Wang, Joanne - TTC...1 Wang, Joanne To: [email protected]; Occhiogrosso, Leonard; Drygas, Tyler...

1

Wang, Joanne

To: [email protected]; Occhiogrosso, Leonard; Drygas, TylerCc: [email protected]: RE: McNicoll Bus Garage - Clarification points on the HHRA - DRAFT RESPONSE

From: MacDonald, Jason Sent: March-12-15 10:51 AM To: 'Barbara Lachapelle'; Howard Shapiro; Nagler, David Cc: Reg Ayre; Dimovski, John; Romano, Lito; Favaro, Marcello Subject: RE: McNicoll Bus Garage - Clarification points on the HHRA - DRAFT RESPONSE

Hi Barb,

Further to your e‐mail message from February 20th shown below, find attached two memos from Intrinsik to address the items you have raised. Glenn Ferguson from Intrinsik developed these responses after in‐depth dialogue with TPH staff over the past week, and I trust these responses will address your concerns. Assuming these responses are acceptable, it is my understanding that there are no further items of concern from TPH to be addressed. Please confirm at your earliest opportunity. Upon confirmation we look forward to receipt of TPH’s final statement regarding public health impacts resulting from the TTC McNicoll Bus Garage project.

As discussed in the memos, minor revisions will be made to the Screening‐Level Human Health Risk Assessment (SLHHRA) to incorporate the changes Glenn has recommended. These changes will not impact the findings of the report. We will provide you with a copy of the SLHHRA as soon as it is available.

Thank you!

Jason MacDonald, P.Eng., PMP

Project Manager, TTC Construction Department 416‐393‐6018 [email protected]

From: Barbara Lachapelle [mailto:[email protected]] Sent: February-20-15 3:46 PM To: Howard Shapiro; Nagler, David; MacDonald, Jason Cc: Reg Ayre; Dimovski, John; Romano, Lito; Favaro, Marcello Subject: RE: McNicoll Bus Garage - Clarification points on the HHRA

Hello, After the initial review of the HHRA and some internal discussions, we are requesting clarification on the following points with respect to the proposed methodology and TRVs to be used in the assessment:

Methodology for assessing Criteria Air Contaminants (CACs)

2

Please provide a rationale for as to why AQBAT is not the appropriate methodology for the assessment of the CACs in this project

Toxicity Reference Values (TRVs)

Please provide a detailed rationale for the use of the following TRVs

1. Chronic, non-cancer TRVs Benzene – ATSDR 9.58 ug/m3 – Cal EPA recently updated CREL to 3 ug/m3 NO2 and PM2.5 – rationale for the use of the proposed TRVs Acetaldeyde – although US EPA value is more conservative, the rationale for using US EPA and not Cal

EPA

2. Chronic, carcinogenic TRVs 1,3 Butadiene – rationale for the use of US EPA rather than the MOE Benzene – rationale for using the IRIS value vs. Cal EPA

3. Acute, non-carcinogenic TRVs (1 hr.) Benzene – rationale for the use of TCEQ value vs. the newly updated Cal EPA 1 hr. value

4. Acute, non-carcinogenic (24 hr.) Benzene – rationale for the use of ATSDR value vs. MOE AAQC

Have a great weekend everyone, Barb

Barbara Lachapelle, MASc, CPHI(C) Environmental Health Specialist Healthy Environments Toronto Public Health 44 Victoria Street, 18th Floor Toronto, Ontario M5C 1Y2 Tel: 416 392-7691 Fax: 416 338-1643 [email protected]

Memo

Date:

March 10, 2015

To: Tyler Drygas, AECOM From: Glenn Ferguson, Ph.D., QPRA

Re: Response to comments provided by Toronto Public Health on the use of Concentration Response Functions (CRFs) to evaluate local CAC risks

Intrinsik has received comments originally made by Toronto Public Health (Barbara Lachapelle) on February 20, 2015. These comments were subsequently forwarded to Intrinsik by AECOM (Tyler Drygas) via email on February 23, 2015. Intrinsik has reviewed the comments made by Toronto Public Health and provided responses to all but Comment #1 in a previous memo, dated March 6th, 2015. The following memo provides a response to the remaining question. Methodology for assessing Criteria Air Contaminants (CACs) Comment #1: Please provide a rationale for as to why AQBAT is not the appropriate methodology for the assessment of the CACs in this project Response to Comment #1: Health Canada’s Air Quality Benefits Assessment Tool (AQBAT) was specifically designed to estimate the human health and welfare benefits or damages associated with changes in Canada’s ambient air quality. The AQBAT model estimates the impacts of air quality on occurrences of health outcomes through the use of concentration response functions (CRFs) which are derived from epidemiological studies. Specifically, AQBAT provides CRFs for the following criteria air contaminants (CACs): carbon monoxide (CO); nitrogen dioxide (NO2); ozone (O3); sulphur dioxide (SO2); fine particulate matter (PM2.5); and coarse particulate matter (PM10). These CRFs provide a correlation between the change in frequency of health outcomes (e.g., acute respiratory symptoms, chronic exposure mortality, respiratory hospital admissions, etc.) with the change in ambient concentrations for these contaminants, on both an acute and chronic basis depending on contaminant. A key element to note is that the Health Canada-endorsed CRFs are specified as normal distributions, rather than discrete values, to account for uncertainty in the underlying dataset. For example, in the case of chronic exposure mortality (for which TPH has evaluated annual average PM2.5 concentrations in their Local Air Quality [LAQ] reports), the mean CRF value is 6.76 x 10-3 with a standard error of 1.50 x 10-3 based on Krewski et al. (2000) reanalysis of the Harvard Six Cities study and the much larger ACS Study. The population size in the original Six Cities Study was 8,111 individuals, while the size of the study population for the ACS Study was 552,138. As such, you have an overall n for the CRF around 560,000.

Response to TPH comments on the use of CRFs in the TTC McNicoll Bus Garage SLHHRA March 10, 2015 Intrinsik Environmental Sciences Inc. – Project # 21640 Page 1

As noted in the PM2.5 chronic exposure mortality example above, these CRFs include fairly large uncertainty bounds around the mean value, despite being developed from such a large study population base. AQBAT itself addresses this through the use of a Monte Carlo probabilistic sampling of the CRF distribution (using the @Risk Excel Addon), thus incorporating the uncertainty into the overall probability density function of the results. Furthermore, AQBAT incorporates pollutant concentration statistics further integrating environmental variability into the analysis. Therefore, simply taking the mean CRF value and applying it to a maximum predicted change in a given contaminant concentration is not what was intended by AQBAT and Health Canada, and likely overestimates the percent change in health statistic when one considers the variability of pollutant concentrations over a given airshed. The frequency of health outcomes is directly dependent on the population exposed to the contaminants. In its calculations, the AQBAT model uses age differentiated population estimates based on the 2001 census, using 5 geographic area types: i) National (i.e., all of Canada); ii) Provinces/Territories (i.e., 13 units); iii) Census Agglomeration Areas – towns with 10,000+ population (i.e., 140 units); iv) Census Metropolitan Areas (CMAs) – cities with 100,000+ populations (27 units); and, v) Census Divisions (i.e., 288 CDs in Canada at the time of model development). The smallest potential population group evaluated within the AQBAT model are the CDs which vary widely in size and population. However, typically they range from a few thousand people to millions of people (i.e., Greater Toronto Area, Metro Vancouver, Montreal, etc.) in size. AQBAT itself expresses the change in incidences of a specific health endpoint in terms of the number of events per million specified population. When discussing the applicability of epidemiological data between exposed populations, a key element is the generalizability of the original study results to a given sample population. In the case of the AQBAT CRFs, you have a study population of more than a half million people being used in AQBAT to characterize potential impacts on populations from thousands to millions of people being exposed to the same CAC concentrations within a given airshed. From a statistical and epidemiological point of view, this relationship starts to break down as you reduce the number of people in your evaluation population. In the case of the City of Toronto LAQ reports, these evaluations are being done on a Ward basis, where the population base is in the tens of thousands (e.g., Ward 5 and 6 have populations of 64,015 and 58,995 as of 2011, respectively). These populations would be consistent with those evaluated within the AQBAT model system and the original research studies used to derive the CRFs. However, it becomes much more difficult to maintain this generalizability for application to potential CAC exposures from the proposed TTC McNicoll Bus Garage, or any similar localized emission source, to the surrounding population. In the case of the McNicoll Bus Garage, predicted emissions are highest directly adjacent to the proposed facility and drop off dramatically as you move away. As such, a very limited number of people may be exposed to the maximum predicted concentration. The following figure provides an annual average concentration isopleth of PM2.5 concentrations as one moves away from the proposed McNicoll bus garage. Based on the results of the modelling, within an approximate area of 1 km2, the predicted annual average contribution from the bus garage for PM2.5 to the surrounding air shed drops from 0.3 µg/m3 at the closest residential receptor at the Mon Sheong centre to less than 0.008 µg/m3 at the edge of the isopleth. If one focuses on the receptor locations at the Mon Sheong centre itself, predicted concentrations drop from 0.3 to 0.075 µg/m3 from one edge of the building to the other, showing the rapid decline in potential particulate contributions even a short distance from the proposed


facility. Finally, the average annual concentration contribution from the proposed facility across the surrounding 1 km2 grid would be 0.072 µg/m3, and is highly skewed by the predicted ambient concentrations in very close proximity to the proposed facility.

Therefore, if one were to use the maximum annual average PM2.5 concentration contribution from the proposed facility in conjunction with the AQBAT CRF to calculate percent change in chronic premature mortality, a very limited sample size may actually be exposed to that concentration change (i.e., less than ten people?). From an epidemiological point of view, putting aside the discussion as to whether the populations are even representative, the error bounds of uncertainty associated with extrapolating the results of the large epidemiological studies used to develop the CRF values to an extremely small sample population would result in one not being able to make a definitive conclusion on the outcome. Ultimately, because effect estimates are only generalizable to large populations, it is simply not possible to precisely estimate the number of premature deaths (related to the predicted percent change in the outcome statistic) for the small number of people living closest to the proposed facility. If one wished to use the AQBAT CRF values to evaluate the impact on an airshed, an appropriate study area with sufficient population size (consistent with that employed within AQBAT) should be used. In this case, one could estimate the change in ambient PM2.5 (and other CAC) concentrations arising from the proposed facility may have to the surrounding Ward. Ward 39 has a population of nearly 55,000 people, of which the isopleth in the above figure only covers a small portion, outside of which the contribution of the proposed facility would be negligible. Given the average incremental annual increase from the propose facility over the 1 km2 grid area is 0.072 µg/m3, compared to an annual average background PM2.5 concentration in the overall airshed of 8.2 µg/m3, it is very unlikely that the average concentration increase related to the proposed facility above background conditions would be detectable, let alone result in an appreciable change in any of the health outcomes considered by the City in their LAQ reports over the appropriate population size.


If for the sake of argument, one uses the average annual increase in PM2.5 concentration predicted to arise from the operation of the proposed bus garage to the surrounding 1 km2 airshed (i.e., 0.072 µg/m3) – acknowledging the population base in this restrictive area is still probably too low from an epidemiological statistical power point-of-view – this results in a predicted incremental increase in premature mortality of 0.049% to this specific subpopulation. Even this is an incorrect application of the data as contributions to the airshed by the source is not consistent across the entire 1 km2 area, as is the core assumption in AQBAT and similar airshed health evaluation models. Given the significant uncertainty involved in this estimate (as discuss above), it is likely a predicted change in health outcomes related to emissions from the proposed facility would not be statistically detectable, and could lead to very misleading conclusions if improperly evaluated. Based on this, it continues to be Intrinsik’s position that it would be inappropriate to apply the Health Canada CRF values in this manner to such a small exposed population size as would be present in the area surrounding the proposed TTC McNicoll Bus Garage.


Memo

Date:

March 11, 2015

To: Tyler Drygas, AECOM From: Glenn Ferguson

Re: Response to comments provided by Toronto Public Health on select TRVs used in the SLHHRA for the proposed TTC McNicoll Bus Garage

Intrinsik has received comments originally made by Toronto Public Health (Barbara Lachapelle) on February 20, 2015. These comments were subsequently forwarded to Intrinsik by AECOM (Tyler Drygas) via email on February 23, 2015. Intrinsik has reviewed the comments made by Toronto Public Health and provided responses in Section 1. In cases where supplemental information was required, this information is provided in Section 2 of this memo. Section 1: Response to TPH Comments Methodology for assessing Criteria Air Contaminants (CACs) Comment #1: Please provide a rationale for as to why AQBAT is not the appropriate methodology for the assessment of the CACs in this project Response to Comment #1: A supplemental document will be provided early next week to provide more detailed referenced discussion on this issue. Toxicity Reference Values (TRVs) Comment #1: Please provide a detailed rationale for the use of the following TRVs (Chronic, non-cancer TRVs):

a) Benzene – ATSDR 9.58 µg/m3 – Cal EPA recently updated CREL to 3 µg/m3 b) NO2 and PM2.5 – rationale for the use of the proposed TRVs c) Acetaldehyde – although US EPA value is more conservative, the rationale for using

US EPA and not Cal EPA

Response to Comment #1:

a) Benzene: TPH noted that Cal EPA recently revised its CREL benchmark to 3 µg/m3, based on statistically significant decreased counts of B-lymphocytes in occupationally exposed populations (Cal EPA, 2014). Upon review of the available TRV derivation information, the Project Team agrees with the TPH recommendation to use the value derived by Cal EPA (2014). The SLHHRA will be revised to use this chronic TRV.

b) NO2: The SLHHRA currently uses a benchmark of 100 µg/m3, which is the US EPA

(2010) annual AAQS. Please see the selection rationale in Section 2 below. No change to the SLHHRA is recommended. PM2.5: The SLHHRA currently uses a benchmark of 8.8 µg/m3, which is the CCME (2012) annual CAAQS for compliance in 2020. Please see the selection rationale in Section 2 below. No change to the SLHHRA is recommended.

c) Acetaldehyde: TPH recommended that the Cal EPA TRV of 140 µg/m³, based on the degeneration of olfactory epithelium observed in rat studies (Cal EPA, 2008), be used for the current assessment. Upon review of the available TRV derivation information, the Project Team agrees with the TPH recommendation to use the value derived by Cal EPA (2008). Though the US EPA IRIS (1991) value used previously in the assessment is more conservative (i.e., 9 versus 140 µg/m3), the Cal EPA TRV provides for the most recent analysis using up-to-date science. The SLHHRA will be revised to use this chronic TRV.

Comment #2: Please provide a detailed rationale for the use of the following TRVs (Chronic, carcinogenic)

a) 1,3 Butadiene – rationale for the use of US EPA rather than the MOE b) Benzene – rationale for using the IRIS value vs. Cal EPA

Response to Comment #2:

a) 1,3-Butadiene: TPH recommends the use of 5.0x10-7 per µg/m3 based on epidemiologic data on leukemia risk from occupational exposure reported in a retrospective cohort study initially derived by TCEQ (2008), which was subsequently adopted by MOE (2012) to derive its AAQC. Upon review of the available TRV derivation information, the Project Team agrees with the TPH recommendation to use the TCEQ (2008) TRV from which the MOE (2012) AAQC was derived. While less conservative than the US EPA IRIS value used in the SLHHRA, it makes use of the most recent toxicological evidence for cancer related to 1,3-butadiene exposures. The SLHHRA will be revised to use this chronic TRV.

b) Benzene: The SLHHRA currently uses the US EPA-derived IUR value of 7.8 x 10-6 per

µg/m3 based on leukemia incidence data in an occupationally exposed population (US EPA IRIS, 2000). Upon review of the available TRV derivation information, the Project Team recommends against the use of the Cal EPA (2008) IUR. Please see the selection rationale in Section 2. No change to the SLHHRA is recommended.

Comment #3: Please provide a detailed rationale for the use of the following TRVs (Acute, non-carcinogenic TRVs (1 hr.))

a) Benzene – rationale for the use of TCEQ value vs. the newly updated Cal EPA 1 hr. value

Response to TPH comments on TRVs used in the TTC McNicoll Bus Garage SLHHRA March 6, 2015 Intrinsik Environmental Sciences Inc. – Project # 21640 Page 2

Response to Comment #3: To summarize, the following TRV was selected:

a) Benzene: Intrinsik initially recommended a 1-hour acute inhalation ReV of 580 µg/m3 from TCEQ (2007) based on immunological effects in mice, while TPH has recommended use of Cal EPA (2014) 1-hour acute inhalation REL of 27 µg/m3. Upon review of the available TRV derivation information, the Project Team agrees with the TPH recommendation to use the value derived by Cal EPA (2014). The SLHHRA will be revised to use this 1-hour TRV for benzene. Refer to Section 2 below for further discussion of this issue.

Comment #4: Please provide a detailed rationale for the use of the following TRVs (Acute, non-carcinogenic TRVs (24 hr.))

a) Benzene –rationale for the use of ATSDR value vs. MOE AAQC Response to Comment #4:

a) Benzene: Intrinsik recommended the use of the ATSDR (2007) MRL of 29 µg/m3 based on immunological effects observed in study animals (rat), while TPH has recommended use of MOE (2011) 24-hour AAQC of 2.3 µg/m3. Upon review of the available TRV derivation information, the Project Team recommends against the use of the MOECC 24-hour AAQC. Please see the selection rationale in Section 2. No change to the SLHHRA is recommended.


Section 2: Selection Rationales NO2 Chronic Inhalation Non-Cancer TRV Selection Rationale (Comment 1b)

• Intrinsik recommended the use of the US EPA (2010) annual AAQS of 100 µg/m3.

• TPH did not provide a recommended RfC for use but requested rationale for the selection of the US EPA (2010) value.

TRVs are available from WHO (2005) (40 μg/m3), US EPA (2010) (100 μg/m3), and Health Canada (2006) (desirable: 60 μg/m3, acceptable: 100 μg/m3). NO2 exposure is associated with respiratory disease, most notably in children. Health Canada (2006) recommended an annual average NAAQO MDL and MAL of 32 and 53 ppb (60 and 100 µg/m3), respectively. However, no further information regarding the derivation of these values was identified. A scientific review of the annual air standard conducted in 1993 suggested that the standard of 100 µg/m³ was based upon the results of a meta-analysis of epidemiological studies conducted in children ages 5 to 12 (US EPA, 1993). Within this review, an increase in 0.015 ppm or 28 µg/m³ of NO2 over an averaging period of 2 weeks was associated with a 20% increase in respiratory symptoms. The NO2 sources included both indoor and outdoor sources, and average concentrations in the studies were noted to range from 0.008 to 0.065 ppm (US EPA, 1993). In 1996, the annual standard was maintained by the US EPA on the basis that, in combination with the short-term standard, the annual standard was protective of both the potential short-term and long-term human health effects of NO2 exposure (US EPA 1996). The US EPA (2010) indicated that the annual standard was upheld due to the uncertainty associated with the potential long-term effects of NO2. As the annual NO2 standard of 100 µg/m³ was recently re-evaluated and upheld, this value was selected for use in the chronic inhalation assessment. The WHO (2005) guideline value of 40 µg/m³ (0.023 ppm) represented an annual value recommended by the WHO International Program on Chemical Safety (IPCS). The WHO IPCS (1997) indicated that the 40 µg/m³ was based on consideration of background concentrations and the observation that adverse health impacts may occur when concentrations in addition to background are above 28 µg/m³. However, as this value was not well substantiated in the available supporting documentation, the US EPA value was used in the chronic assessment. Recommendation: The chronic exposure limit of 100 µg/m3 reported by the US EPA (2010) is recommended for use in the assessment due to its scientific defensibility compared to other viable exposure limits.


PM2.5 Chronic Inhalation Non-Cancer TRV Selection Rationale (Comment 1b)

• Intrinsik recommended the use of the CCME (2012) CAAQS for compliance, 2020 of 8.8 µg/m3.

