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____________________________________
)
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 )
____________________________________)
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
additional reports and abstracts dealing with lung biology, inhalation toxicology, and risk
assessment.
function (National Heart, Lung, and Blood Institute), pulmonary pathology (University of
Vermont Lung Center), analytical and quantitative microscopy (Woods Hole Marine Biological
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
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
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
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
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
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.
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,
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
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
4
acceptable. These target (hypothetical) cancer risks are much smaller than the combined risk
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
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),
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
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
5
extrapolations from observations at high levels of exposure, or because of other kinds of indirect
evidence.
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
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
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
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.
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-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
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
25. The final results, for chronic inhalation exposure guidelines, yielded three, health-
All three of these agency derivations are based on being protective of health, including for
9
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
the CalOEHHA REL (3 µg/m3), and reduced it further by a relative source contribution (RSC)
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
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
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
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
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,
34. The AAL is thus a factor of 163,000 to 326,000-fold below the lowest benzene
11
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,
39. All three of these derivations are based on being protective of health, including
40. Studies of indoor air have shown that people are exposed to indoor concentrations
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-
concentration, and reduced it further by a relative source contribution (RSC) factor of 5, to arrive
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
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
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
50. The MassDEP formaldehyde AAL is nearly 100,000-fold (86,250-fold) below the
animals.
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
14
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:
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
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.
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
concentration, and reduced it further by a relative source contribution (RSC) factor of 5, to arrive
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
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
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.
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
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
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-
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
68. As compared to the MassDEP TEL of 2 µg/m3, the ATSDR acute inhalation MRL
69. As compared to the MassDEP TEL of 0.07 µg/m3, the ATSDR acute inhalation
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
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
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
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
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
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
(a) If 100,000 people were continuously exposed (each day, 24 hrs/day) over
(b) The probability for any one person of being diagnosed with a
(c) If human lifetime were not limited, an exposed individual might expect
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
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
the stated MassDEP policies to protect the public health.” But, this is
(b) p. 10, point 26: “Thus, the TELs for ambient air limit total chemical
(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
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).”
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
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
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
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
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
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-
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
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
unacceptable cancer risks from existing ambient air. However, if the average formaldehyde
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
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
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
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.
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
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
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
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
(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
fact, Dr. Clapp’s next sentence in point 17 states “The default assumption
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
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
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
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
(a) p. 6, point 27: “an established body of science that unequivocally links air
(b) p. 7, point 31: “it is well established that air pollution (what type, at what
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
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
“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
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
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
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
104. In his pre-filed testimony, Dr. Nordgaard cites the Shi et al. (2016)45
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
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
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
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
applicable to a single location and Nordgaard erroneously asserts it to apply to “an increase in
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.
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
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
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
Peter A. Valberg
41