as compared to the state of Massachusetts. There was one statistically significant

elevation, during one time period (2006-2010), for females in Hingham, but this elevation was

not observed in the subsequent time period (2011-2015). MADPH (2017)43 cautions that

increases or decreases in cancer incidence over time may not be due to true changes in cancer

incidence but may arise instead as a result of important data limitations:

“It should be emphasized that apparent increases or decreases in cancer incidence


over time might reflect changes in diagnostic methods or case reporting rather
than true changes in cancer incidence. Four other limitations must be considered
when interpreting cancer incidence data for Massachusetts cities and towns:
under-reporting in areas close to neighboring states; under-reporting for cancers
that may not be diagnosed in hospitals; cases being assigned to incorrect
cities/towns; and standardized incidence ratios based on small numbers of cases.”

102. In point 74 of his testimony, Dr. Landrigan alleges: “Yet another limitation in

environmental guidelines is that they are not based solely on protection of human health. All

guidelines are compromises, inasmuch as they take into consideration economic and other

factors in addition to health protection in setting legal limits.” This is not the case for the

MassDEP TELs and AALs, which are solely health-based screening-level guidelines that do not

take into account other factors, such as economics. As discussed in the pre-filed written

testimony of Dr. Sandra J.S. Baird of MassDEP,44 they are developed according to a highly

conservative (i.e., health-protective) process and are intended to assure health protection.

103. At the conclusion of his pre-filed testimony on p. 18 (point 85), Dr. Landrigan

asserts that “the existing levels of formaldehyde, benzene, and other air toxics in Weymouth and

the other areas measured in the Health Impact Assessment constitute “air pollution” within the

43
Massachusetts Dept. of Public Health (MADPH), Office of Data Management and Outcomes Assessment. May
2017. "Cancer Incidence in Massachusetts 2009 - 2013: City and Town Supplement."
44
Baird, SJS. [Massachusetts Dept. of Environmental Protection (MassDEP)]. March 26, 2019. "Pre-filed direct
testimony Sandra J.S. Baird, Ph.D. [In the matter of Algonquin Gas Transmission, LLC]." Submitted to
Massachusetts Dept. of Environmental Protection (MassDEP), Office of Appeals and Dispute Resolution. OADR
Docket Nos. 2019-008 through 2019-013 Weymouth. 84p.

36
definition set forth in 310 C.M.R. 7.01, because they are injurious to human life.” However, his

pre-filed testimony provides no quantitative support for this statement. As previously discussed,

the existing ambient-air levels of chemicals such as formaldehyde and benzene do not reach

levels where adverse health effects would be expected, and Dr. Landrigan does not offer a

quantitative human health risk assessment that demonstrates how the existing ambient-air levels

lead to unacceptable risks.

REBUTTAL TO DR. NORDGAARD

104. In his pre-filed testimony, Dr. Nordgaard cites the Shi et al. (2016)45

epidemiological study as reporting findings supporting a linear relationship between mortality

and PM2.5 levels “far below” the US EPA NAAQS. However, Dr. Nordgaard fails to discuss

how the Shi et al. (2016) study suffers from several key methodological limitations that

contribute to uncertainty in the study results and restrict it to providing suggestive, rather than

causal, evidence of increased PM2.5-mortality risks at PM2.5 levels below the NAAQS. The study

authors themselves acknowledge some of these study limitations.

105. The analysis by Shi et al. (2016) was conducted among Medicare enrollees in the

New England area in the US from 2003 to 2008. While the authors used several estimates of the

12-month average PM2.5 concentrations prior to death or censoring, the validity of the PM2.5

estimates was limited by uncertainties in the input variables, such as the Aerosol Optical Depth

(AOD) data. In particular, satellite-based AOD measurements can be biased by unresolved

cloud, water vapor, and smoke interference. Because Medicare records do not provide

information on address changes, the authors had to assume that subjects remained at the same

45
Shi, L; Zanobetti, A; Kloog, I; Coull, BA; Koutrakis, P; Melly, SJ; Schwartz, JD. 2016. "Low-concentration
PM2.5 and mortality: Estimating acute and chronic effects in a population-based study." Environ. Health Perspect.
124 (1): 46-52. doi: 10.1289/ehp.1409111.

37
address for the duration of the study period. Also, upon consideration of the potential

mechanisms underlying the PM2.5 effect on mortality, the 12-month period prior to death is not

likely to be the relevant PM2.5 exposure window. Shi et al. (2016) did not have information on

cause of death, and hence did not exclude deaths from unnatural causes (i.e., suicide, automobile

accidents, falls), which likely biased the results. Finally, no individual-level confounders were

adjusted for in the analyses, which severely undermined the validity of the observed

concentration-response relationship.

106. In using results from this single study to estimate a mortality rate among older

adults associated with PM2.5 emissions from the compressor station, Dr. Nordgaard disregards

the well-accepted caveat that statistical correlations are not equivalent to causation (Rhomberg et

al., 201146; MacMahon and Trichopoulos, 199647). In a recent critical review of associational

and causal relations between fine particulate matter and mortality, Cox (2017)48 demonstrated

how even relatively strong associations between PM2.5 and mortality are not sufficient to draw

conclusions about a causal relationship. There exist only a limited number of epidemiological

correlations suggesting PM2.5-mortality associations at PM2.5 levels below the current US EPA

NAAQS, while there is a general lack of health effects evidence from other lines of

investigation, namely laboratory-animal results, human clinical exposure results, and data on

mechanism, all of which would be necessary to support the plausibility of low-level ambient

PM2.5 exposure causing premature mortality.