• TPH did not provide a recommended RfC for use but requested rationale for the selection of the CCME (2012) value.

TRVs are available from CCME (2012) (compliance 2015: 10 μg/m3, compliance 2020: 8.8 μg/m3), US EPA (2010) (12 μg/m3), and WHO (2006) (10 μg/m3). PM2.5 exposure is associated with various adverse health effects and an increased risk of mortality. The CCME (2012) derived two annual average CAAQS of 10 µg/m3 (for compliance by 2015) and 8.8 µg/m3 (for compliance by 2020) for PM2.5. Though a supporting document was available (CCME, 2012), the specific basis of the annual average values with respect to health was not provided. The US EPA (2010) derived an annual average NAAQS of 12 µg/m3 based on epidemiological evidence relating ambient concentrations of PM to different adverse health effects (increased risk of mortality, cardiovascular-related effects, and respiratory morbidity). The WHO (2006) derived a chronic inhalation AQG of 10 µg/m3 based on alterations in survival rates in the American Cancer Society (ACS) study and the Harvard Six Cities Study (Krewski et al., 2000). These investigation reported robust associations between long-term exposure to PM2.5 and altered rates of mortality. The concentration of exposure in the ACS and Harvard Six Cities Study was 18 µg/m3 and 20 µg/m3 respectively. Statistical uncertainty in the risk estimate was apparent in the ACS study at a concentration of 13 µg/m3 (Krewski et al., 2000). The WHO (2006) also cited a study by Dockery et al. (1993) that showed increased health risks associated with chronic inhalation of PM2.5 in cities at concentrations of 11 and 12.5 µg/m3. The WHO (2006) therefore selected an AQG of 10 µg/m3 as this value would most likely be below the mean concentration associated with adverse effects reported in the literature. Recommendation: The 2020 compliance CAAQS (chronic inhalation value) of 8.8 µg/m³ derived by CCME (2012) is recommended for use in the assessment as it is the most conservative value and is the regulatory standard for Canada.


Benzene Chronic Inhalation Cancer TRV Selection Rationale (Comment 2b)

• Intrinsik initially recommended an IUR of 2.2 x 10-6 per µg/m3 from US EPA IRIS (2000) based on leukemia incidence data in an occupationally exposed population.

• TPH recommended use of Cal EPA (2008) IUR of 2.9x10-5 per µg/m3 The US EPA IRIS (2000) presented a range of potential IURs of benzene. The key data sets employed in the US EPA IRIS cancer assessment were those by Rinsky et al. (1981, 1987), which were also critically analyzed by Paustenbach et al. (1993), Crump and Allen (1984), Crump (1992, 1994), and the US EPA (1998). The Rinsky et al. (1981, 1987) studies examined the incidence of leukemia in exposed white male workers in the rubber hydrochloride department of a pliofilm plant. The more comprehensive follow-up study (Rinsky et al., 1987) involved the evaluation of 1,165 workers who were exposed for at least 1 day between 1965 and 1981. Individual assessments of cumulative exposure were calculated for each worker based on air sampling data. Inhalation unit risks of 2.2 x 10-6 to 7.8 x 10-6 per µg/m3 were extrapolated based on a low dose linear model using maximum likelihood estimates for leukemia in humans (US EPA IRIS, 2000). MOE (2011) recommended an IUR of 2.2x10-6 (µg/m3)-1 that was based on US EPA IRIS (2000). The Cal EPA (2008) derived an URF of 2.9 x10-5 (µg/m3)-1 based on epidemiological studies of Chinese workers. Although it is not very clear, the basis of the Cal EPA (2008) value seemed to be the studies by Yin et al. (1994, 1996). The Chinese cohort studies that served as the basis of the Cal EPA (2008) derivation were some of the studies determined by the US EPA to have methodological issues (poor exposure characterization, co exposure to other agents, data quality) to the point where the study was not adequate for quantitative assessment. The US EPA IRIS (2000) IUR value, in contrast, was based on a study that has been critically analyzed by several other studies. As such, the Cal EPA (2008) IUR was not used in the chronic inhalation assessment of benzene. Recommendation: The IUR 7.8 x 10-6 per µg/m3 reported by the US EPA (2000) is recommended for use in the assessment due to its scientific defensibility compared to other viable exposure limits and conservatism over the low-range risk estimate also provided by the US EPA and recommended by the MOECC.


Benzene Acute 1-hour Inhalation Cancer TRV Selection Rationale (Comment 3)

• Intrinsik initially recommended a 1-hour acute inhalation ReV of 580 µg/m3 from TCEQ (2007) based on immunological effects in mice.

• TPH recommended use of Cal EPA (2014) 1-hour acute inhalation REL of 27 µg/m3. Cal EPA (2014) has recently derived a 1-hour acute inhalation REL based on decreased early nucleated red cell counts observed during a developmental toxicity study in mice by Keller and Snyder (1988). In the critical study by Keller and Snyder (1988), pregnant female mice were exposed to benzene for 6 hours per day for 10 days during gestation (days 6-15). A LOAEL of 5 ppm (16,000 µg/m3) benzene was seen in two day neonates with no NOAEL being detected. The LOAEL was converted to a Human Equivalent Concentration (HEC) using RGDR. Given that the observed critical effect was systemic, a default value of 1 was used for the RGDR. A cumulative uncertainty factor of 600 (SQRT10 for the use of LOAEL, 10*SQRT10 for extrapolation from animals to humans, and 2*SQRT10 for human variability) was applied to the HEC (LOAEL) to provide the acute 1-hour inhalation value of 0.008 ppm (27 µg/m3). The TCEQ (2007) derived a 1-hour inhalation ReV of 580 µg/m3 that was based on depressed peripheral lymphocytes and depressed mitogen-induced blastogenesis of femoral B- lymphocytes in C57BL/6J male mice. The key study by Rozen et al. (1984) exposed mice to benzene via inhalation for 6 hours per day for 6 days and reported a LOAEL of 10.2. The TCEQ (2007) adjusted the LOAEL for benzene exposure reported by Rozen et al. (1984) to 18.5 ppm (59.1 mg/m3), using Haber’s law and a default approach for converting exposures of more than one hour to a 1 hour exposure level. The LOAEL (ADJ) was converted to a Human Equivalent Concentration (HEC) LOAEL using RGDR. In the case that the animal blood to gas partition coefficient is greater than the human blood to gas partition coefficient, a default value of 1 is used for the RGDR. Thus, the LOAEL (HEC) was calculated to be 18.5 ppm. A cumulative uncertainty factor of 100 (3 for inter-species variability, 10 for intra-species variability, 3 for use of a LOAEL, and 1 for database uncertainty) was applied by the TCEQ (2007) to the LOAEL (HEC). The TCEQ (2007) also stated that lymphocyte count depression was a sensitive sentinel effect that was not a serious nature, and the reported decreased lymphocyte count at 10.2 ppm appeared to be within the normal range. The result was an acute ReV of 580 µg/m3 that was based on immunological effects. Recommendation: While there is considerable uncertainty with respect to considering a one-time 1-hour exposure to benzene as potentially causing developmental toxicity and thus regulating as such, the approach taken by Cal EPA in the derivation of their value is reasonable and protective. Given this and that the derived TRV is more conservative than the previously selected TCEQ benchmark, Intrinsik agrees with TPH’s recommendation to select the Cal EPA TRV for the evaluation of acute 1-hour exposure to benzene.


Benzene Acute 24-Hour Inhalation TRV Selection Rationale (Comment 4)

• Intrinsik recommended the use of the ATSDR (2007) MRL of 29 µg/m3 based on immunological effects observed in study animals (rat).

• TPH recommended use of MOE (2011) 24-hour AAQC of 2.3 µg/m3. The MOE (2011) derived a 24-hour health-based inhalation AAQC of 2.3 µg/m3 for benzene. This value was converted from the MOE (2011) annual AAQC, which was derived from the US EPA IRIS (2000) IUR value of 2.2 x 10-6 (µg/m3)-1. As noted by previously (comment 2b), the US EPA IRIS (2000) IUR selected by MOE (2011) is the low-end risk estimate. The annual AAQC was derived assuming an incremental lifetime cancer risk level of one-in-one million. The 24-hour AAQC was converted from the annual AAQC by multiplying the annual value by a factor of 5. This factor was used based on empirical monitoring data, ratios of concentrations observed for different averaging times, and meteorological considerations (MOE, 2011). The ATSDR (2007) derived an acute MRL of 0.009 ppm (29 µg/m3) that was based on reduced lymphocyte proliferation following mitogen stimulation in mice in the study by Rozen et al. (1984). Male C57BL/6J 0, 32.6, 99, 320, or 960 mg/m³ benzene in whole body dynamic inhalation chambers for 6 hours/day on six consecutive days (ATSDR 2007). The control group was exposed to filtered, conditioned air only. Significant depression of femoral lipopolysaccharide induced B colony forming ability was observed at the 10.2 ppm exposure level in the absence of a significant depression of total number of B cells. Peripheral lymphocyte counts were depressed at all exposure levels. The ATSDR (2007) adjusted a LOAEL of 10.2 ppm (32.6 mg/m³) from intermittent to continuous exposure (6/24 hours) to a concentration of 2.55 ppm (8.16 mg/m³). The duration adjusted LOAEL was converted to a HEC for a category 3 gas causing respiratory effects. The average ratio of the animal blood: air partition coefficient would be greater than 1; thus, a default value of 1 was used in calculating the HEC (ATSDR 2007). As a result, a HEC (LOAEL) of 2.55 ppm (8.16 mg/m³) was identified. A cumulative uncertainty factor of 300 (10 for the use of LOAEL, 3 for extrapolation from animals to humans, and 10 for human variability) was applied to the adjusted LOAEL to provide the MRL of 0.009 ppm (29 µg/m3). The acute-duration MRL is protective of inhalation exposures of 14 days or less. Recommendation: The MOE (2011) 24-hour AAQC for benzene is established from a policy point-of-view to ensure compliance on a daily basis so that annual exposures may not result in exceedances of the cancer-based TRV. The Ministry’s intention was simply to not have to wait for a year of operation to determine that a facility being evaluated under O. Reg. 419 was out of compliance and causing potential cancer-based health risks. Rather, the intention was to catch issues early (i.e., repeated exceedances of the 24-hour compliance benchmark) before it becomes a true risk from a cancer point-of-view. Ultimately, there is little scientific justification for the establishment of a 24-hour acute benchmark based on a chronic, long-term exposure endpoint such as leukemia. Furthermore, the MOECC used policy-based, not science-based, extrapolation factors to convert the long-term chronic benchmark into a compliance-based 24-hour benchmark. It is also worth noting that the MOECC has historically cautioned against using such 24-hour AAQC values, derived for compliance purposes, as appropriate acute benchmarks as part of an HHRA. Given this, Intrinsik recommends continuing to use the ATSDR 24-hour acute benchmark for benzene in the current assessment.


6605 Hurontario Street, Suite 500, Mississauga, Ontario ▪ L5T 0A3 Tel: 905-364-7800 ▪ Fax: 905-364-7816 ▪ www.intrinsikscience.com

TTC MCNICOLL BUS GARAGE

TRANSIT PROJECT ASSESSMENT PROCESS

SCREENING LEVEL HUMAN HEALTH RISK ASSESSMENT (SLHHRA) OF AIR QUALITY

IMPACTS

FINAL REPORT

April 22, 2015 Prepared For: AECOM Canada 4th Floor, 30 Leek Crescent

Richmond Hill, Ontario L4B 4N4

FINAL REPORT

TTC McNicoll Bus Garage Transit Project Assessment Process – SLHHRA of Air Quality Impacts April, 2015 Intrinsik Environmental Sciences Inc. – Project #20-21640

TTC MCNICOLL BUS GARAGE TRANSIT PROJECT ASSESSMENT PROCESS - SCREENING LEVEL HUMAN HEALTH RISK ASSESSMENT OF AIR QUALITY IMPACTS -

DISCLAIMER AND SIGNOFF Intrinsik Environmental Sciences Inc. (Intrinsik) provided this report for AECOM Canada Limited. (hereafter referred to as AECOM), and their client the Toronto Transit Commission (TTC), solely for the purpose stated in the report. The information contained in this report was prepared and interpreted exclusively for AECOM and the TTC and may not be used in any manner by any other party. Intrinsik does not accept any responsibility for the use of this report for any purpose other than as specifically intended by AECOM and the TTC. Intrinsik does not have, and does not accept, any responsibility or duty of care whether based in negligence or otherwise, in relation to the use of this report in whole or in part by any third party. Any alternate use, including that by a third party, or any reliance on or decision made based on this report, are the sole responsibility of the alternative user or third party. Intrinsik does not accept responsibility for damages, if any, suffered by any third party as a result of decisions made or actions based on this report. Intrinsik makes no representation, warranty or condition with respect to this report or the information contained herein other than that it has exercised reasonable skill, care and diligence in accordance with accepted practice and usual standards of thoroughness and competence for the profession of toxicology and environmental assessment to assess and evaluate information acquired during the preparation of this report. Any information or facts provided by others, and referred to or utilized in the preparation of this report, is believed to be accurate without any independent verification or confirmation by Intrinsik. This report is based upon and limited by circumstances and conditions stated herein, and upon information available at the time of the preparation of the report. Intrinsik has reserved all rights in this report, unless specifically agreed to otherwise in writing with AECOM and the TTC. Prepared by: Intrinsik Environmental Sciences Inc. ________________________ Glenn Ferguson, Ph.D., QPRA Vice President – Eastern Region / Senior Scientist

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Table of Contents

Page

EXECUTIVE SUMMARY ............................................................................................................... I 1.0 INTRODUCTION ............................................................................................................... 1 2.0 PROPOSED APPROACH ................................................................................................ 2

2.1 Screening Level Human Health Risk Assessment (SLHHRA) ....................................... 2 2.2 Problem Formulation ...................................................................................................... 4 2.3 Exposure Assessment .................................................................................................... 5 2.4 Hazard Assessment ........................................................................................................ 5 2.5 Risk Characterization ...................................................................................................... 7

2.5.1 Estimating Potential Risk ......................................................................................... 7 2.5.1.1 Threshold Chemicals (Non-carcinogens) ......................................................... 7 2.5.1.2 Non-Threshold Chemicals (i.e., Genotoxic Carcinogens) ................................ 8

2.5.2 Interpretation of Risk Estimates ............................................................................... 8 2.5.2.1 Threshold Chemicals (Non-carcinogens) ......................................................... 8 2.5.2.2 Non-Threshold Chemicals (i.e., Genotoxic Carcinogens) ................................ 9

3.0 PROBLEM FORMULATION ........................................................................................... 11 3.1 Site Characterization .................................................................................................... 11 3.2 Chemical Characterization ............................................................................................ 12

3.2.1 Overview of Characteristics of Diesel Emissions .................................................. 12 3.2.2 Selection of Chemicals of Concern (COC) ............................................................ 13

3.2.2.1 Criteria Air Contaminants (CACs) .................................................................. 13 3.2.2.1.1 Carbon Monoxide (CO) ............................................................................... 13 3.2.2.1.2 Oxides of Nitrogen (NOx) ............................................................................ 14 3.2.2.1.3 Particulate Matter (PM) ............................................................................... 16

3.2.2.2 Volatile Organic Contaminants (VOCs) .......................................................... 18 3.2.2.2.1 1,3-Butadiene .............................................................................................. 18 3.2.2.2.2 Acetaldehyde .............................................................................................. 19 3.2.2.2.3 Acrolein ....................................................................................................... 20 3.2.2.2.4 Benzene ...................................................................................................... 21 3.2.2.2.5 Formaldehyde ............................................................................................. 22

3.2.2.3 Polycyclic Aromatic Hydrocarbons (PAHs) .................................................... 23 3.3 Receptor Characterization ............................................................................................ 24 3.4 Identifying Exposure Scenarios and Pathways ............................................................. 24

3.4.1 Exposure Scenarios .............................................................................................. 24 3.4.2 Exposure Pathways ............................................................................................... 24

4.0 EXPOSURE ASSESSMENT ........................................................................................... 25 4.1 Estimation of Ambient Ground Level Air Concentrations .............................................. 25 4.2 Exposure Analysis of Particulate Matter ....................................................................... 27

4.2.1 Ultrafine Particulate Matter .................................................................................... 28 5.0 HAZARD ASSESSMENT ............................................................................................... 29

5.1 Acute Inhalation Toxicity Reference Values ................................................................. 29 5.2 Chronic Inhalation Toxicity Reference Values .............................................................. 30

6.0 RISK CHARACTERIZATION .......................................................................................... 32 6.1 Acute Inhalation Assessment Results .......................................................................... 32 6.2 Chronic Inhalation Assessment Results ....................................................................... 33

6.2.1 Non-Carcinogenic Risks ........................................................................................ 33 6.2.2 Carcinogenic Risks ................................................................................................ 33

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7.0 UNCERTAINTY ANALYSIS ........................................................................................... 35 8.0 DISCUSSION AND CONCLUSIONS .............................................................................. 39 9.0 REFERENCES ................................................................................................................ 42

List of Tables Page

Table 4-1 Location of Regional Monitoring Station used to Estimate Background Concentrations for each COC (Novus, 2014) ...................................................... 26

Table 4-2 Summary of Predicted Maximum Ground-Level Air Concentrations (µg/m3) in Study Area ........................................................................................................... 26

Table 5-1 Summary of Selected Acute Non-carcinogenic Inhalation TRVs ........................ 29 Table 5-2 Summary of Chronic Non-carcinogenic and Carcinogenic Inhalation TRVs ....... 30 Table 6-1 Worst-case Acute Risk Predictions for Background and Proposed Project-

Related Emissions in the Study Area .................................................................. 32 Table 6-2 Worst-case Chronic Non-Cancer Risk Predictions for Background and

Proposed Project-Related Emissions in the Study Area ..................................... 33 Table 6-3 Worst-case Incremental Lifetime Cancer Risk Predictions for Proposed

Project-Related Emissions in the Study Area ...................................................... 34 Table 7-1 Major Assumptions Used in the Current Assessment ......................................... 36

List of Figures

Page

Figure 2-1 Overview of Standard Risk Assessment Framework ............................................ 4 Figure 3-1 Map of Proposed Study Area and Sensitive Receptor Locations (Novus, 2014) 11 Figure 3-2 Schematic Diagram of the Cycle of Reactive Oxidized N species in the

Atmosphere (US EPA, 2008a) ............................................................................. 15 Figure 3-3 Comparison of PM Fractions with a Range of Biological Entities from Pollen

to Molecules (adapted from Brook et al., 2004) ................................................... 16 Figure 8-1 Predicted Hourly Cumulative NO2 Concentrations at the Worst-case Receptor

Location in 2010 .................................................................................................. 40

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GLOSSARY OF TERMS This glossary is intended to provide the reader with working definitions of many of the technical terms and acronyms which appear in the risk assessment. Various government agencies and organizations may have different definitions for these terms; thus the definitions are intended only to provide guidance to the reader as to how these terms are used within this report. Sources for these definitions include a variety of documents prepared by the Ontario Ministry of the Environment and Climate Change (MOECC), United States Environmental Protection Agency (US EPA), New York State Department of Health, Health Canada, U.S. Federal Drug Administration (USFDA), International Programme on Chemical Safety (IPCS), Agency for Toxic Substances and Disease Registry (ATSDR), and the World Health Organization (WHO). 90th Percentile The 90th percentile of a set of measurements is the value below which 90% of the results fall. AAQC See Ambient Air Quality Criteria. Acute Occurring over a short time. An acute or short-term exposure can result in short term or long-term health effects. An acute effect happens within a short time after an exposure (i.e., may be minutes or days). Agency for Toxic Substances and Disease Registry (ATSDR) As an agency of the U.S. Department of Health and Human Services, the mandate of ATSDR is to serve the public by using the best science, taking responsive public health actions, and providing trusted health information to prevent harmful exposures and disease related to toxic substances. Further information can be found on http://www.atsdr.cdc.gov/. Ambient Environmental or surrounding conditions. Ambient air is usually outdoor air (as opposed to indoor air). Ambient Air Quality Criteria (AAQC) Air quality criteria established for specific chemicals and substances above which there is the risk of potential for adverse effects. These effects can be health-based, or protective of other important endpoints (e.g., corrosion, odour, staining, etc.). In Ontario, these criteria are usually developed for annual averages or on a 24-hour basis in µg/m3, though criteria are also available for 1-hour and 10-minute exposure durations for select chemicals. Asthmatics / asthma Asthmatics are people who suffer from asthma, a disease involving episodes (“asthma attacks”) where the breathing tubes become constricted making it difficult to breath. ATSDR See Agency for Toxic Substances and Diseases Registry.

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Background level A typical or average level or concentration of a chemical or substance in the environment, without any contribution from the proposed project. Benchmark A reference point (such a regulatory standard or guideline) against which a measurement can be compared (as a noun), or the act of comparing a measurement to a reference value (as a verb). Canadian Council of Ministers of the Environment (CCME) A group comprised of 14 environment ministers from the federal, provincial and territorial governments which promotes effective intergovernmental cooperation and coordinated approaches to inter-jurisdictional issues such as air pollution and toxic chemicals. Although the CCME establishes nationally-consistent environmental standards, strategies and objectives, it has no authority to enforce them on individual jurisdictions. Carcinogen / Carcinogenic A substance or chemical that can cause cancer. Knowledge that a chemical or substances can cause cancer is usually obtained from laboratory studies in animals. Only infrequently do we know that a substance definitely causes cancer in humans. Sometimes the cancer effect is dependent on the type of exposure. CCME See Canadian Council of Ministers of the Environment. Chemical of Concern (COC) A chemical of concern is a contaminant identified as of interest for evaluation as part of the risk assessment. Chronic Occurring over a long period of time, several weeks, months or years, depending on the exposed species. COC See Chemical of concern. Concentration The proportion of one substance contained in a given amount of a specific media. The unit is a concentration unit which has two components: the numerator (i.e., quantity of chemical present) and the denominator (i.e., quantity of the media or volume of solution in which the chemical is present). For example, an NO2 concentration of 10 µg/m3 represents 10 µg of NO2 present within 1 cubic metre of air. Concentration Ratio (CR) The concentration is similar to the hazard quotient, where the exposure and exposure limit are expressed as concentrations (rather than as doses). See Hazard quotient. Conservative In the context of the current assessment, a conservative assumption or approach refers using a precautionary approach in establishing the value so as to not underestimate potential exposures, or relatedly health risks.

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Contaminant A substance that is present in an environment where it does not belong. CR See Concentration ratio. Cumulative ground-level air concentrations Predicted total ground-level air concentrations, based upon adding the modelled contribution from the proposed project to the measured regional background air concentrations. Data gap Refers to a type of data which is unavailable or limited, and which would likely reduce uncertainty in the risk assessment if it were to be available or if the data set were more complete. Dermal Referring to the skin. For example, dermal absorption means absorption through the skin. Dose The amount of chemical or substance taken in or absorbed by an exposed individual. Dose often takes body weight into account. For example, to receive equivalent doses of medicine, children are given smaller amounts than adults. The unit is mg/kg for example. The dose rate is the frequency that the dose is applied, such as "mg/kg body weight per day". Acute toxicity usually refers to single doses, while chronic toxicity refers to given dose rates. Dose-response relationship The relationship between the amount of a substance absorbed (i.e., dose) and the resulting changes in body function or health (i.e., response). EA Environmental Assessment. Effect Change in the state or dynamics of an organism, system, or (sub)population caused by the exposure to an agent. Endpoint An adverse effect on a living system (from single organisms to entire ecosystems) which is studied in an experiment, or an adverse effect whose prevention or minimization is the basis of a benchmark. See also Effect and Benchmark. Emissions Materials released to the environment from a source. Emissions may be released from localized sources (such as an industrial smokestack), diffuse sources (such as a landfill site) or mobile sources (such as an automobile or locomotive). EPR Environmental Project Report. The EPR document, as specified under Ontario Regulation 231/08, document the results of a transit project assessment process, and the consultation undertaken. See also Transit Project Assessment Process (TPAP).

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Exceedance Refers to predicted ground-level air concentrations which are greater than, or exceed, the corresponding regulatory benchmark for that averaging period. Exposure Exposure is any contact with a chemical by swallowing, breathing or direct contact (such as through the skin or eyes). Exposure may be either short term (acute) or long term (chronic). Exposure can vary greatly, and is often associated with specific activities or behaviours of people or ecological organisms. It is quantified as the amount of a substance that can be absorbed, or the amount available for inhalation or ingestion. Exposure assessment A process that estimates or measures the amount of a chemical or substance that enters or comes into contact with a person or ecological organism. An exposure assessment also takes into consideration the length of time and the nature of a population exposed to a chemical. Exposure pathway The pathway a chemical, substance or agent may take to reach or cause exposure of humans or other living organisms. Pathways link a source of a chemical, substance or agent (i.e., soil) to its eventual entry into the body. Exposure route The route through which a substance can enter the body. Exposure scenario A combination of facts, assumptions, and inferences that define a discrete situation where potential exposures may occur. These may include the source, the exposed population, the time frame of exposure, microenvironment(s), and activities. Scenarios are often created to aid exposure assessors in estimating exposure under varying conditions. Guideline Recommended limit for some parameter or substance in a specific medium and/or environment. For example, health guidelines are upper limits of exposure, below which adverse health effects are absent or minimized. Hazard Inherent property of an agent or situation having the potential to cause adverse effects when an organism, system, or (sub)population is exposed to that agent or situation. Hazard assessment The hazard assessment involved identifying and understanding potential health outcomes that can result from exposure to each COC and the conditions under which the outcomes might be observed. The hazard, or toxicity, assessment methodology is based on the fundamental dose response principle. That is, the response of biological systems to chemical exposures increases in proportion to the concentration of a chemical in critical target tissues where adverse health outcomes may occur. Hazard quotient (HQ) The ratio of estimated site-specific exposure to a single chemical over a specified period to the estimated daily exposure level, at which no adverse health effects are likely to occur. This risk characterization metric is typically used in the evaluation of non-carcinogenic chemicals. Also known as an exposure ratio (ER).

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Health Canada (HC) The Canadian Federal department responsible for helping Canadians maintain and improve their health. Health assessment A process to determine the health impacts related to particular events or circumstances, such as the release of a chemical, substance or agent into the environment. It includes a health interpretation of all the information known about the situation. The information may include some or all of the following: site investigation (environmental sampling and studies), exposure assessment, risk assessment, biological monitoring and health effects studies. The information is used to advise people how to prevent or reduce their exposures, to determine if remedial actions are necessary, or the need for additional studies. The types of studies carried out in a health assessment can include studies of the environment (soil measurements, chemical availability, etc.) or studies of the people living in the environment (epidemiological studies or biological monitoring studies). HHRA See Human health risk assessment. Human health risk assessment (HHRA) A risk assessment focused on estimating potential human health risks to a defined set of individuals from exposure to a particular agent or agents. The HHRA process includes four basic steps: problem formulation (hazard identification), exposure assessment, hazard assessment, and risk characterization. HQ See Hazard quotient. Ingestion Taking a substance into the body by swallowing it, whether incidentally or purposely. Inhalation Breathing or inhaling air, and the substances it contains, into the lungs. Interstitialization The process by which ultrafine particles are penetrate through the pulmonary alveoli, and are sequestered in the interstitial space within the lung tissue. Mode of Action The mode of action of a substance is defined as the general recognition of the broad biochemical pathways (such as DNA synthesis, protein synthesis, cholesterol synthesis) which are inhibited or affected by a substance. The mode of action is distinguished from the mechanism of action of a substance, which is defined as the mechanism by which a toxicologically active substance produces an effect on a living organism or in a biochemical system. The mechanism of action is usually considered to include an identification of the specific targets to which a toxicologically active substance binds or whose biochemical action it influences.

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Modelling The process by which scientists consider many scenarios of exposure for the purpose of determining the associated health risks. A selected scenario may be preferred for a given site when information is known about the site and about the behaviour of the chemical or substance. In most cases modelling involves the use of mathematical equations to inter-relate the factors critical to the process being studied. These mathematical equations have been developed through studies of factor inter-relationships. Models are used to predict events expected in the future, or that have occurred in the past, when direct measurements are not feasible. Models can be used to assist in designing studies to obtain direct measurements of the processes of concern. MOECC See Ontario Ministry of the Environment and Climate Change. NAAQOs See National Ambient Air Quality Objectives. NAPS See National Air Pollution Surveillance network. National Air Pollution Surveillance (NAPS) network The NAPS network, a joint initiative of Environment Canada and various provinces (including Ontario), territories and some municipal governments, to monitor ambient concentrations of key COC (primarily SO2, NO2, ozone, fine particulate matter, and carbon monoxide) at key monitoring stations across Canada. These measurements are used by the provinces to report the Air Quality Index and by Environment Canada to report the Air Quality Health Index (AQHI). National Ambient Air Quality Objectives (NAAQOs) NAAQOs are the benchmark against which Canada assess the impact of anthropogenic activities on air quality and ensures that current emission control policies are successfully protecting human health and the environment. The federal government sets NAAQOs on the basis of recommendations from the Federal-Provincial Working Group on Air Quality Objectives and Guidelines consisting of representatives from both Health Canada and Environment Canada, as well as their relevant provincial counterparts. NOAEL See No observed adverse effect level. No observed adverse effect level (NOAEL) The highest dose in an experiment which did not cause an adverse effect. NOx See Oxides of Nitrogen Ontario Ministry of the Environment and Climate Change (MOECC) Provincial body responsible for development, implementation, and enforcement of regulations, as well as various programs and initiatives, which address environmental issues having local, regional and/or global effects. Formerly known as Ministry of the Environment (MOE). Oral By mouth. Oral exposure refers to exposure by swallowing a material. Also see Ingestion.

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Oxides of Nitrogen (NOx) Oxides of nitrogen (NOx), including nitric oxide (NO) and nitrogen dioxide (NO2) gases, are produced by both natural and human activities, primarily formed by the reaction of atmospheric oxygen and nitrogen during high temperature combustion processes. PAH PAH is an acronym for polycyclic aromatic hydrocarbons. All PAH contain only carbon and hydrogen, and are produced as by-products of incomplete combustion. They are commonly found in soot, and are emitted during the combustion of fossil fuels and wood. Particulate matter (PM) A general term that refers to dust, soot, and smoke that is emitted from such sources as factories, vehicles, and fires. A numeric subscript indicates the upper limit of the particles of interest (i.e., PM10 refers to particulate matter less than 10 microns in aerodynamic diameter). Parts per billion (ppb) Units of concentration (i.e., µg/kg, ng/g, etc.) Parts per million (ppm) Units of concentration (i.e., µg/g, mg/kg, etc.) Physico-chemical properties The physical and chemical characteristics of a substance. Examples of physico-chemical properties include boiling point, melting point, colour, odour, solubility, vapour pressure, etc. PM See Particulate matter. PM10 Particulate matter which is less than 10 µm in diameter. This size of particulate is small enough so as to be easily inhaled into the lungs. This is the primary particulate size fraction evaluated for potential health impacts by the HHRA. PM2.5 Particulate matter which is less than 2.5 µm in diameter. This size of particulate is small enough so as to be easily inhaled deep into the lower lungs (i.e., alveolar), and potentially absorbed directly into the blood stream. ppb See Parts per billion. ppm See Parts per million. Problem Formulation Initial stage of the risk assessment, where information is gathered and interpreted to plan and focus the risk assessment. RA See Risk assessment.

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Receptor An individual (person, plant, animal) that could come into contact with hazardous substances. In the context of air dispersion modelling, a sensitive receptor can also refer to a specific geographical location at which ground-level air concentrations are predicted. Reference concentration (RfC) An estimated air concentration of a specific chemical or substance which is likely to be without risk of deleterious effects to people, animals or plants, even if the exposure continues over a lifetime. Typically expressed in mg/m3 or µg/m3. Reference dose (RfD) An estimate of a rate of exposure of people, animals or plants that is likely to be without risk of deleterious effects, even if the exposure continues over a lifetime. Reference doses are adjusted for sensitive sub-groups of the population. Typically expressed in mg/kg bodyweight/day or µg/kg bodyweight/day. Respiratory Tract The respiratory tract consists of the nose, mouth, windpipe, lungs and related structured required for breathing. RfC See Reference concentration. RfD See Reference dose. Risk Risk, in the context of a human health risk assessment, is the likelihood of injury, disease or death that will be caused by an action or condition. Risk Assessment (RA) A process that estimates the likelihood or chance that people or the environment may experience adverse effects from a particular series of events or circumstances, such as exposure to chemicals, substances or agents. The four steps of a risk assessment are:

problem formulation (also known as hazard identification);

toxicity/effects assessment;

exposure assessment; and,

risk characterization.

Note: Likelihood is a quantitative term related to "probability", "chance" or to "risk". Risk characterization Final phase of the risk assessment, where the exposure and effects/toxicity information are combined to evaluate potential impacts, and provide a qualitative or quantitative characterization of health risk. Risk management The process of deciding how to reduce or eliminate possible adverse effects on people’s health and the environment by considering the risk assessment, engineering factors (i.e., can engineering procedures or equipment do the job, for how long and how well?) and social, economic and political concerns.

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Route of exposure The way in which a person or other organism in the natural environment may come in contact with a chemical, substance or agent. These are typically through inhalation, ingestion, or via dermal absorption. For example, drinking (ingestion) and bathing (skin contact) are two different routes of exposure to chemicals that may be found in water. See "Exposure." Safe In common language, safe means free from harm or risk. In scientific language, any exposure to most chemicals, substances or agents have some risk, although that risk may be extremely small. Therefore, scientifically, safe means at very low or negligible risk. Scenario A hypothetical situation evaluated in a HHRA. Screening Level Human Health Risk Assessment (SLHHRA) A screening level human health risk assessment (SLHHRA) is a qualitative or quantitative evaluation of risk typically based on a “worst-case” exposure scenario rather than verifiable site-specific conditions. As an initial scoping of potential risk, the SLHHRA approach relies on available data to provide conservative estimates of exposure and risk based on a worst-case scenario, so that exposures and risks are not underestimated. The intent is to determine whether there is the potential for adverse health impacts under these worst-case exposure scenarios for the relevant COC emitted from the proposed project, identify any data gaps limiting the assessments ability to appropriately estimate exposures and risk, and eliminate any COC and pathways of exposure which are not a concern moving forward for any further analyses. SDB Standards Development Branch. The branch of the MOECC largely responsible for technical review of environmental risk assessments in Ontario. SLHHRA See Screening Level Human Health Risk Assessment. Threshold The dose or exposure below which an adverse effect is not expected. Total Suspended Particulates (TSP) A measure of the total number of particles of solid or liquid matter - such as soot, dust, aerosols, fumes and mist - found in a sample of ambient air. Typically assumed to be composed of suspended particulate that have aerodynamic diameters less than 40 μm. Toxicity A general term that can refer either to a substance’s toxic potency, or the type(s) of effects that a substance can have (for example, ocular toxicity refers to effects on the eye; respiratory system toxicity refers to effects on the respiratory system). Toxicity assessment Step in the risk assessment process involving the evaluation of the toxicological properties and effects of a chemical, with special emphasis on establishment of dose response characteristics.

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Toxicity Reference Value (TRV) A toxicity reference value, or TRV, is an estimate of the dose (in this document, usually a daily dose over a long period of time) of a substance that is associated with a specific level of risk, or that is considered to be safe. Toxicity reference values are used to evaluate whether estimated or measured exposures are likely to cause adverse health effects. Toxicity reference values are also used to develop guidelines and standards, such as drinking water quality guidelines. TPAP See Transit Project Assessment Process. Transit Project Assessment Process (TPAP) In June 2008, the Province of Ontario approved a new Transit Project Assessment Process (TPAP) for undertaking transit-related projects with the introduction of Ontario Regulation 231/08 entitled “Transit Projects and Greater Toronto Transportation Authority Undertakings”. The TPAP Regulation provides a framework for an accelerated consultation and objection process for completing the assessment of potential environmental impacts of a transit project, so that decision-making can be completed within a six month approval window. TRV See Toxicity reference value. TSP See Total suspended particulates. UF See Uncertainty factor. g Microgram (1 x 10-6 grams). UFP See Ultrafine Particulate Matter. Ultrafine Particulate Matter (UPM) UFP constitute particulate matter smaller than 0.1 microns (or 100 nanometres) in size (i.e., PM0.1). Due to their small size, UFPs are considered to be respirable particles and are able to travel deep within the lung with the potential to penetrate tissue and undergo interstitialization, and therefore are not easily removed from the body. Uncertainty analysis A detailed examination of the potential sources of variability and uncertainty within the data, and their influence on risk assessment results. See Uncertainty Factor. Uncertainty Factor (UF) One of several factors used in calculating the reference dose from experimental data. UFs are typically used to account for such uncertainties as: (1) the variation in sensitivity among humans (i.e., intraspecies); (2) the uncertainty in extrapolating animal data to humans (i.e., interspecies); (3) the uncertainty in extrapolating data obtained in a study that covers less than the full life of the exposed animal or human; (4) the uncertainty in using LOAEL data rather than NOAEL data

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(see LOAEL and NOAEL); and, (5) uncertainties associated with the adequacy of the database of experimental data. United States Environmental Protection Agency (US EPA) The federal agency responsible for developing and enforcing regulations to implement environmental laws enacted by Congress. EPA is responsible for researching and setting national standards for a variety of environmental programs, and delegates to states and tribes the responsibility for issuing permits and for monitoring and enforcing compliance. US EPA See United States Environmental Protection Agency. WHO See World Health Organization. World Health Organization (WHO) The United Nations agency which works in a variety of ways and with a variety of agencies internationally to attain the highest level of physical, mental, and social well-being for all people.

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EXECUTIVE SUMMARY Overview of the Study

To accommodate increasing ridership demand in the future, the Toronto Transit Commission (TTC) is proposing the construction of a new bus garage at Kennedy Road and McNicoll Avenue in Scarborough, Ontario. The intended use of the garage is to store new standard and articulated TTC buses, along with some of the current in service fleet. As part of the ongoing Transit Project Assessment Process (TPAP) Environmental Assessment (EA), Intrinsik Environmental Sciences Inc. (Intrinsik) was retained by AECOM Canada Limited (AECOM), on behalf of the TTC, to assess the potential human health implications associated with expected emissions from buses using the garage to individuals in the surrounding area. As such, to evaluate the potential local air quality impacts of bus emissions arising from the planned TTC McNicoll bus garage, a screening level human health risk assessment (SLHHRA) was completed. The SLHHRA can be used to determine the worst-case health implications of these emissions to potentially sensitive individuals living, working, or playing in the surrounding communities. The current human health risk assessment was conducted according to widely accepted risk assessment methodologies and guidance published and endorsed by regulatory agencies including the Ontario Ministry of the Environment and Climate Change (MOECC), Health Canada, the Canadian Council of the Ministers of the Environment (CCME), and the United States Environmental Protection Agency (US EPA). The SLHHRA, in particular the selection of appropriate regulatory benchmarks, was conducted in consultation with Toronto Public Health. What is a Screening Level Human Health Risk Assessment (SLHHRA)?