46
Rhomberg, LR; Bailey, LA; Goodman, JE; Hamade, A; Mayfield, D. 2011. "Is exposure to formaldehyde in air
causally associated with leukemia? - A hypothesis-based weight-of-evidence analysis." Crit. Rev. Toxicol. 41 (7):
555-621.
47
MacMahon, B; Trichopoulos, D. 1996. Epidemiology Principles and Methods. 2nd Edition. Lippincott Williams
and Wilkins (Philadelphia, PA), 347 pp.
48
Cox, LA Jr. 2017. "Do causal concentration-response functions exist? A critical review of associational and
causal relations between fine particulate matter and mortality." Crit. Rev. Toxicol. doi:
10.1080/10408444.2017.1311838.

38
107. Notwithstanding the methodological limitations of the Shi et al. (2016) study and

the unsupported premise that its statistical correlations are equivalent to causation, Dr.

Nordgaard incorrectly applies results from the Shi et al. (2016) study in his calculation of an

increased mortality rate for older residents in the Fore River Basin due to the proposed

compressor station emissions. This incorrect calculation demonstrates Dr. Nordgaard’s lack of

understanding of epidemiological studies and air quality data. First of all, it’s important to

remember that the Shi et al. (2016) article reports an “association,” that is, a statistical

correlation, which should not be taken as establishing a casual connection between PM2.5 and

mortality. Secondly, and specifically, he performs the following calculation: (2.14% mortality

rate / 10 µg/m3 PM2.5) x (2.3 µg/m3 x facility impact PM2.5) = 0.4922% mortality rate (Paragraph

63), with the 2.14% mortality rate per 10 µg/m3 drawn from Shi et al. (2016) for two-day

exposures and the 2.3 µg/m3 24-hour PM2.5 proposed compressor station maximum impact drawn

from MassDEP (2019)49 Table 3. This is an apples to oranges comparison, as one number

focuses on two-day exposures and the other on 24-hour exposures. Longer term exposures are

typically lower than shorter-term exposures, indicating that Dr. Nordgaard’s calculation is likely

an overestimate. Moreover, the 2.3 µg/m3 is a one-day-per-year maximum impact level

applicable to a single location and Nordgaard erroneously asserts it to apply to “an increase in

mortality rate in the [entire] Fore River Basin.”

108. The Shi et al. (2016) article provides no clear framework for causal

determinations. In fact, Shi et al. (2016) consistently use the word “associated” as opposed to

“causes” when describing their conclusions. The Clean Air Science Advisory Committee also

49
Massachusetts Dept. of Environmental Protection (MassDEP), Bureau of Air and Waste. January 11, 2019. "Air
Quality Plan Approval." Submitted to Algonquin Gas Transmission, LLC (Houston, TX) 27p.

39
noted that it is problematic to assert causality based on a subjective view of the overall data.

Although in its criteria-pollutant review documents, US EPA provides descriptions of the

research studies and speculates extensively on possible modes of action, the agency's causal

determinations are not sufficiently supported. Accordingly, the CASAC recommended in its

letter to US EPA Administrator Andrew Wheeler that US EPA revisit arguments that support

determinations of causality for specific associations of PM2.5 levels with life-threatening effects

such as mortality and hospitalizations.50 As the CASAC stated, without such demonstrations of

the logic involved, the US EPA is not providing the needed transparency to support the validity

of its causality conclusions.

109. In his concluding points, p. 16 - 18 (e.g., point 86), Dr. Nordgaard asserts that the

applicant will cause a “condition of air pollution,” but he provides no quantitative analysis to

show that the incremental concentrations predicted by the air dispersion analysis will cause air

pollution aside from quoting that “such concentrations and such duration” is “potentially

injurious” to humans, animals, or vegetation (point 74).

CONCLUSIONS

110. As a toxicologist and a practitioner of human health risk assessment for many

years, my overall conclusion is that the proposed Weymouth compressor station, for the

operating conditions defined in the MassDEP Air Quality Plan Approval, cannot be expected to

pose unreasonable health risks to populations in the Fore River Basin area. This conclusion is

based on my assessment of the modeled air quality impacts of the proposed facility and existing

air quality in the Fore River Basin area. Additional air modeling has been conducted by the

50
US EPA, Clean Air Scientific Advisory Committee (CASAC) April 11, 2019. "Letter Report to A. Wheeler (US
EPA) re: CASAC Review of the EPA’s Integrated Science Assessment for Particulate Matter (External Review
Draft - October 2018)." EPA-CASAC-19-002. 205p

40
Town of Weymouth’s expert Hinckley, which suggests that, for certain assumed facility

operating conditions at start up, small exceedances of the formaldehyde and benzene AALs and

TELs may sometimes occur at locations to the east within and just outside the facility fence line

in the vicinity of the Kings Cove Conservation Area. Whether conducted correctly or not, these

modeling results do not change my opinion. First, maximum modeled concentrations for

locations along and nearby to the facility fence line are not representative of population

exposures across the Fore River Basin area. It is broadly recognized that incremental ambient air

concentrations associated with facility air emissions decrease rapidly with distance from the

emission sources due to atmospheric dispersion and dilution. In other words, air emissions are

not transported en bloc to distant locations, and air concentrations projected to occur very close

to a facility’s emission sources should not be viewed as being representative of exposure levels

for populations living at more distant locations from the facility, especially for populations

spread across multiple communities. Second, it is extremely unlikely that any person, including

those using Kings Cove Conservation Area, could be exposed on a continuous, annual basis to

start up emissions at those locations of the modeled exceedances. Finally, as has been discussed

in this testimony, the modeled exceedances are far less than an order of magnitude above the

pertinent AALs and TELs, which means that even with a lifetime of exposure at the modeled

levels, no adverse health effects would be expected.

Signed under the pains and penalties of perjury on May 7, 2019.

Peter A. Valberg

41