A SLHHRA is a qualitative or quantitative evaluation of risk typically based on a “worst-case” exposure scenario rather than verifiable site-specific conditions. As an initial scoping of potential risk, the SLHHRA approach relies on available data to provide conservative estimates of exposure and risk based on a worst-case scenario, so that exposures and risks are not underestimated. The intent is to determine whether there is the potential for adverse health impacts under these worst-case exposure scenarios for the chemicals of concern (COC) emitted from the proposed facility, identify any data gaps limiting the assessments ability to estimate exposures and risk, and eliminate any COC and pathways of exposure which are not a concern moving forward for any future analyses. Should the SLHHRA indicate the potential for the risk, the process provides an excellent foundation on which additional data gathering and analysis can be conducted, in support of a more detailed quantitative human health risk assessment (HHRA). Ultimately, due to the conservative approach and assumptions used, a SLHHRA cannot predict whether potential health risks will occur. Rather, a SLHHRA can only determine if significant human health risks are unlikely. In many cases, a detailed HHRA may be necessary to address the inherent conservatism and uncertainty built into the SLHHRA process, to permit a detailed quantification of actual human health risks related to airborne emissions from the bus garage, should the SLHHRA indicate the potential for human health impacts. Overall, the SLHHRA follows the standard HHRA framework that is composed of the following steps:

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i) problem formulation;

ii) exposure assessment;

iii) hazard assessment; and,

iv) risk characterization. Typically, the assessment results provided in the risk characterization step can be used by risk managers to develop appropriate mitigation plans to prevent adverse health risks, should they be warranted. However, given that this is a screening level assessment, it is likely that should the potential for health risks be identified, a more detailed human health risk assessment would be recommended to provide a more comprehensive evaluation of site-specific health risks around the proposed bus garage. What are the Project-Related Health Concerns?

To accommodate increasing ridership demand, the Toronto Transit Commission (TTC) is proposing to construct a new bus garage on McNicoll Avenue, just east of Kennedy Road in Scarborough, Ontario. The intended use of the garage is to store new standard and articulated TTC buses, along with some of the current in service fleet, and for general maintenance and repair on these buses. The majority of emissions considered in this assessment are due to idling buses, while emissions from natural gas-fired heating equipment were also considered.

(Legend: Proposed facility outlined in blue, the property boundary line in red, and each receptor location in yellow)

Map of Proposed Study Area and Sensitive Receptor Locations The closest sensitive receptor to the proposed facility is an existing senior citizens’ residence, located approximately 20 m west of the facility’s property boundary line. As part of the air dispersion modelling, the Air Quality Study team predicted maximum ground-level air concentrations at 21 discrete sensitive receptor locations within the Study Area, including the existing senior citizen’s residence, any proposed daycare facility on the nearby property to the east, and three churches.

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What are the Chemicals of Concern?

The primary concern for the current assessment is emissions from TTC buses using the proposed McNicoll garage and surrounding roadways, and the potential health implications associated with emissions from these diesel-powered vehicles on the surrounding community. As such, one must understand the typical contaminants emitted by diesel engines to properly select the chemicals of concern for the current study. Sulphur dioxide was not included as a COC in the current assessment due to the use of low sulphur fuels by the TTC. Potential emissions from a backup diesel generator and heating equipment within the garage were also considered as part of the Air Quality Study. The main concern associated with boiler exhaust due to the combustion of natural gas would be the release of oxides of nitrogen (NOx). Based upon the primary components present in diesel exhaust from the worst case vehicle fleet using the proposed garage, as well as the boiler exhaust from the proposed garage itself, the following contaminants were evaluated in the Air Quality Study and selected as COC for the current screening level assessment:

Criteria Air Contaminants (CACs) Volatile Organic Contaminants (VOCs)

Carbon monoxide (CO) Oxides of nitrogen (NOx) Inhalable coarse particulate matter (PM10) Respirable fine particulate matter (PM2.5)

1,3-Butadiene Acetaldehyde Acrolein Benzene Formaldehyde

Polycyclic Aromatic Hydrocarbons (PAHs)

Benzo[a]pyrene (as a surrogate for the carcinogenic PAH group)

How were the Chemicals of Concern Evaluated?

Each of the chemicals of concern were evaluated on both a short-term “acute” and long-term “chronic” basis. Where relevant for the specific chemical, both cancer and non-cancer end-points were evaluated. Finally, the predicted worst-case contributions from the both the proposed facility and associated increased roadway traffic to local air quality, as well as the overall cumulative air quality (i.e., typical regional background concentrations plus the contribution from the proposed facility and associated vehicle traffic on adjacent roadways) in the community, were evaluated at each of the key sensitive receptor locations identified in the Figure above. What were the Results of the Assessment?

Based on the results of the assessment, and given the considerable conservatism built into both the Air Quality Assessment and the SLHHRA itself, no unacceptable health risks related to emissions from the proposed bus garage and associated vehicle traffic would be expected. In fact, estimated emissions from the proposed Project represent a minimal to negligible contribution of the overall cumulative exposures for all of the COC predicted for the sensitive receptor locations around the proposed facility.

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TTC McNicoll Bus Garage Transit Project Assessment Process – SLHHRA of Air Quality Impacts April, 2015 Intrinsik Environmental Sciences Inc. – Project #20-21640 Page 1


1.0 INTRODUCTION To accommodate increasing ridership demand in the future, the Toronto Transit Commission (TTC) is proposing the construction of a new bus garage at Kennedy Road and McNicoll Avenue in Scarborough, Ontario. The intended use of the garage is to store new standard and articulated TTC buses, along with some of the current in service fleet. As part of the ongoing Transit Project Assessment Process (TPAP) Environmental Assessment (EA), Intrinsik Environmental Sciences Inc. (Intrinsik) was retained by AECOM Canada Limited (AECOM), on behalf of the TTC, to assess the potential human health implications associated with expected emissions from buses using the garage to individuals in the surrounding area. As such, to evaluate the potential local air quality impacts of bus emissions arising from the planned TTC McNicoll bus garage, a screening level human health risk assessment (SLHHRA) was completed. The SLHHRA can be used to determine the health implications of these emissions to potentially sensitive individuals living, working, or playing in the surrounding communities. This assessment is not intended to evaluate risks to nearby residents unrelated to the planned bus garage (beyond that which is inherently required to estimate the overall cumulative worst-case concentration from the regional airshed), nor is it intended to evaluate potential health risks during construction activities (addressed elsewhere in the EA), or arising from occupational exposures (i.e., workers within the bus garage). The focus of the current assessment is solely on the impacts on the surrounding communities of airborne emissions from buses and other vehicles using the planned bus garage as part of the proposed service expansion. Overall, this project is being completed in accordance with the TPAP regulation (Ontario Regulation 231/08). This regulation does not provide specific guidance on human health risk assessment methodology, nor specifically guidance required to complete a SLHHRA. The current human health risk assessment was conducted according to widely accepted risk assessment methodologies and guidance published and endorsed by regulatory agencies including the Ontario Ministry of the Environment and Climate Change (MOECC), Health Canada, the Canadian Council of the Ministers of the Environment (CCME), and the United States Environmental Protection Agency (US EPA). The current assessment was designed and conducted in the spirit of O. Reg. 153/04 (i.e., the approach to brownfields risk assessments in Ontario, as required by the MOECC), but is not intended to meet the regulatory policy or administrative requirements of a brownfields RA under this regulation (i.e., this assessment is not being conducted for the purposes of registering a Record of Site Condition with the MOECC). The SLHHRA, in particular the selection of appropriate regulatory benchmarks, was conducted in consultation with Toronto Public Health.

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2.0 PROPOSED APPROACH In general, a human health risk assessment (HHRA) is a scientific study that evaluates the potential for the occurrence of adverse health effects from exposures of people (receptors) to chemicals of concern (COC) present in surrounding environmental media (e.g., air, soil, sediment, surface water, groundwater, food and biota, etc.), under existing or predicted exposure conditions. HHRA procedures are based on the fundamental dose-response principle of toxicology. The response of an individual to a chemical exposure increases in proportion to the chemical concentration in critical target tissues where adverse effects may occur. The concentrations of chemicals in the target tissues (the dose) are determined by the degree of exposure, which is proportional to the chemical concentrations in the environment where the receptor resides, works or visits. All chemicals (anthropogenic and natural) have the potential to cause environmental effects in people and the ecosystem. However, it is the chemical concentration, the route of exposure, and the inherent toxicity of the chemical that determines the level of environmental effect and potential for unacceptable risk to the exposed receptor. As illustrated in the diagram to the right, if all three components are present (i.e., where the three circles intersect), the possibility of adverse risk exists. The prediction of an individual’s exposure to specific chemicals in the environment and the potential risks resulting from such exposures can be determined through the completion of a quantitative HHRA. For the current investigation, a screening level human health risk assessment (SLHHRA) has been used to evaluate the potential impacts of projected emissions from vehicles present at the proposed TTC McNicoll bus garage, and to determine the health implications to potentially sensitive individuals living, working, or playing in the surrounding communities, under “worst-case” exposure conditions. The following section provides a brief overview of the SLHHRA approach to evaluating potential health risk. 2.1 Screening Level Human Health Risk Assessment (SLHHRA) A screening level human health risk assessment (SLHHRA) is a qualitative or quantitative evaluation of risk typically based on a “worst-case” exposure scenario rather than verifiable site-specific conditions. As an initial scoping of potential risk, the SLHHRA approach relies on available data to provide conservative estimates of exposure and risk based on a worst-case scenario, so that exposures and risks are not underestimated. The intent is to determine whether there is the potential for adverse health impacts under these worst-case exposure scenarios for the relevant COC emitted from the proposed facility, identify any data gaps limiting the assessments ability to appropriately estimate exposures and risk, and eliminate any COC and pathways of exposure which are not a concern moving forward for any further analyses. Should the SLHHRA indicate the potential for the risk, the process provides an excellent foundation on which additional data gathering and analysis can be conducted, in support of a more detailed quantitative human health risk assessment (HHRA). Ultimately, due to the conservative approach and assumptions used, a SLHHRA cannot predict whether potential

Receptor

Exposure Hazard

Risk

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health risks will occur. Rather, a SLHHRA can only determine if significant human health risks are unlikely. In many cases, a detailed HHRA may be necessary to address the inherent conservatism and uncertainty built into the SLHHRA process, to permit a detailed quantification of actual human health risks related to airborne emissions from the assessed bus garage, should the SLHHRA indicate the potential for human health impacts. It should be noted that there is no specific regulatory guidance for the completion of a SLHHRA for a transportation source, such as the proposed TTC bus garage, beyond the recommendations provided by the Standards Development Branch (SDB) of the MOECC in a memo to GO Transit for the proposed expansion of the Oshawa to Bowmanville corridor (MOE, 2009a). As noted in their memo, the MOECC does provide some guidance for screening level risk assessments (for contaminated sites) as part of O. Reg. 153/04, and specifically the 2005 Ministry Procedures document (refer to http://www.ene.gov.on.ca/envision/gp/5404e.pdf). As such, the current SLHHRA was conducted according to widely accepted risk assessment methodologies and guidance published and endorsed by regulatory agencies including the MOECC (as noted above), Health Canada, the Canadian Council of the Ministers of the Environment (CCME), and the United States Environmental Protection Agency (US EPA). Overall, the current SLHHRA follows the standard HHRA framework (see Figure 2-1) that is composed of the following steps:

i) problem formulation;

ii) exposure assessment;

iii) hazard assessment; and,

iv) risk characterization. Typically, the assessment results provided in the risk characterization step can then be used by risk managers to develop appropriate mitigation plans to prevent adverse health risks, should they be warranted. However, given this is a screening level assessment, it is likely that should the potential for health risks be identified, a more detailed human health risk assessment could be recommended to provide a more accurate evaluation of site-specific health risks around the proposed bus garage.

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Figure 2-1 Overview of Standard Risk Assessment Framework 2.2 Problem Formulation The first step in the SLHHRA process is an information gathering and interpretation stage that plans and focuses the study on critical areas of concern for the Project. Problem formulation defines the nature and scope of the work to be conducted, permits practical boundaries to be placed on the overall scope of work and ensures that the assessment is directed at the key areas and issues of concern. This step is critical to the success of the SLHHRA as sound planning during the problem formulation step reduces the need for significant modifications once the SLHHRA has begun. The data gathered and evaluated in this step provides information into the physical layout and characteristics of the assessment area, possible exposure pathways, potential human receptors, COC, and any other specific areas or issues of concern to be addressed. The key tasks that comprise the problem formulation step of this SLHHRA include the following:

Chemical characterization, which involves the identification of the COC;

Site characterization, which consists of a review of available project-specific data to identify factors affecting the availability of chemicals to potential receptors;

Receptor characterization to identify “receptors of concern”, which include those individuals with the greatest probability of exposure to chemicals from the proposed bus garage and those that have the greatest sensitivity to these chemicals; and,

Identification of exposure scenarios and pathways takes into account chemical-specific parameters, such as solubility and volatility, characteristics of the site, such as physical geography, as well as the physiology and behaviour of the receptors.

The outcome of these tasks forms the basis of the approach taken in the current assessment. The following subsections describe the methodological details and outcomes of problem formulation, specific to identification of chemicals, receptors and pathways.

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2.3 Exposure Assessment The exposure assessment evaluates data related to all chemicals, receptors and exposure pathways and routes identified during the problem formulation phase. As noted previously, the assessment of potential occurrences of adverse effects from chemicals is based on the dose-response concept that is fundamental to the responses of biological systems to chemicals (Filov et al., 1979; Amdur et al., 1991). Since it is not usually practical to measure concentrations of chemicals at the actual site where the adverse response occurs within tissues and cells, these concentrations are estimated based on either the dose of the chemical that actually enters a receptor or, more commonly, by the concentrations in various environmental media that act as pathways for exposure. The degree of exposure of individuals to chemicals from the environment therefore depends on the interactions of a number of parameters, including:

The concentrations of chemicals in various environmental media as determined by the magnitude of point sources as well as background or ambient concentrations;

The characteristics of the chemicals of potential concern which affect environmental fate and persistence (e.g., physical-chemical properties);

The impact of site-specific characteristics, such as geology, geography and hydrogeology, on chemical behaviour;

The physiological and behavioural characteristics of the receptors (e.g., respiration rate, soils/dusts intake, time spent at various activities and in different environmental areas); and,

The various physical, chemical and biological factors that determine the bioavailability of chemicals from various exposure pathways.

The primary objective of the current exposure assessment was to predict, using a series of conservative assumptions, the rate of exposure of individuals present near the proposed bus garage to the COC through various exposure scenarios and pathways identified in the problem formulation step. 2.4 Hazard Assessment The hazard assessment involves identifying and understanding potential health outcomes that can result from exposure to each COC and the conditions under which the outcomes might be observed. The hazard, or toxicity, assessment methodology is based on the fundamental dose response principle. That is, the response of biological systems to chemical exposures increases in proportion to the concentration of a chemical in critical target tissues where adverse health outcomes may occur. Two basic and quite different chemical categories are commonly recognized by regulatory agencies, depending on the compound’s mode of toxic action, and applied when estimating toxicological criteria for humans (FDA, 1982; US EPA, 1989). These are the threshold approach (or the no-observed-adverse-effect levels [NOAELs]/benchmark dose with extrapolation/uncertainty factor approach) typically used to evaluate non-carcinogens, and the non-threshold approach (or the mathematical model-unit risk estimation approach), typically used for carcinogenic compounds. In the case of threshold chemicals, a benchmark or threshold level must be exceeded for toxicity to occur. A NOAEL can be identified for threshold chemicals, which is the dose or amount of the chemical that results in no observable response in the most sensitive test species and test endpoint. The application of uncertainty or safety factors to the NOAEL provides an

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added level of protection, allowing for derivation of a toxicity reference value (TRV) that is expected to be safe to sensitive individuals following exposure for a prescribed period of time. Non-threshold chemicals are capable of producing cancer by altering genetic material. Regulatory agencies such as Health Canada and the US EPA assume that any level of long term exposure to carcinogenic chemicals is associated with some “hypothetical cancer risk”. However, as there is no non-threshold chemicals selected as COCs for the current assessment, this particular approach will not be discussed further. The terminology used to define threshold and non-threshold TRVs differs according to the source and type of exposure and often varies between regulatory jurisdictions. Generic nomenclature has been developed, with the following terms and descriptions commonly used. Reference concentration (RfC): A reference concentration (or RfC) refers to the acceptable level of an airborne chemical for which the primary route of exposure is inhalation, and applies to either short term acute (e.g., 1-hour or 24-hour) or long term chronic exposure periods. It is expressed as a concentration of the chemical in air (i.e., micrograms per cubic metre, µg/m3) and applies only to chemicals acting through a threshold mode of toxicological action. For chemicals such as irritants and some combustion gases, short term or acute non-systemic toxicity is frequently observed at the points of entry into the body (i.e., the respiratory tract, eyes, and skin, for air-borne contaminants). In these cases, because the toxicity is enacted simply by direct contact between the receptor and the contaminated medium, the concentration in the air to which the receptor is exposed is the important measure of exposure, rather than the internal dose associated with multiple exposure pathways. For chemicals with these characteristics, short term RfCs are used to characterize health risk, and are intended to be protective of the general population. The toxicity of a chemical has been observed to vary between acute (short term) and chronic (long term) exposure. Thus, it is important to differentiate TRVs based on duration of exposure. The two TRV durations used in the current HHRA can be described as follows:

Acute: the amount or dose of a chemical that can be tolerated without evidence of adverse health effects on a short term basis. These benchmarks are routinely applied to conditions in which exposures extend from minutes through several hours or several days only (ATSDR, 2006). For the current HHRA, risks will be evaluated based upon 1 or 24-hour exposure periods, where a relevant acute TRV for that time period is available.

Chronic: the amount of a chemical that is expected to be without effect, even when exposure occurs continuously or regularly over extended periods, possibly lasting for periods of at least a year, and possibly extending over an entire lifetime (ATSDR, 2006).

As it would be inappropriate to establish a generic hierarchy of source agencies by which to select TRVs given the breadth of COCs evaluated in a typical human health assessment, when TRVs for a particular COC were available from multiple regulatory agencies, all of the TRVs were reviewed and the professional judgment of experienced toxicologists was used to select the most appropriate TRV. The most critical considerations in selecting TRVs were the source (it must have been derived by a reputable agency), the data used to derive the benchmark, the date the TRV was derived (it must be as up to date as possible), and its relevance in terms of duration and route of exposure. Health Canada (2010) provides a list of acceptable jurisdictions that maybe be used to determine toxicity reference values. In some occasions, additional jurisdictions outside this list can be selected based on the professional judgement of an experienced toxicologist.

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2.5 Risk Characterization The final step of a risk assessment is risk characterization. This involves the estimation, description, and evaluation of risk associated with exposure to COC by comparing the estimated exposure to the appropriate TRV for a specific chemical or group of compounds. Risk characterization involves the comparison of estimated exposures (identified in the exposure assessment) with TRVs (identified during the hazard/toxicity assessment) to identify potential human health risks. This comparison is typically expressed as a Concentration Ratio (CR) or Hazard Quotient (HQ) for non-carcinogenic chemicals and is calculated by dividing the predicted exposure by the TRV. In the case of carcinogenic chemicals, potential risk estimates are typically presented as an Incremental Lifetime Cancer Risk (ILCR). These metrics are discussed in further detail below. Separate assessments were completed for short term (acute) and long term (chronic) durations because the health outcomes produced by some COC depend on the duration of exposure. It is important to distinguish between the health outcomes that might result from acute exposures versus effects that may occur following chronic exposures. In the chronic assessment, further distinction was made between inhalation and multiple pathway exposures (i.e., oral and dermal) since the pathway of exposure could also influence the potential health outcomes associated with each of the COC. In recognition of the influence of these exposure variables, risk estimates are typically segregated into three exposure categories:

Acute inhalation (1-hour and 24-hour durations);

Chronic inhalation (annual average durations); and,

Chronic multiple pathways (i.e., oral and dermal exposures). However, in the current assessment, deposition on to soil and home gardens is not considered to be a significant pathway, and was not considered further in the current assessment. 2.5.1 Estimating Potential Risk 2.5.1.1 Threshold Chemicals (Non-carcinogens) Concentration Ratios (CR)

CR values were used to evaluate the acute and chronic health risk from exposure to chemicals via inhalation. CR values were calculated by dividing the predicted ground-level air concentration (for 1-hour, 24-hour or annual average exposure durations) by the appropriate toxicity reference value (i.e., RfC), according to the following example equation:

duration

durationduration RfC

AirCR

Where:

CRduration = the duration-specific CR (unitless), calculated for 1-hour, 24-hour and chronic durations, as appropriate

[Air]duration = the predicted ground-level air concentration (µg/m3) for the specific time duration

RfCduration = the RfC (µg/m3) for the specific time duration

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2.5.1.2 Non-Threshold Chemicals (i.e., Genotoxic Carcinogens) Incremental Lifetime Cancer Risks (ILCR)

ILCR estimates were used to evaluate the increased cancer risk resulting from a lifetime of exposure to non-threshold genotoxic carcinogenic chemicals. ILCR estimates provided the incremental lifetime cancer risk resulting from emissions from the proposed facility, based upon the incremental change between the current and proposed future local air quality as a result of the use of the proposed facility. Direct Air Inhalation

ILCR estimates resulting from direct air inhalation were calculated as follows:

URAirILCR Local ][

Where:

ILCR = the incremental (or additional) lifetime cancer risk (unitless)

[Air]∆Local = the predicted annual average ground-level air concentration (µg/m3) change between current versus future air quality with the operation of the proposed facility

UR = the COC-specific unit risk (µg/m3)-1

2.5.2 Interpretation of Risk Estimates The interpretation of the various risk evaluation metrics, as well as the appropriate benchmark by which to evaluate whether the predicted risk is acceptable or not, are discussed in the following section. 2.5.2.1 Threshold Chemicals (Non-carcinogens) If the risk assessment evaluates risks associated with a single source (such as inhalation), the selection of a CR or HQ of 1.0 as an indication that predicted exposures do not exceed the toxicity reference values is appropriate. For example, as gaseous chemicals such as NOx only occur in air, and not in other media, the appropriate CR benchmark is 1.0 (i.e., 100% of the TRV is used as the evaluation benchmark). For chronic multi-media exposures, the Canadian Council of Ministers of the Environment (CCME, 2006) allotted 20% of the total exposure to any one source during the derivation of its health-based soil quality criteria. This was based on the assumption that exposure to COC may occur via five potential sources: air, food, water, soil, and consumer products. This means that, in the absence of a multi-media assessment that takes into account multiple sources, the TRV should be apportioned for the single source under consideration. HQ values that are less than 0.2 represent a situation in which Project-related exposures (e.g., facility-related emissions) account for less than 20% of the TRV. Therefore, no adverse health risks are expected to be associated with the estimated level of exposure. When predicted risks are greater than the benchmark level (e.g., CR/HQ value greater than 1.0 or 0.2), this may indicate the potential for adverse health outcomes in sensitive individuals or in some of the exposure scenarios considered. Re-evaluation of such HQs and CRs is important since both the exposure estimates and the toxicological criteria are based on a series

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of conservative assumptions, particularly when considering the maximum “worst-case” exposure scenarios. Concentration Ratio (CR)

Acute CR values less than 1.0 indicate that estimated chemical concentrations in air are less than the applicable RfC, and thus, adverse health outcomes would not be expected to occur. As this is usually a straight comparison between predicted short term air concentrations (i.e., for 1-hour and 24-hour exposure durations) and the regulatory RfC, the resulting CR value is receptor-independent (i.e., the same value is calculated for all receptor types). For short term exposure durations, a benchmark representing the entire TRV (i.e., a CR benchmark value of 1.0) is typically used, rather than only allocating 20% to the inhalation assessment (i.e., a CR benchmark value of 0.2). The reason for the difference between benchmarks of 1.0 and 0.2, relates to the definition of each type of TRV. For example, a chronic RfD is the average daily intake, derived from multiple sources and pathways that an individual could experience which are not expected to result in an adverse health outcome, regardless of the source of exposure. An acute TRV is typically specific to a chemical concentration within a single environmental medium (i.e., air) that can be tolerated without adverse health outcomes occurring on a short term basis. These benchmarks are routinely applied to conditions in which exposures extend over several hours or several days. As a result, a portion of any short term TRV is not typically apportioned for various source attributions. In general, interpretation of the CR values proceeded as follows: CR ≤1

Signifies that the estimated exposure is less than or equal to the TRV (i.e., the assumed safe level of exposure). This shows that negligible health risks are predicted. Added assurance of protection is provided by the high degree of conservatism (protection) incorporated in the derivation of the TRV.

CR >1

Signifies the exposure estimate exceeds the regulatory TRV. This suggests that the potential for an elevated level of risk may be present for some COC. The significance of which must be balanced against the high degree of conservatism incorporated in the risk assessment (i.e., the margin of safety is reduced but not removed entirely).

2.5.2.2 Non-Threshold Chemicals (i.e., Genotoxic Carcinogens) Incremental Lifetime Cancer Risk (ILCR)

Non-threshold chemicals that can alter genetic material (i.e., genotoxic) are capable of producing cancer. Regulatory agencies such as Health Canada and the US EPA have therefore assumed that any level of long term exposure to a carcinogenic compound is associated with some “hypothetical cancer risk”. As a result, regulatory agencies have typically employed acceptable ILCR levels (i.e., incremental cancer risks over and above background cancer incidence) between 1-in-100,000 and 1-in-1,000,000. ILCRs generally consider risks related to a particular facility (facility alone) in that the cancer risks are expressed on an incremental or additional basis as compared to cancer risks related to all sources.

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As this HHRA is being conducted as part of the EIA process for the Province of Ontario, a benchmark ILCR of 1-in-1,000,000 (1 x 10-6) was selected, based upon MOECC policy for risk assessments in Ontario. The definition of a benchmark ILCR of 1-in-1,000,000 is a policy based decision, not a scientifically derived value. An ILCR of 1-in-1,000,000 increases a person’s lifetime cancer risk from 0.400000 (based on the 40% lifetime probability of developing cancer in Canada) to 0.400001. It is recognized that some amount of the “background” cancer risk of 40% is likely associated with exposures to environmental pollution. It must be noted, however, that an ILCR of 1-in-1,000,000 (a level below which the MOECC considers acceptable) represents a 0.00025% increase over the background cancer incidence, an increase that cannot be detected using epidemiological data from the study area (Health Canada, 2010). It is noted that other regulatory agencies, including Health Canada, consider an ILCR of 1-in-100,000 as the de minimus risk level considered protective of public health. In general, interpretation of the ILCR values proceeded as follows: ILCR ≤ 1.0 x 10-6 (1E-06)

Signifies that the estimated exposure results in an incremental lifetime cancer risk less than or equal to 1-in-1,000,000 (i.e., within the accepted level of risk set by MOECC and 10 times lower (more conservative) than that set by the Health Canada). This shows that negligible health risks are predicted. Added assurance of protection is provided by the high degree of conservatism (protection) incorporated in the derivation of the TRV and exposure estimate.

ILCR > 1.0 x 10-6 (1E-06) ≤ 1.0 x 10-5 (1E-05)

Signifies the estimated exposure results in an incremental lifetime cancer risk greater than the acceptable regulatory-established cancer risk benchmark of 1-in-1,000,000, but less than the 1-in-100,000 benchmark accepted by Health Canada.

ILCR > 1.0 x 10-5 (1E-05)

Signifies the estimated exposure results in an incremental lifetime cancer risk greater than the acceptable regulatory-established cancer risk benchmark of 1-in-100,000. This suggests that the potential for an elevated level of risk may be present for some COC. The significance of which must be balanced against the high degree of conservatism incorporated in the risk assessment (i.e., the uncertainty is reduced but not removed entirely).

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3.0 PROBLEM FORMULATION 3.1 Site Characterization To accommodate increasing ridership demand in the future, the Toronto Transit Commission (TTC) is proposing the construction of a new bus garage located on McNicoll Avenue, just east of Kennedy Road in Scarborough, Ontario. The intended use of the garage is to store new standard and articulated TTC buses, along with some of the current in service fleet, and for general maintenance and repair on the buses. The majority of emissions considered in this assessment are due to buses idling within the proposed facility or related vehicle use on adjacent roadways, while emissions from natural gas-fired heating equipment within the garage were also considered (Novus, 2014).

(Legend: Proposed facility outlined in blue, the property boundary line in red, and each receptor location in yellow)

Figure 3-1 Map of Proposed Study Area and Sensitive Receptor Locations (Novus, 2014)

The closest sensitive receptor to the proposed facility is an existing senior citizens’ residence, located approximately 20 m west of the facility’s property boundary line. The vacant land to the east of the facility (i.e., 2150 McNicoll Avenue) is zoned under Scarborough General Zoning Bylaw 24982 as Heavy, General and Special Industrial (M, MG and MS). Despite the industrial nature of this zoning, the Bylaw does permit for educational facilities, daycares and places of worship within this zone. While there are currently no publically-made plans for development, and no building permits on the property, potential risks related to the future establishment of such a facility on these lands was considered in the current assessment. To provide the necessary ground-level air concentrations, Novus predicted maximum ground-level air concentrations at 21 discrete sensitive receptor locations within the Study Area (Novus, 2014).

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3.2 Chemical Characterization The primary concern for the current assessment is emissions from TTC buses using the proposed McNicoll garage and nearby roadways, and the potential health implications associated with emissions from these diesel-powered vehicles on the surrounding community. As such, one must understand the typical contaminants emitted by diesel engines to properly select the chemicals of concern for the current study. Potential emissions from heating equipment within the garage and the standby diesel generator were also considered as part of the Air Quality Study. The main concern associated with boiler exhaust due to the combustion of natural gas would be the release of oxides of nitrogen (NOx). 3.2.1 Overview of Characteristics of Diesel Emissions In brief, diesel engines operate through the injection of fuel into air within a combustion chamber at high pressure and temperature (US EPA, 2002a). The ignition of injected fuel results in the release of chemical energy, and the expanding combustion gases pushing a piston prior to being released into the atmosphere. The amount of injected fuel controls the power output of the engine. Diesel exhaust emissions are constituted of a complex mixture of chemical and physical components, including gases, vapours, and fine particles (known as “soot”), that are formed through the complete and incomplete combustion of fuel (US EPA, 2002a; Health Canada, 2006a). Major gaseous products emitted include oxygen, nitrogen, water vapour, carbon dioxide (CO2), carbon monoxide (CO), oxides of nitrogen (NOx), sulphur dioxide (SO2), and volatile organic compounds (VOC) (i.e., low-molecular-weight hydrocarbons) (WHO, 1996; US EPA, 2002a). Such gaseous hydrocarbons include benzene, 1,3-butadiene, aldehydes (e.g., formaldehyde, acetaldehyde, acrolein), polycyclic aromatic hydrocarbons (PAHs), and nitro-PAHs (US EPA, 2002a). Generally, diesel engines operating without emission controls emit high concentrations of particles, NOx, and aldehydes and low concentrations of CO and hydrocarbons. The NOx in diesel exhausts contain a higher fraction of NO2 than exhaust from gasoline engines because the excess air intake of diesel engines allows greater conversion of NO to NO2. Diesel particles are complex, covering a range of sizes and morphologies, and having a myriad of chemical components that vary with engine characteristics, operating conditions, and fuels (WHO, 1996; US EPA, 2002a). Diesel particulate is released directly from diesel-powered engines, but can also be formed from the gaseous compounds emitted by diesel-powered engines (i.e., secondary formation (US EPA, 2002a)). Diesel particulate emissions are composed of elemental carbon (EC) as the central core and chemical species that condense onto these nuclei when exhaust gases cool (US EPA, 2002a). Typically, adsorbed organic compounds contribute 10 to 30% of the total particulate matter (PM) and originate from fuel and lubricating oil (WHO, 1996). Particles are also composed of much smaller amounts of inorganic compounds including sulphate, nitrates, metals, and other trace elements which originate from diesel oil and engine material (Health Canada, 2006a). PAHs, nitro-PAHs, and oxidized PAH derivatives can also be present on diesel exhaust particles (US EPA, 2002a). Diesel engines characteristically release significant amounts of PM, typically producing particles at a rate about 20-times greater than from gasoline engines; however, over the past decade, modifications of diesel engine components have significantly reduced particle emissions (WHO, 1996; US EPA, 2002a). Diesel exhaust emissions are significantly reduced by the use of engine designs that exploit clean-diesel technologies and use such features as particle traps/filters to remove particles and

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catalytic converters to reduce levels of carbon monoxide and gaseous hydrocarbons emitted into the environment (WHO, 1996). The use of low-sulphur diesel fuel also effectively reduces emission of sulphur particulates, and ensures that sulphur emissions do not impair the effectiveness of catalytic converters and particles filter devices. 3.2.2 Selection of Chemicals of Concern (COC) Based upon the primary components present in diesel exhaust from the worst case vehicle fleet using the proposed garage, as well as the boiler exhaust from the proposed garage itself, the following contaminants were evaluated in the Air Quality Study (Novus, 2014) and selected as COC for the current screening level assessment:

Criteria Air Contaminants (CACs) Volatile Organic Contaminants (VOCs)

Carbon monoxide (CO)

Oxides of nitrogen (NOx)

Inhalable coarse particulate matter (PM10)

Respirable fine particulate matter (PM2.5)

1,3-Butadiene

Acetaldehyde

Acrolein

Benzene

Formaldehyde

Polycyclic Aromatic Hydrocarbons (PAHs)

Benzo[a]pyrene (as a surrogate for the carcinogenic PAH group)

Sulphur dioxide was not included as a COC in the current assessment due to the use of low sulphur fuels by the TTC. The following sections provide a brief description of each selected COC, and their typical sources within the environment (both natural and anthropogenic). 3.2.2.1 Criteria Air Contaminants (CACs) 3.2.2.1.1 Carbon Monoxide (CO) Carbon monoxide (CO) is a colourless and odourless gas (WHO, 1999). The compound is a trace constituent of the atmosphere, usually present at concentrations less than 0.001% (Ernst and Zibrak, 1998; WHO, 1999). CO is a product of the incomplete combustion of carbon-containing fuels (i.e., fossil fuel combustion, biomass burning), produced at the earth’s surface by both natural processes and human activities (US EPA, 2000a). Global budgets suggest that combustion processes produce about 40% of annual CO emissions (WHO, 1999). The atmospheric oxidation of methane (CH4) and non-methane hydrocarbons is an additional source of anthropogenic and naturally occurring CO, accounting for approximately 50% of annual emissions (WHO, 1999). The remainder of emissions is thought to be accounted for by the production of CO via organic matter oxidation in surface waters and soils, and as a metabolic by-product of plants. Human activities are estimated to be responsible for two thirds of global CO production (US EPA, 2000a). Specific sources are generally divided into five categories: transportation/mobile sources, stationary source fuel combustion, industrial processes, solid waste disposal, and miscellaneous sources (WHO, 1999). Transportation sources include both on-road vehicles (e.g., passenger cars, trucks, buses, and motorcycles) and non-road (e.g., aircraft, trains, vessels, agricultural and construction equipment, industrial machinery, lawnmowers, etc.). While CO emissions have steadily decreased since 1970, an estimated decrease of 24.7% in

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total CO emissions observed in the United States between 1988 and 1997, the fractional contribution of on-road vehicles consistently represents the single largest contributing source of emissions (WHO, 1999; US EPA, 2000a). Stationary sources (e.g., coal-, gas-, oil-fired heating or power generation plants, residential wood-burning) account for approximately 23% of CO emissions in the United States, much of the CO produced as a result of inefficient operating practices or combustion techniques (US EPA, 2000a). In 2005, Environment Canada estimated that over 9.5 million tonnes of CO were released in Canada, not accounting for the release of CO from open sources (e.g., forest fires, prescribed burning) (Environment Canada, 2006). Approximately 76% of emissions were attributed to transportation sources (Environment Canada, 2006). Thus, atmospheric concentrations of CO in urban areas are typically higher than in rural areas (Ernst and Zibrak, 1998). Residential fuel wood combustion, upstream oil and gas, and the wood and aluminum industries, accounted for the majority other emissions (Environment Canada, 2006). CO is also produced endogenously via biochemical processes in the human body through both the normal catabolism of hemoglobin (Ernst and Zibrak, 1998), and the biotransformation of halomethanes (WHO, 1999). Therefore, a low background concentration of the compound is detected in the blood (Ernst and Zibrak, 1998). Inhalation is the primary route of human exposure to non-endogenous CO. Once inhaled, CO will bind to haemoglobin in the blood to form carboxyhaemoglobin (COHb) (US EPA, 2000a), a compound that inhibits the capacity of the blood to carry oxygen (Environment Canada, 2006). It is generally assumed that people are exposed to higher levels of CO indoors compared to the outdoor environment when fossil fuels and other combustion processes are used in an indoor setting (US EPA, 2000a). CO can be formed indoors by malfunctioning, or misused combustion appliances, combustion engines and tobacco smoke (US EPA, 2000a). 3.2.2.1.2 Oxides of Nitrogen (NOx) Nitrogen is the most abundant element in ambient air, existing primarily as N2 (Cal EPA, 2007). Oxides of nitrogen (NOx), including nitric oxide (NO) and nitrogen dioxide (NO2) gases, are produced by both natural and human activities, primarily formed by the reaction of atmospheric oxygen and nitrogen during high temperature combustion processes (Environment Canada, 2006). Specific anthropogenic sources of NOx include transportation, stationary source fuel combustion, industrial processes, solid waste disposal, and other sources (e.g., forest fires) (US EPA, 1993). Approximately 2.4 million tonnes of NOx were released in Canada in 2005, not accounting for the emissions from open sources (e.g., forest fires, prescribed burning) (Environment Canada, 2006). The primary emitting sources were on-road and off-road transportation (53 % of emissions), the upstream oil and gas industry (19% of emissions), and fossil-fuelled electric power plants (10% of emissions) (Environment Canada, 2006). Even in the absence of human activity, NOx is ubiquitous in the environment, produced naturally by biological and abiological processes in soils, biomass burning, lightning, and to a lesser extent by oxidation of ammonia, stratospheric intrusion, and oceans (US EPA, 1993; Cal EPA, 2007). NOx released via combustion processes (e.g., motor vehicles, fossil fuel power stations) is mostly in the form of NO and to a lesser extent NO2 (usually less than 10%) (WHO, 1997). In the presence of ozone (O3) or in a photochemically active reactive atmosphere, NO is quickly oxidized to NO2 (US EPA, 1993; WHO, 1997). NO2 is subject to further extensive atmospheric transformations, ultimately leading to the formation of strong oxidants (i.e., ozone) and the conversion of NO2 to nitric acid (NO3) (Forastiere et al., 2006). NO3 may be found as a vapour, or deposited on particular matter or other surfaces; NO3 levels can affect visibility (Cal EPA, 2007). Ammonium nitrate (NH4NO3) particles may be subsequently produced from NO3 via reaction with ammonia (NH3) in the atmosphere (Cal EPA, 2007). Thus, through the

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photochemical reaction sequence initiated by solar-radiation-induced activation of NO2, the newly generated pollutants are an important source of nitrate particles currently measured as PM2.5. For these reasons, NO2 is a key precursor of a range of secondary pollutants whose effects on human health are well-documented (Forastiere et al., 2006). NO and NO2 can also undergo reactions to form other oxides of nitrogen (both in indoor and outdoor air) including HNO2, HNO3, nitrogen trioxide (NO3), dinitrogen pentoxide (N2O5), peroxyacetyl nitrate (PAN) and other organic nitrates (WHO, 1997). Figure 3-1 (from US EPA, 2008a) provides a schematic diagram of the cycle of reactive oxidized N species in the atmosphere, and demonstrates the potential for inter-conversion of various NOx species in the environment. It should be noted that the “NOx” group of chemicals are generally considered to consist of all nitrogen-containing compounds shown inside the large dashed-line box.

Figure 3-2 Schematic Diagram of the Cycle of Reactive Oxidized N species in the Atmosphere (US EPA, 2008a)

Significant concentrations of NOx can be found in both ambient and indoor air (WHO, 1997); heaters and gas stoves may produce substantial amounts of NO2 in indoor settings (Cal EPA, 2007). Human exposures to NOx vary greatly from indoors to outdoors and from urban to nonurban areas. NOx due to the proximity to combustion sources (traffic or industry) and exposure is also dependant on the time of day and season (WHO, 1997). During the summer months, photochemical reactions tend to increase the ratio of NOx to NO. The primary route of exposure to NOx is through inhalation. Ambient concentrations of NO and NOx tend to be greatest in the cities (WHO, 1997). Higher concentrations of NO are commonly found in street canyons due to vehicular emissions (WHO, 1997). In rural areas, where there is less vehicular traffic, NOx may have spent considerable time in the atmosphere and thus undergone reactions to produce significant concentrations of other species, such as HNO3 and PAN (i.e., 1-(2-pyridylazo)-2-naphthol) (WHO, 1997). While the NOx emitted and produced in the atmosphere are removed via wet precipitation and dry deposition, NOx in indoor air dissipates via infiltration into household materials (WHO, 1997).

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It is important to note that while NOx is emitted from a diesel engine, nitrogen dioxide (NO2) is the most toxicological significant of the oxides of nitrogen. As NO is considerably less toxic than NO2, it is important to accurately estimate the actual amount of NO2 present at the receptor location related to the emissions from diesel vehicles using the proposed facility. In the case of the current project, Novus (2014) modelled specifically the NO2 emissions from the diesel buses using the proposed facility, as well as the standby diesel generator. 3.2.2.1.3 Particulate Matter (PM) PM consists of airborne particles in solid or liquid form, the size of ambient PM ranging from approximately 0.005 to 100 microns (µm) in aerodynamic diameter (WHO, 2000) (Figure 3-3).

0.01µm 1µm 10µm 100µm0.1µm

0.05µm 0.5µm 5µm 50µm

Limit of vision

PM10Thoracic Particles

PM 2.5-10Coarse fraction

PM 2.5Fine particles

PM 0.1Ultra fine particles

pollenRBCSalmo nellaVirusMolecule S.aureu s

Figure 3-3 Comparison of PM Fractions with a Range of Biological Entities from Pollen to Molecules (adapted from Brook et al., 2004)

PM is operationally separated into three groups: total suspended particulate (TSP), inhalable coarse particles (PM10) and fine or respirable particles (PM2.5) (Environment Canada, 2000a). It is important to recognize that TSP contains all particles smaller than 44 microns; PM10 contains all particles with a mean aerodynamic diameter of less than 10 microns; and PM2.5 contains particles smaller than 2.5 microns as well as ultrafine PM of less than 0.1 micron (US EPA, 2004). The largest particles (coarse particles in particular) form the highest proportion of the mass of ambient particles; the smallest, ultrafine particles, comprise only 1 to 8% of this mass. PM is ubiquitous in the environment as it is emitted from both natural and anthropogenic sources. Suspended particulate may be emitted directly into the atmosphere (i.e., primary PM), or can be formed in the atmosphere from precursor gases via physical and chemical transformations (i.e., secondary PM), such as nitrogen oxides (NOx) reacting to form nitrate PM (Environment Canada, 2006). When characterizing possible health effects associated with exposure to PM it is important to consider the source and the associated chemical composition of particulate mixtures.

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It should be noted that some regulatory jurisdictions (such as the California EPA) consider diesel particulate to be carcinogenic, and evaluate the risk arising from this mixture group in its entirety. However, a more recent scientific review by the US EPA generally disagreed with this approach, and concluded that while diesel exhaust is “likely to be carcinogenic in humans by inhalation” at environmental or higher exposure conditions, due to the uncertainty in available exposure-response data, a specific cancer potency benchmark for diesel exhaust could not be derived. For purpose of the current assessment, particulate matter (i.e., PM10 and PM2.5), in itself, is not considered to be carcinogenic. Rather, the potential carcinogenicity of the diesel particulate mixture is considered to be primarily a result of the carcinogenic nature of various chemicals adsorbed to the surface of the particulate, with the PM (such as PM2.5) being the delivery vehicle by which these carcinogenic chemicals are carried deep into an individual’s lungs. For the current assessment, a number of the VOCs (specifically 1,3-butadiene, acetaldehyde, benzene, and formaldehyde) and the PAH group are considered to be carcinogenic, and the implications of exposure to these diesel particulate contaminants to the surrounding community has been evaluated. The potential health impact of ultrafine particulate matter (i.e., PM0.1) is also an emerging area of scientific enquiry. Currently there are no established regulatory benchmarks or standardized approaches to evaluation of the health impact related to exposures to this particulate matter fraction. For the current assessment, the ultrafine fraction was considered as part of the evaluation of health impacts related to the PM2.5 (i.e., particulate matter less than 2.5 microns in size) group. This approach is agreement with the position established by the US EPA in its 2012 National Ambient Air Quality Standard (NAAQS) for particulate matter (PM), where the agency declined to establish a distinct PM standard for UFPs (US EPA, 2013), and a recent Health Effects Institute (HEI) expert panel that extensively reviewed the scientific literature on UFPs published since 1997 and found that the current evidence “is not sufficiently strong to conclude that short-term exposures to UFPs have effects that are dramatically different from those of larger particles” (HEI, 2013). Inhalable Coarse Particles (PM10) Characteristics of coarse particles include composition and sources. Coarse PM10 is composed of suspended soil or street dust, fly ash from uncontrolled combustion of coal, oil, and wood, nitrates/chlorides/sulfates from HNO3/HCl/SO2 reactions with coarse particles. It also includes oxides of crustal elements (Si, Al, Ti, Fe), CaCO3, CaSO4, NaCl, sea salt, bacteria, pollen, mold, fungal spores, plant and animal debris, tire, brake pad, and road wear debris. Sources of PM10 include resuspension of particles deposited onto roads; suspension from disturbed soil (e.g., farming, mining, unpaved roads); construction and demolition, and uncontrolled coal and oil combustion. PM10 has become the indicator for purposes of regulating the coarse fraction (referred to as thoracic coarse particles or coarse-fraction particles; generally including particles with a nominal mean aerodynamic diameter greater than 2.5 μm and less than or equal to 10 µm, or PM10-2.5) (US EPA, 2008b) According to 2005 estimates, open sources (e.g., paved and unpaved roads, construction operations, agricultural tilling and wind erosion, etc.) account for approximately 90% of total PM10 emissions in Canada (Environment Canada, 2006). Fixed site monitoring of 24-hour

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concentrations showed that the long term mean PM10 concentrations in Canada during the mid-1980s to mid-1990s ranged from 11 to 42 µg/m3 at urban sites and rural sites in the mid-1990s experienced PM10 concentrations ranging between 11 and 17 µg/m3 (Health Canada, 1999). Fine Particles (PM2.5) Fine PM (PM2.5) and its precursor gases largely originate from combustion processes (Health Canada, 1999). PM is typically composed of sulphate, nitrate, ammonium, inorganic and organic carbon compounds and heavy metals such as lead and cadmium (Health Canada, 1999). Sulphate has repeatedly been shown to be the most abundant single component of fine particles (PM2.5). The sulphate component of PM tends to be acidic in nature. Primary precursor pollutants in the formation of secondary PM2.5 include SO2, NOx, VOCs, and NH3 (Environment Canada, 2006). According to 2005 estimates, open sources (e.g., paved and unpaved roads, forest fires and prescribed burning, construction operations, etc.) account for approximately 64% of total PM2.5

emissions in Canada (Environment Canada, 2006), while industrial processes (e.g., wood and pulp and paper industries), non-industrial fuel combustion (e.g., residential heating), and transportation (e.g., diesel vehicles) account for the majority of other emissions (Environment Canada, 2000a). Measured concentrations of PM2.5 at urban and rural sites ranged from 6.9 to 20.2 µg/m3 and 7.0 to 10.5 µg/m3, respectively (Health Canada, 1999). Refer to Section 4.2.1 for a further discussion of ultrafine particulate matter (PM0.1). 3.2.2.2 Volatile Organic Contaminants (VOCs) 3.2.2.2.1 1,3-Butadiene 1,3-Butadiene is a highly reactive, colourless gas with a mild aromatic odour and is formed by both natural processes and human activities (Environment Canada, 2000b; TCEQ, 2008). The main environmental source of 1,3-butadiene is the incomplete combustion of fossils fuels (US EPA, 2002b). The compound is also produced commercially via the catalytic dehydrogenation of n-butane and n-butene, the oxidative dehydrogenation of n-butene, and as a by-product in the manufacture of ethylene, for use in various industrial processes (US EPA, 2002b). 1,3-Butadiene is predominantly used as an intermediate in the production of polymers such as polybutadiene, styrene-butadiene rubbers and latexes, and nitrilebutadiene rubbers (Environment Canada, 2000b). Transportation sources account for the majority of 1,3-butadiene emissions in Canada, including emissions from gasoline- and diesel-powered on-road vehicles, off-road motor vehicles, and aircraft, and to a lesser extent, lawnmowers, marine vessels and rail (Environment Canada, 2000b). In the United States, these sources produce approximately 78.8% of the total 1,3-butadiene emitted (US EPA, 2002b), with a similar fractional contribution reported in Canada (Environment Canada, 2000b). Other anthropogenic sources of atmospheric 1,3-butadiene include fugitive or accidental release during production, storage, transport, or disposal of the compound; industrial production and use accounts for approximately 1.6% of total 1,3-butadiene emissions in the United States (US EPA, 2002b). Miscellaneous combustion sources (e.g., biomass burning, petroleum refining) produce approximately 19.6% of total emissions (US EPA, 2002b). Biomass combustion (e.g., forest fires) is a major natural source of 1,3-butadiene, releases from forest fires accounting for between 28 to 65% of total annual emissions in Canada; however, the concentrations measured consistently in urban and industrial areas are

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not likely a product of forest fires due to the short atmospheric half-life of the compound (Environment Canada, 2000b). Due to the high volatility of 1,3-butadiene, it is expected to partition to the atmosphere where it is subject to rapid degradation via photo-initiated reactions (ATSDR, 1993). The dominant and most rapid breakdown pathway is the gas-phase reaction with photo-chemically produced hydroxyl radicals. Reactions with other electrophillic oxidants (i.e., ozone, nitrate radicals, and molecular oxygen) are also expected to be significant. Breakdown products include acrolein, formaldehyde, and furan (Environment Canada, 2000b). Despite the relatively fast breakdown of 1,3-butadiene in the ambient environment, the compound is ubiquitous at very low concentrations in urban and suburban environments, typically in the range of 0.1 to 1.0 ppb (Environment Canada, 2000b; US EPA, 2002b). This is due to the widespread presence of combustion sources of the compound. The primary route of human exposure to 1,3-butadiene is inhalation, with the indoor environment a potentially significant source of exposure when environmental tobacco smoke and fugitive emissions indoor combustion source (e.g., wood stoves or fireplaces) are taken into consideration (US EPA, 2002b). 3.2.2.2.2 Acetaldehyde Acetaldehyde is a colorless liquid with a pungent fruity odour, and is ubiquitous in the ambient environment (US EPA, 2000b). Acetaldehyde is predominantly used as a chemical intermediate in the production of acetic acid and a number of other chemicals (US EPA, 1994). To a lesser extent, it is used as a fragrance, deodorizer, and flavouring agent in food (Environment Canada, 2000c). Acetaldehyde is a product of incomplete combustion, this constituting the main direct source of both naturally and anthropogenically produced compound (Environment Canada, 2000c). The secondary formation of acetaldehyde in the atmosphere as a result of photochemical oxidation of VOC is also a major environmental source (Environment Canada, 2000c). In Canada, on-road motor vehicles were the largest direct environmental source of acetaldehyde, according to 1994 estimates (Environment Canada, 2000c). To a lesser extent, aircraft, off-road gasoline-powered and diesel-powered engines, wood-burning stoves, furnaces, power plants, waste incinerators, cigarettes, and cooking of certain types of food, are all sources. Anthropogenic sources also include industrial on-site releases such as emissions from chemical manufacturing plants, pulp and paper mills and forestry product plants, tire rubber plants, and petroleum refining and coal processing plants (Environment Canada, 2000c). Additionally, the degradation of sewage, hydrocarbons and solid biological wastes release acetaldehyde into the environment (WHO, 1995). In the United States, emissions of acetaldehyde formed as a product of the incomplete combustion of wood in residential fireplaces and stoves are higher than releases from industrial activities (US EPA, 2000b). While reliable release estimates are not available for naturally produced acetaldehyde (i.e., forest fires, brush fires) or for the secondary formation of acetaldehyde in atmosphere via the oxidation of non-methane hydrocarbons in the background troposphere and in photochemical smog, it is expected that these sources are very large (WHO, 1995; Environment Canada, 2000c). Breakdown of acetaldehyde in the troposphere predominant occurs via photo-oxidation reactions with hydroxyl radicals (Environment Canada, 2000c). Major breakdown products include phenol peroxyacetyl nitrate, formaldehyde, peroxyacetic acid and acetic acid. To a lesser extent, acetaldehyde may also react with other oxidants in the atmosphere (i.e., ozone, nitrate radicals, and hydroperoxyl radical), transfer into precipitation and clouds, or be removed by dry deposition.

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Small amounts of acetaldehyde are produced endogenously as a metabolic intermediate in human metabolism and respiration of higher plants, and as a product of alcohol fermentation (WHO, 1995). The compound is also formed in the body through the metabolism of ethanol by alcohol dehydrogenase; the consumption of alcoholic beverages and the subsequent breakdown of ethanol in the body is the main source of exposure of the general population (WHO, 1995; Environment Canada, 2000c). Humans are also exposed to acetaldehyde through the inhalation of ambient and indoor air (Environment Canada, 2000c), and potentially via ingestion since acetaldehyde occurs naturally in certain foods (e.g., coffee, fruits). 3.2.2.2.3 Acrolein Acrolein is a clear to yellowish liquid with an acrid odour, and is ubiquitous is the ambient environment (MOE, 2005). Acrolein is predominantly used as a chemical intermediate in the production of acrylic acid. It is also used in a variety of industrial and commercial applications including use as a slimicide, an aquatic herbicide, a sulfide scavenger in oil field floodwater systems, a tissue fixative in histology, etc. (MOE, 2005). Acrolein is a product of incomplete combustion, this constituting the main direct source of anthropogenically produced compound (Environment Canada, 2000d). The secondary formation of acrolein in the atmosphere by the reaction and photodecomposition of other volatile pollutants, such as propylene, 1,3-butadiene, and other diolefins , is also a major environmental source (MOE, 2005). Vehicular sources account for the majority of acrolein emissions in Canada, including emissions from gasoline- and diesel-powered on-road vehicles (Environment, 2000d). Aircraft, marine, railway vehicles, and other off-road motor vehicles also potentially contribute to emissions. Other anthropogenic combustion sources of acrolein include waste incinerators, furnaces, coal-based electric power generation plants, agricultural burns, and cigarette smoking (Environment Canada, 2000d); however, reliable release estimates are not available for most environmental sources. Acrolein represents up to 8% of the total aldehydes generated from vehicles and residential fireplaces and 13% of total atmospheric aldehydes (Ghilarducci and Tjeerdema, 1995). Natural releases of acrolein are primarily from forest fires, fermentation processes, and as a volatile component of oak wood oil (MOE, 2005). Acrolein is not produced commercially in Canada, and thus, is not released to the environment via production and associated processes (Environment Canada, 2000d). Globally, the mean and maximum background concentrations of acrolein detected in ambient urban air are 15 and 32 µg/m3, respectively (WHO, 1992); Canadian urban background air concentrations are typically lower than these concentrations, maximum concentrations of acrolein not exceeding 2.5 µg/m3 when measured under the National Air Pollution Surveillance between 1989 and 1995 (Environment Canada, 2000d). Due to the high vapour pressure and water solubility of acrolein, it is highly mobile in the environment and is expected to partition to the atmosphere as a vapour (US EPA, 2003; MOE, 2005). Acrolein is highly reactive and degrades readily; hence, it is not persistent in the environment (Environment Canada, 2000d). Removal of acrolein from the atmosphere primarily occurs due to photo-oxidation reactions with hydroxyl radicals, and to a lesser extent, by reaction with other oxidants (i.e., ozone, nitrate radicals), wet deposition, and direct photolysis (Environment Canada, 2000d). Major atmospheric breakdown products include carbon monoxide, formaldehyde, and glycolaldehyde (MOE, 2005). Acrolein is present in most living organisms, as a product of the metabolism of spermine, spermidene, glycerol, allyl formate, allyl alcohol, the anticancer drug cyclophosphamide, and as a product of the UV radiation of the lipid triolein in skin (Ghilarducci and Tjeerdema, 1995; MOE, 2005). Small amounts of acrolein are present in humans, produced endogenously by the peroxidation of lipid membranes and metabolism of α hydroxy amino acids and polyamines

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(ATSDR, 2007a). Additionally, acrolein is detected in many unprocessed foods as a product of microbial and vegetative biochemical processes, and in various processed foods released by the heating of animal and vegetable oils (MOE, 2005). Humans may be exposed to acrolein through the inhalation of ambient and indoor air and by ingestion of certain foods. Indoor air concentrations of acrolein may be 2- to 20-fold higher than outdoor air concentrations, major sources indoor sources including combustion appliances and tobacco smoking (WHO, 1992; Environment Canada, 2000b). 3.2.2.2.4 Benzene Benzene is a volatile, colourless liquid with a sweet odour. It is produced by both natural and anthropogenic activities (ATSDR, 2007b). Benzene is recovered commercially from petroleum, coal, and natural gas sources for use as a solvent, and as an intermediate in the manufacture of a number of chemicals including ethylbenzene/styrene, cumene, cyclohexane, and nitrobenzene (WHO, 1993; ATSDR, 2007b). Nitrobenzene is subsequently used the production of urethanes, chlorobenzene, and maleic anhydride (ATSDR, 2007b). Benzene is also an important natural component of gasoline that acts as anti-knock agent in unleaded fuel, typically evident in gasoline at levels below 1% by volume in Canada (Health Canada, 2007; ATSDR, 2007b). Canadian data indicate a trend toward decreasing concentrations of benzene in the air in both urban and rural areas (HEI, 2007). Data from the US for 95 sites monitoring urban ambient air indicate a 47% decrease in benzene concentrations between 1994 and 2000 (US EPA, 2006). During this period, the mean urban concentration in Canada dropped from approximately 3.3 to 1.8 µg/m3. In 1994, 90% of the sites reported concentrations below 6.2 µg/m3, and by 2004 the concentrations were below 3.0 µg/m3. Over the same time period, there was a corresponding decrease in the benzene content of Canadian gasoline (HEI, 2007). Benzene is ubiquitous in the atmosphere, detected in ambient air in rural and urban areas at mean background concentrations of approximately 1 and 5 to 20 µg/m3, respectively (WHO, 2000). Benzene predominantly partitions into air when released into the environment and exists mainly as a vapour in the atmosphere (ATSDR, 2007b). The most significant source of benzene in the Canadian environment is vehicular emissions, including releases associated with automobile exhaust and refueling operations (ATSDR, 2007b; Health Canada, 2007). Combustion of gasoline and other diesel fuels contribute over 75% of benzene emitted to the atmosphere (Health Canada, 1993). Other significant anthropogenic sources include fugitive emissions from the production of benzene and other chemicals, and to a lesser extent, residential fuel combustion, solvent uses, and other industrial sources (Health Canada, 1993). Tobacco smoke is a significant source of benzene in indoor air (ATSDR, 2007b). Natural sources of benzene, contributing low-level concentrations of compound to the environment, include forest fires, volcanoes, crude oil seeps and plant volatiles (Health Canada, 1993). Degradation of benzene in the atmosphere is relatively rapid, reported atmospheric half-lives ranging from 0.1 to 21 days (Health Canada, 1993). The dominant breakdown pathway of benzene in the atmosphere is the reaction with photo-chemically produced hydroxyl radicals (ATSDR, 2007b). Major breakdown products may include phenol, nitrophenol, nitrobenzenes, and various ring-opened dicarbonyl compounds (WHO, 1993). Benzene may also react with other oxidants in the atmosphere (i.e., ozone, nitrate radicals, and molecular oxygen); however, such reactions are considered insignificant due to slow rates of reaction (ATSDR, 2007b). Inhalation is the primary route of human exposure to benzene (ATSDR, 2007b). In general, people living in cities and industrial areas are exposed to higher levels of benzene from inhalation than those living in rural areas (ATSDR, 2007b). In addition, members of the general

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population living near hazardous waste sites, petroleum refining operations, petrochemical manufacturing sites, and gas stations may be exposed to higher levels of benzene in air (ATSDR, 2007b). Generally, concentrations of benzene in indoor air are higher than those in outdoor air (Health Canada, 2007). 3.2.2.2.5 Formaldehyde Formaldehyde is a colourless gas with a strong, irritating odour. It is formed by natural and anthropogenic activities, primarily via combustion processes (Environment Canada, 2001). Formaldehyde is also produced commercially by the catalytic oxidation of methanol (ATSDR, 1999). Formaldehyde is used in a variety of applications including use as a chemical intermediate in the production of amino and phenolic resins and fertilizer, and as a preservative in a variety of consumer products (e.g., cosmetics, foodstuffs, and household cleansers) (WHO, 1989). Large quantities of formaldehyde are also formed in the atmosphere through the photochemical oxidation of natural and anthropogenic VOCs, these reactions considered secondary sources of the compound (Environment Canada, 2001). Formaldehyde is produced by various natural sources including forest fires, animal wastes, and may be emitted by bacteria, algae, plankton, and vegetation (ATSDR, 1999; Environment Canada, 2001). According to 1997 estimates, on-road motor vehicles were the largest direct anthropogenic source in Canada, acetaldehyde released as a product of incomplete combustion (Environment Canada, 2001). Other significant combustion sources include aircraft and marine sector releases, and to a lesser extent, wood-burning stoves, fireplaces, furnaces, power plants, agricultural burns, waste incinerators, cigarette smoking and the cooking of food (Environment Canada, 2001). Industrial discharges account for far less of the formaldehyde released into the environment than vehicular sources. Comparatively, it is estimated that industrial sources emit less than 15% of the total amount of emitted by on-road motor vehicles. According to 1995 estimates, 66.7% of the total industrial air emissions in Canada were produced by the wood industries (MOE, 1998). Formaldehyde is also detected in emissions from other industries, such as tire and rubber plants, petroleum refining and coal processing plants, textile mills and industries that produce chemical and chemical product, non-metallic mineral product, and paper and allied products (MOE, 1998; Environment Canada, 2001). While reliable release estimates are not available for naturally produced formaldehyde (e.g., forest fires) or for the secondary formation of formaldehyde in atmosphere, releases from these sources are expected to be greater than emissions from direct anthropogenic activities (Environment Canada, 2001). Estimates suggest that up to 70 to 90% of the total formaldehyde found in the urban atmosphere may be a product of the photo-oxidation of precursor compounds. Background concentrations of formaldehyde in ambient outdoor air are estimated to range from 0.14 to 0.96 µg/m3 in uncontaminated areas, from about 2 to 4 µg/m3 in major Canadian urban centres, and from about 5 to 10 µg/m3 in major urban centres around the world (MOE, 1998). Additionally, studies have found that indoor air concentrations of formaldehyde are often higher than outdoor air levels (MOE, 1998; ATSDR, 1999; Liteplo and Meek, 2003). This is due to the presence of various sources of formaldehyde in the indoor environment including pressed wood products, permanent press fabrics, fiberglass products, decorative laminates, paper goods, paints, wallpaper, and cosmetics and combustion sources (e.g., stoves, heaters, burning cigarettes) (ATSDR, 1999). Formaldehyde is also present in most living organisms, as a natural product of animal metabolism (ATSDR, 1999). It is both a degradation product in the breakdown of amino acids and an intermediate in the production of various essential chemicals (MOE, 1998); glycine and serine are the major sources of endogenous formaldehyde (ATSDR, 1999). Varying levels of

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formaldehyde are present in the human body at all times, and all cells posses the metabolic capability to breakdown the compound (ATSDR, 1999). Humans are also exposed to formaldehyde through the inhalation of ambient and indoor air and potentially via ingestion of foods (ATSDR, 1999). 3.2.2.3 Polycyclic Aromatic Hydrocarbons (PAHs)

PAH are a large class of organic compounds (>100 compounds) made up of carbon and hydrogen grouped into two or more fused aromatic rings (ATSDR, 1995; WHO, 1998). PAHs almost always occur in the environment as complex mixtures which are difficult to characterize; the chemical constituents of the mixtures generally vary with the source (WHO, 1998). PAHs are primarily formed during the incomplete combustion of organic matter, including the burning of gas, oil, coal, complex petroleum products, products of coal liquefaction processes, plant and animal matter, garbage, wood (biomass), and tobacco (Cal EPA, 1994). To a far lesser extent, PAHs may be produced by diagenesis or biosynthesis, and are found naturally in coal derivatives and petroleum (Environment Canada, 1994). Sources in the environment include natural (volcanic eruptions, peat fires, forest fires, and burning crude oil or shale) and anthropogenic sources (burning of fossil fuels, coke oven emissions, aluminum smelters, coal combustion, conversion industries, vehicle exhaust, tobacco smoke, incinerators, and biomass burning) (Cal EPA, 1994). PAHs may be present in relatively high concentrations in some manufactured products despite the fact that most compounds are not generally manufactured commercially (ATSDR, 1995). PAHs are largely emitted to the atmosphere adsorbed onto PM, but may also be found in the gaseous phase (ATSDR, 1995). PAHs are found in water and soil largely from deposition of air emissions (Environment Canada, 1994). According to 1990 estimates, forest fires were the largest source of atmospheric PAHs in Canada (representing 47% of total emission inventoried) (Environment Canada, 1994). The aluminum smelting industry, residential wood heating, open-air fires/agricultural burning, incineration by saw mills, and transportation represent other significant sources of PAHs in Canada. As indicated in Health Canada (2006b), as well as most other regulatory guidance, the assessment of risks related to exposures to carcinogenic PAHs is primarily conducted through the use of potency or toxicity equivalence factors (PEF or TEF). TEFs allow large groups of compounds with a common mechanism of action such as PAHs to be assessed when limited data is available for all but one of the compounds (i.e., benzo(a)pyrene or b[a]p). Through this approach, exposures to each of the carcinogenic PAHs are adjusted by their carcinogenic potency relative to benzo[a]pyrene. These potency-adjusted exposures can then be summed to provide an overall exposure to the group of carcinogenic PAHs, based on benzo[a]pyrene as the primary surrogate. For the current assessment, emission data for the entire family of PAHs were available as a toxicological equivalence of benzo[a]pyrene (i.e., b[a]p-TEQ). Using this approach, the quantity of each PAH emitted by the diesel vehicles was adjusted for its toxicological potency versus benzo[a]pyrene (i.e., it’s TEF), and summed to produce an overall b[a]p-TEQ emission rate for PAHs emitted from the proposed facility. Benzo[a]pyrene, itself, is a five-ring PAH that accounts for less than five percent of the total amount of atmospheric PAHs (Cal EPA, 1994), but is a persistent compound, poorly volatile, slightly soluble in water, readily sorbed to air and dust particles and one that tends to partition predominantly in soil and sediments (Cal EPA, 1994). Benzo[a]pyrene has an equally distributed electronic density leading it to be metabolized as a carcinogen (ATSDR, 1995).

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Humans are exposed to PAHs through the inhalation of ambient air, tobacco smoke, wood smoke, and consumption of PAHs in foods (ATSDR, 1995). While most direct releases of benzo[a]pyrene are to the atmosphere, there are some suggestions that the dominant pathway of human exposure is the food chain (Hattemer-Frey and Travis, 1991). Ingestion of benzo[a]pyrene in contaminated water are much more minor pathways of exposure. 3.3 Receptor Characterization A human receptor is a hypothetical person (e.g., infant, toddler, child, adolescent, or adult) who resides, attends school/daycare, and/or works in the area being investigated and is, or could potentially be, exposed to the chemicals identified as being of potential concern. The assessment must be sufficiently comprehensive to ensure inclusion of those receptors with the greatest potential for exposure to COC, and those who have the greatest sensitivity, or potential for developing adverse health outcomes from these exposures. For the assessment of inhalation risks, as a straight comparison between predicted short term, acute (i.e., for 1-hour and 24-hour exposure durations) and long term, chronic (i.e., annual average exposures) air concentrations and the corresponding regulatory benchmark (RfC) is made, the resulting CR value is receptor-independent (i.e., the same value is calculated for all receptor types). 3.4 Identifying Exposure Scenarios and Pathways 3.4.1 Exposure Scenarios The main sources of emissions from the proposed facility will be emissions from idling buses inside the facility prior to going into service, emissions from the buses as they travel on nearby roadways, emissions from boilers used to heat the facility, and exhaust from any use of the standby diesel generator. For the current screening level assessment, an exposure scenario consisting of individuals living in the nearby senior citizen’s residence, any proposed daycare facility on the nearby property to the east, or visiting the nearby churches, being exposed on both a short-term (acute) and long-term (chronic) basis to these emissions was evaluated. 3.4.2 Exposure Pathways The primary exposure pathway under evaluation in the current assessment is the inhalation of the COC by individuals living, working or playing in the area around the proposed facility. Deposition onto soils is not viewed as a significant risk for the COCs selected for the current assessment given the predicted emission concentrations and the surrounding land-use, and as such, oral and dermal exposures were not evaluated.

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4.0 EXPOSURE ASSESSMENT The exposure assessment evaluates data related to all chemicals, receptors and exposure pathways and routes identified during the problem formulation phase. Given the nature of the proposed project, the primary source of COC to the environment will be via emissions from buses present at the proposed facility and travelling on the nearby roads, as well as emissions from natural gas boilers used to heat the facility. For the inhalation exposure assessment, specific rates of exposure were not calculated. Rather, ambient air concentrations (measured or modelled) of each COC (expressed as µg/m3) were compared to acceptable air concentrations (also expressed as µg/m3). The inhalation exposure assessment identified potential health risks from acute and chronic exposures (via direct air inhalation only) for all of the COC at each of the assessed human health receptor locations. As deposition onto soils was not viewed as a significant risk for the COCs selected for the current assessment given the predicted emission rates, oral and dermal exposures were not evaluated. 4.1 Estimation of Ambient Ground Level Air Concentrations The main sources of emissions from the proposed facility will be emissions from idling buses inside the facility prior to going into service, emissions from boilers used to heat the facility, and exhaust from a standby diesel generator. Fugitive emissions were also considered from re-suspended particulate matter from buses driving on-site, from the paint booth and shop space, from the storage tanks and vehicles in the parking lot (Novus, 2014). Emissions were also considered from vehicles travelling to and from the proposed facility on adjacent roads – specifically the impact of the additional bus traffic on Redlea Avenue as well as the additional employee vehicle traffic coming to and from work at the proposed Facility (Novus, 2015). Novus (2014) modelled worst-case ground-level air concentrations for each of the COC at each of the 21 sensitive receptor locations assuming worst-case future operations at the facility based on meteorological data collected between 2006 and 2010. Hourly vehicle distribution at the TTC Mount Dennis facility was used to predict the maximum number of buses proposed at the McNicoll bus garage. Based on this information, and a maximum idling time of 10 minutes for any vehicle within the facility, hourly bus movements at the McNicoll facility were predicted. Emissions data from the buses, the boilers servicing the facility, and a standby diesel generator were used by Novus (2014) to model the air dispersion of these COC using the US EPA’s AERMOD dispersion model (an MOECC-approved model), and to estimate worst-case ground-level air concentrations at the receptor locations around the proposed facility. Refer to the Air Quality Report (Novus, 2014) and the Redlea/McNicoll Roadway Assessment Report (Novus, 2015) for a detailed discussion of the methodology used to estimate ground-level air concentrations. When evaluating the impact of a project on local air quality, it is important for the evaluation to include a general estimate of baseline (i.e., “background”) ambient air quality in the region. By combining both existing local background air quality with the estimated contribution from the proposed facility, a conservative estimation of cumulative exposures can be estimated. An appropriate reasonable worst-case regional background concentration for diesel and diesel-related COC for the study area was estimated by Novus (2014) using ambient air quality data

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collected from a number of distinct federal and provincial monitoring stations near the study area between 2009 and 2013. These monitors are part of the National Air Pollution Surveillance (NAPS) network operated by the MOECC and Environment Canada. However, a number of these monitoring stations lie some distance from the study area, itself. In particular, ambient concentrations of the aldehydes considered in the assessment were monitored in Windsor, as none of the monitors in the GTA currently record ambient concentrations of aldehydes. Table 4-1 provides a list of the COC and the regional monitoring station used to estimate worst-case background conditions for the Study Area.

Table 4-1 Location of Regional Monitoring Station used to Estimate Background Concentrations for each COC (Novus, 2014)

Chemical of Concern Worst-Case Regional Monitoring Station

Station Location (MOECC/NAPS ID) Address CO Toronto West (ID 35125) 125 Resources Road NO2 (1-hour) Toronto East (ID 33003) Kennedy Rd./Lawrence Ave NO2 (24-hour) Toronto North (ID 34020) Hendon Ave./Yonge St. PM2.5 Toronto East (ID 33003) Kennedy Rd./Lawrence Ave Acetaldehyde Egbert (ID 64401) Simcoe RR56/Murphy Road Acrolein Windsor (ID 60211) College Avenue/Prince Road Benzene Etobicoke North (ID 60413) Elmcrest Road 1,3-Butadiene Etobicoke South (ID 60435) 461 Kipling Avenue Formaldehyde Egbert (ID 64401) Simcoe RR56/Murphy Road

The station with the highest five year maximum value for each COC and averaging period was selected to represent background concentrations in the study area. The maximum measured concentration for each COC from monitoring data collected between 2009 and 2013 was selected to represent a reasonable worst-case background scenario for the overall regional airshed. Table 4-2 provides a summary of the maximum predicted ground level air concentrations for both the proposed facility and associated roadway contribution, for each averaging period (i.e., 1-hour, 8-hour, 24-hour, and annual average) at the worst-case receptor location for each COC evaluated within the Study Area, as well as the measured historical regional background concentrations (where available). These maximum predicted worst-case ground level air concentrations were used to evaluate potential health risks arising from acute and chronic exposures to these COC.

Table 4-2 Summary of Predicted Maximum Ground-Level Air Concentrations (µg/m3) in Study Area

Chemical of Concern Background Roadway

Contribution a Proposed Facility Cumulative

1-Hour Concentrations Criteria Air Contaminants Carbon Monoxide (CO) 2131 72.3 (3.2%) 79.0 (3.5%) 2282 Nitrogen Dioxide (NO2) 156 18.4 (5.5%) 158.0 (47.5%) 332 Volatile Organic Chemicals Acetaldehyde 3.1 0.83 (16.2%) 1.2 (23.4%) 5.1 Acrolein 0.13 0.15 (39.9%) 0.10 (26.1%) 0.38 Benzene 2.3 0.26 (7.5%) 0.9 (26.0%) 3.5 Formaldehyde 8.2 1.8 (14.7%) 2.5 (19.9%) 12.5

8-Hour Concentrations

Criteria Air Contaminants Carbon Monoxide (CO) 1845 29.9 (1.6%) 22.0 (1.2%) 1897

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Table 4-2 Summary of Predicted Maximum Ground-Level Air Concentrations (µg/m3) in Study Area


Contribution a Proposed Facility Cumulative

24-Hour Concentrations Criteria Air Contaminants Nitrogen Dioxide (NO2) 90.0 2.3 (1.9%) 32.0 (25.7%) 124 Fine Particulate (PM2.5) 36.0 1.4 (3.6%) 1.60 (4.1%) 39.0 Respirable Particulate (PM10) 66.7 1.7 (2.4%) 2.00 (2.8%) 70.4 Volatile Organic Chemicals Acetaldehyde 3.1 0.10 (3.1%) 0.11 (3.3%) 3.3 Acrolein 0.13 0.019 (11.1%) 0.020 (11.9%) 0.17 Benzene 2.3 0.047 (1.9%) 0.19 (7.6%) 2.5 Formaldehyde 8.2 0.23 (2.6%) 0.25 (2.9%) 8.7

Annual Average Concentrations

Criteria Air Contaminants Nitrogen Dioxide (NO2) 31.2 0.34 (0.9%) 5.4 (14.6%) 36.9 Fine Particulate (PM2.5) 8.2 0.22 (2.5%) 0.30 (3.4%) 8.7 Volatile Organic Chemicals Acetaldehyde 1.3 0.014 (1.0%) 0.020 (1.5%) 1.3 Acrolein 0.038 0.0025 (5.6%) 0.0040 (9.0%) 0.045 Benzene 0.77 0.0075 (0.9%) 0.02 (2.5%) 0.80 Butadiene (1,3-) 0.057 0.0015 (2.5%) 0.002 (3.3%) 0.061 Formaldehyde 3.1 0.030 (0.9%) 0.050 (1.6%) 3.2 Polycyclic Aromatic Hydrocarbons (PAHs) Benzo[a]pyrene-TEQ NA b NA 0.00008 NA Note: (X%) values represent the percentage of the overall cumulative maximum ground-level air concentration represented by

contributions from the proposed facility. a Roadway contribution includes the impact of the additional bus traffic on Redlea Avenue as well as the additional employee

vehicle traffic. b NA = Not available. PAHs are not routinely measured at any of the provincial/federal monitoring locations. As such, no regional

background information is available. PAHs were also not evaluated as part of the Novus (2015) roadway assessment; however, PAH contributions from buses travelling along the roadways would be expected to be significantly less than the emissions from idling buses within the proposed facility.

4.2 Exposure Analysis of Particulate Matter The size of the airborne particles to which people are exposed is one of the most important aspects in determining the potential for health risk resulting from PM exposure. Size is directly related to where particles will be deposited in specific parts of the respiratory tract. Particles larger than about 10 microns (µm) in aerodynamic diameter (>PM10) are deposited almost exclusively in the nose, throat, and upper respiratory tract, and tend to be coughed out or swallowed over a very short period of time. This size range is considered outside the inhalable range for people, since these particles are too large to be deposited in the lung. Health effects associated with particles greater than PM10 are considered less critical compared to fractions less than 10 microns in size since they are less likely to be absorbed into the body via inhalation. Fine and ultrafine particles (<2.5 µm), on the other hand, are small enough to reach the alveoli (air spaces) deep in the lungs. In general, it may be assumed that the smaller the particle, the greater the potential to reach respiratory structures such as alveoli where blood-gas exchange occurs. Inhaled fine and ultrafine particles can also carry adsorbed chemical pollutants to the deeper lung structures. Smaller particles tend to be present in greater numbers, and they possess a greater total surface area than larger particles of the same mass. The potential impacts of human exposure to the respirable fraction of PM (i.e., PM2.5) is emphasized in the current HHRA, rather than the broader size fraction represented by total suspended particulate (i.e., TSP, comprising particles ranging up to 44 µm in size). The

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inhalable fraction (i.e., PM10) is also widely used to evaluate potential health issues, since this size of particle primarily affects tissues in the upper airways, but can also travel deep into the lung. When both sets of data are available (PM10 and PM2.5), the PM2.5 data tends to carry more weight in determining the potential for health risks because of the large body of scientific literature characterizing both the epidemiological and toxicological properties of the finer size fraction. Refer to the US EPA Quantitative Health Risk Assessment for Particulate Matter (US EPA, 2010) for further discussion. 4.2.1 Ultrafine Particulate Matter One area of ongoing research is into the health implications of ultrafine particulate matter (UFP). UFP constitute particulate matter smaller than 0.1 microns (or 100 nanometres) in size (i.e., PM0.1). Due to their small size, UFPs are considered to be respirable particles and are able to travel deep within the lung with the potential to penetrate tissue and undergo interstitialization and therefore are not easily removed from the body. These smaller particles also have proportionally greater surface area per mass than larger particles, which can interact more readily with cell surfaces and can adsorb more of other chemicals, which in turn can have toxicological impacts on cells. Like PM2.5, UFP can also lead to cardiopulmonary and respiratory disease, as well as stimulate immune and non-immune pathogenic process, oxidative stress, inflammatory mediator release, and other systemic effects (Oberdörster, 2000). Currently there are no established regulatory benchmarks or standardized approaches to evaluation of the health impact related to exposures to this particulate matter fraction. However, it is important to note that the UFP fraction is collected in monitoring equipment as a subset of the PM2.5 fraction, and as such the health effects arising from exposure to UFPs are inherently accounted for in the epidemiological studies used to establish health-based regulatory benchmarks for PM2.5. Both in vivo and in vitro studies of various UFP species are currently ongoing in a variety of animal models to better establish the toxicological profiles necessary for the establishment of regulatory benchmarks used in risk assessment (refer to the nanotechnology and ultrafine particle research provided by the US EPA National Center for Environmental Research at http://www.epa.gov/ncerqa/nano/research/particle_index.html for further information). For the current assessment, the UFP fraction was considered as part of the evaluation of health impacts related to the PM2.5.

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5.0 HAZARD ASSESSMENT The following section provides the acute and chronic inhalation TRV for each COC evaluated in the current assessment. For the purposes of the current screening level risk assessment, the most conservative TRV from a variety of credible regulatory agencies was selected for each COC and averaging period. It should be noted that there are National Ambient Air Quality Objectives (NAAQOs) established by Health Canada and provincial Ambient Air Quality Criteria (AAQCs) established by the Ontario Ministry of the Environment under O. Reg. 419/05 for a number of the COCs. While still in regulatory force both provincially and federally, these benchmarks are often dated (i.e., NO2, SO2) and may not represent the most recent scientific or regulatory knowledge on health effects related to exposures to these COCs. However, to provide relevant context to current provincial regulation, potential risks were also evaluated based upon the appropriate provincial AAQC, where not selected as the primary regulatory benchmark for that COC. As this is a screening level human health risk assessment, typically the most conservative and stringent of the available criteria (where appropriate), was selected, in consultation with Toronto Public Health. 5.1 Acute Inhalation Toxicity Reference Values The acute (i.e., for 1-hour and 24-hour exposure durations) non-carcinogenic inhalation TRVs for each COC, as well as the key critical health outcomes and regulatory source for each TRV, are provided in Table 5-1.

Table 5-1 Summary of Selected Acute Non-carcinogenic Inhalation TRVs

COC Acute Non-Carcinogenic Inhalation TRVs (µg/m3)

1-hour 24-hour Value Critical Effect Source Value Critical Effect Source

Criteria Air Contaminants (CACs)

CO 15,000 Carboxyhemoglobin blood

level of less than 1% Health Canada,

2006b 6,000 a Carboxyhemoglobin blood

level of less than 1% Health Canada,

2006b

NO2 200 Effects in the pulmonary function of asthmatics

WHO, 2005 200 Respiratory irritant Health Canada,

2006b

PM2.5 NV - - 25 Lowest levels at which total, cardiopulmonary and lung cancer mortality have been

shown to increase

WHO, 2005 PM10 NV - - 50

Volatile Organic Chemicals (VOCs) 1,3-Butadiene NV - - NV - -

Acetaldehyde 470 Sensory irritation; bronchi,

eyes, nose, throat OEHHA, 2014 500 Tissue damage MOE, 2012

Acrolein 2.5 Eye irritation OEHHA, 2014 0.4 Nasal lesions (chronic) MOE, 2009b

Benzene 27 Developmental

hematotoxicity in fetal andneonatal mice

OEHHA, 2014 29 Reduced lymphocyte

proliferation following mitogen stimulation

ATSDR, 2005

Formaldehyde 55 Mild and moderate eye

irritation OEHHA, 2014 65

Chronic human health effects and short term odour irritation

MOE, 2012

NV No acute regulatory toxicity reference values are available for that specific averaging time. a CO is evaluated for 1-hour and 8 hour exposure time periods, from a toxicological and regulatory point-of-view. For the current table, the

TRV provided for CO in the 24-hour column represented a TRV for an 8-hour exposure period.

It should be noted that, in the absence of any available acute-specific TRVs in the regulatory literature, 24-hour AAQC specified by the MOECC under O. Reg. 419/05 (i.e., MOE, 2012) were

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used to evaluate acute 24-hour health risks. Though they are expressed as 24-hour exposure period criteria, due to the nature of how the MOECC derives their 24-hour AAQC, these typically are based on chronic endpoints, rather than acute. As chronic TRVs are typically much more conservative than acute TRVs for the same COC, it is expected that this will result in an overestimation of potential acute risks. In the absence of acute TRVs, this is viewed as a conservative approach to evaluating risks for this exposure period. 5.2 Chronic Inhalation Toxicity Reference Values The chronic non-carcinogenic and carcinogenic inhalation TRVs for each COC (where they were available), as well as the key critical health outcomes and regulatory source for each TRV, are provided in Table 5-2.

Table 5-2 Summary of Chronic Non-carcinogenic and Carcinogenic Inhalation TRVs

COC Chronic Toxicity Reference Values

Non-Carcinogenic Inhalation TRVs (µg/m3) Carcinogenic Inhalation Unit Risk Values (µg/m3)-1 Value Critical Outcome Source Value Critical Outcome Source

Criteria Air Contaminants (CACs) CO NV - - NC - - NO2 40 Health effects WHO, 2005 NC - -

PM2.5 8.8

Lowest levels at which total, cardiopulmonary and lung cancer mortality have been shown to increase

CCME, 2012 NC - -

Volatile Organic Chemicals (VOCs)

1,3-Butadiene 2 Ovarian atrophy US EPA IRIS, 2002; OEHHA,

2014 5.0 x 10-7 Leukemia incidence data

(human) TCEQ, 2008

Acetaldehyde 140

Degenerative, inflammatory and

hyperplastic changes of the nasal mucosa in

animals

OEHHA, 2014 2.7 x 10-6 Nasal tumour incidence (rat)

OEHHA, 2011

Acrolein 0.35 Lesions in respiratory

epithelium OEHHA, 2014 NC - -

Benzene 3 Decreased peripheral

blood cells in Chinese workers

OEHHA, 2014 2.9 x 10-5 Leukemia incidence (occupational exposure)

OEHHA, 2011

Formaldehyde 9

Nasal obstruction and discomfort, lower airway

discomfort, and eye irritation

OEHHA, 2014 6.0 x 10-6 Nasal squamous carcinoma incidence (rat)

OEHHA, 2011

Polycyclic Aromatic Hydrocarbons (PAHs)Benzo[a]pyrene-TEQ NV - - 1.1 x 10-3 Respiratory tract tumor OEHHA, 2011

NC This chemical is not considered to be a carcinogen. NV No value. No chronic TRVs are available for this COC.

It should be noted that some regulatory jurisdictions (such as the California EPA) consider diesel particulate to be carcinogenic. However, a more recent scientific review by the US EPA (in 2002) concluded that while diesel exhaust is “likely to be carcinogenic in humans by inhalation” at environmental or higher exposure conditions, due to the uncertainty in available exposure-response data, a cancer unit risk/cancer potency for diesel exhaust could not be derived (US EPA, 2002a). For the purpose of the current assessment, PM (i.e., PM10 and PM2.5), in itself, is not considered to be carcinogenic. Rather, the potential carcinogenicity of the diesel particulate mixture is a

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result of the carcinogenic nature of various chemicals adsorbed to the surface of the particulate, with the PM (such as PM2.5) being the delivery vehicle by which these carcinogenic chemicals are carried deep into an individual’s lungs. For the current assessment, a variety of VOCs (specifically hazardous air pollutants or HAPs) and the PAH group are considered to be carcinogenic, and the implications of exposure to these diesel particulate contaminants to the surrounding community has been evaluated.

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6.0 RISK CHARACTERIZATION The following section provides the results of the acute and chronic assessment of risks related to emissions from the proposed facility (both vehicle and heating related) at the worst-case sensitive receptor location. As noted previously, potential acute human health inhalation risks were evaluated for both 1-hour and 24-hour exposure periods for individuals living, working or playing in the community surrounding the proposed TTC bus garage. In both cases, the worst-case 1-hour or 24-hour period of cumulative exposures was selected from the evaluated sensitive receptor locations around the proposed facility, which would account for the impacts of worst-case meteorological conditions, bus activity patterns, facility heating requirements, and regional air quality. For the assessment of potential chronic human health risks to individuals living, working, or playing in the community surrounding the proposed TTC bus garage, the maximum worst-case ground level air concentrations predicted at the sensitive receptor locations around the proposed facility were evaluated based upon an annual average exposure period. 6.1 Acute Inhalation Assessment Results Table 6-1 provides a summary of the maximum predicted acute 1-hour, 8-hour, and 24-hour inhalation risks at the worst-case receptor location for each COC.

Table 6-1 Worst-case Acute Risk Predictions for Background and Proposed Project-Related Emissions in the Study Area


Contribution Proposed Facility Cumulative

1-Hour Concentrations Criteria Air Contaminants Carbon Monoxide (CO) 0.14 0.0048 0.0053 0.15 Nitrogen Dioxide (NO2) 0.78 0.092 0.79 1.7 Volatile Organic Chemicals Acetaldehyde 0.0066 0.0018 0.0026 0.011 Acrolein 0.052 0.061 0.040 0.15 Benzene 0.084 0.010 0.033 0.13 Formaldehyde 0.15 0.033 0.045 0.23

8-Hour Concentrations Criteria Air Contaminants Carbon Monoxide (CO) 0.31 0.0050 0.0037 0.32

24-Hour Concentrations Criteria Air Contaminants Nitrogen Dioxide (NO2) 0.45 0.012 0.16 0.62 Fine Particulate (PM2.5) 1.4 0.057 0.064 1.6 Respirable Particulate (PM10) 1.3 0.034 0.040 1.4 Volatile Organic Chemicals Acetaldehyde 0.0062 0.00020 0.00022 0.0066 Acrolein 0.33 0.047 0.050 0.42 Benzene 0.078 0.0016 0.0066 0.086 Formaldehyde 0.13 0.0035 0.0038 0.13 Note: Bolded and shaded CR values in shaded cells indicate predicted risks exceeded the CR benchmark of 1.0 (i.e., predicted ground-level air

concentrations exceeded the regulatory benchmark).

Results of the inhalation assessment for the acute exposure periods (i.e., 1-hour, 8-hour, and 24-hour) indicated that none of the COCs individually exceeded the corresponding regulatory benchmark or TRV. However, predicted cumulative risks (i.e., background + project

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contributions) for NO2 in the 1-hour exposure period did marginally exceed the health-based acute benchmark. Also, the 24-hour exposures to particulate matter (both PM10 and PM2.5) exceeded the regulatory benchmark for both the background and cumulative conditions. However, in the case of particulate matter, the contribution from project-related emissions was negligible (i.e., approximately 3 to 5% of the total cumulative concentration). 6.2 Chronic Inhalation Assessment Results 6.2.1 Non-Carcinogenic Risks Table 6-2 provides a summary of the maximum predicted chronic non-carcinogenic inhalation risks at the worst-case receptor location for each COC.

Table 6-2 Worst-case Chronic Non-Cancer Risk Predictions for Background and Proposed Project-Related Emissions in the Study Area


Contribution Proposed

Facility Cumulative


Criteria Air Contaminants Nitrogen Dioxide (NO2) 0.78 0.009 0.14 0.92 Fine Particulate (PM2.5) 0.93 0.025 0.034 0.99 Volatile Organic Chemicals Acetaldehyde 0.0091 0.00010 0.00014 0.0095 Acrolein 0.11 0.0071 0.011 0.13 Benzene 0.26 0.0025 0.0067 0.27 Butadiene (1,3-) 0.029 0.00075 0.0010 0.030 Formaldehyde 0.34 0.0033 0.0056 0.35 Note: Bolded and shaded CR values in shaded cells indicate predicted risks exceeded the CR benchmark of 1.0 (i.e., predicted ground-

level air concentrations exceeded the regulatory benchmark).

Results of the inhalation assessment for the chronic exposure period (i.e., annual average) for non-carcinogenic endpoints indicated that none of the COCs individually exceeded the corresponding health-based benchmark. 6.2.2 Carcinogenic Risks Table 6-3 provides a summary of the maximum predicted chronic carcinogenic inhalation incremental lifetime cancer risks (ILCR) at the worst-case receptor location for each COC. For the purpose of evaluating carcinogenic risks related to an airborne emission source as part of an Environmental Assessment (EA) process, the evaluation of incremental lifetime cancer risks versus the Ontario regulatory benchmark of acceptable incremental cancer risk (i.e., one-in-one-million or 1 x 10-6) is done by calculating the incremental increase in lifetime cancer risk related to emissions predicted for the proposed project above those predicted for background conditions (i.e., the incremental lifetime cancer risks related to addition of emissions from the proposed facility versus status quo).

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Table 6-3 Worst-case Incremental Lifetime Cancer Risk Predictions for Proposed Project-Related Emissions in the Study Area

Chemical of Concern Roadway

Contribution Proposed Facility Total Project


Volatile Organic Chemicals

Acetaldehyde 3.8 x 10-8 5.4 x 10-8 9.2 x 10-8

Benzene 2.7 x 10-7 5.8 x 10-7 8.5 x 10-7

Butadiene (1,3-) 7.5 x 10-10 1.0 x 10-9 1.8 x 10-9

Formaldehyde 1.8 x 10-7 3.0 x 10-7 4.8 x 10-7

Polycyclic Aromatic Hydrocarbons

Benzo[a]pyrene and related ND 8.8 x 10-8 8.8 x 10-8 Note: Bolded and shaded ILCR values in shaded cells indicate predicted risks exceeded the ILCR benchmark of 1.0 x 10-6 (i.e., one-in-one million

acceptable incremental lifetime cancer risk benchmark).

b NA = Not available. PAHs were not evaluated as part of the Novus (2015) roadway assessment.

Results of the assessment indicated that none of the COC emitted from the proposed facility resulted in an incremental lifetime cancer risk exceeded the provincial benchmark for acceptable incremental lifetime cancer risk of one-in-one-million (i.e., 1.0 x 10-6). It should be noted that PAHs were not evaluated as part of the Novus (2015) roadway assessment. However, PAH contributions from buses travelling along the roadways would be expected to be significantly less than the emissions from idling buses within the proposed facility. Even if one conservatively assumed the PAH contribution from the roadway vehicles was equivalent to the concentration of PAHs emitted from the proposed bus garage, the total Project incremental lifetime cancer risks would still be well below the provincial ILCR benchmark (i.e., 1.8 x 10-7 versus 1.0 x 10-6).

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7.0 UNCERTAINTY ANALYSIS In any HHRA, screening level or detailed, the intention is to obtain the most accurate evaluation of risk based upon the available data and state of knowledge, without underestimating the potential health risks. With any such assessment, there are always a number of administrative and technical boundaries that limit the ability of the assessment to quantify risk with absolute certainty. The following section provides an overview of the key administrative and technical boundaries inherent within the current assessment. Quantitative human health assessments involve assigning numerical values to input parameters in an appropriate exposure or risk model to obtain a quantitative estimate of risk. Numerical values are required for parameters describing chemical concentrations in environmental media, chemical fate and transport, human exposure and toxic response. These values may be measured, assumed, prescribed or based on published literature. Variability and uncertainty in the input parameters or risk model result in variability and uncertainty in the estimate of risk. The US EPA (2000) advocates that the risk characterization process maintain transparency, clarity, consistency, and reasonableness. The goal of risk characterization is to clearly communicate the key findings of the assessment and to provide a clear and balanced assessment of the strengths and limitations of the process. Risk characterization involves both scientific and policy based decision making, thereby resulting in a decision making process that blends both elements. When assumptions are made during the risk assessment process, either because of data gaps or knowledge gaps, each can result in some degree of uncertainty in the overall conclusions. In order to understand the uncertainties within the assessment and to ensure that the implications of these uncertainties are understood and addressed, it is important to document and characterize them. To ensure that the risk assessment does not underestimate the potential for the occurrence of adverse effects, it is necessary to make assumptions that are conservative (protective). In other words, assumptions should be made that tend to overestimate exposure, toxicity and risk, rather than underestimate these parameters. The following sections describe uncertainty within the current assessment, and discuss the potential impacts of these limitations on the conclusions drawn from the assessment. Given the tendency for the assumptions described below to overestimate both exposure and toxicity, it is likely that the risk characterization errs on the side of caution and over predicts risk. A summary of the conservative assumptions that were incorporated into the assessment can be found in Table 7-1, arranged according to the steps of the risk assessment paradigm. Examination of the table shows that conservatism was introduced at virtually every step of the assessment, and extended to both the exposure and toxicity assessment of the overall human health assessment.

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Table 7-1 Major Assumptions Used in the Current Assessment

Risk Assessment

Paradigm Assumption Discussion of Conservatism

Problem Formulation

21 discrete receptor locations were selected in the area surrounding the proposed facility to represent the most sensitive or highly exposed individuals living, working or playing in the surrounding community.

Care was taken to select residential locations around the facility that would likely demonstrate the highest potential impacts from bus and facility emissions. As one moves away from the proposed facility geographically, airborne concentrations related to facility emissions would be expected to drop significantly.

Chemical characterization and selection of COC were based upon the primary contaminants of importance in diesel emissions.

The key chemicals with respect to diesel emissions from the perspective of either regulatory or public health were selected as COC for the current assessment. Diesel particulate emissions include a large number of different chemicals. While the selected COC typically represent the most toxic of the chemicals in this mixture, the current assessment does not attempt to evaluate all of the contaminants emitted from the proposed buses.

Oral and dermal exposures to certain COCs were screened out of the current assessment based on previous experience.

With the exception of the PAH group, due to their physical-chemical nature none of the COCs would be expected to deposit onto soils following emission and cause potential oral or dermal exposures to nearby residents. The evaluation of oral and dermal exposures to the PAH group was screened off given the very low emissions estimated for this group. Previous experience on similar projects has demonstrated that there would have to be significantly greater emissions of PAHs to result in any potential risk from soil-deposited exposures.

Measured background air quality is intended to provide an indication of air quality throughout the GTA, and as such may not be exactly representative of baseline air quality in the community surrounding the proposed project.

An appropriate background concentration for diesel and diesel-related COC for the study area was prepared using five years of ambient air quality data from a number of distinct federal and provincial monitoring stations near the study area. A number of these monitoring stations lie some distance from the study area, itself. In particular, ambient concentrations of the aldehydes considered in the assessment were monitored in Windsor. Refer to the air quality technical study for further details.

Exposure Assessment

Current air quality in the vicinity of the proposed facility was estimated by combining the worst-case measured GTA background pollutant concentrations with the worst-case modelled diesel emissions from the project itself.

Worst-case cumulative exposures to the COCs were estimated by adding the worst-case regional background concentrations from the last five years of monitoring with the worst-case ground-level air concentrations predicted from emissions of the proposed facility. This is likely to be overly conservative, as the worst-case conditions for each are unlikely to occur at the same time.

Exposure Assessment (continued)

Ground-level air concentrations of COCs related to emissions from the proposed facility were estimated based on mathematical air dispersion models.

The SLHHRA relied on the results of air dispersion modelling to evaluate the health risks from direct inhalation exposure as well as to predict inhalation health risks. The MOECC has discussed matters of confidence and uncertainty in the predictions of dispersion models with regard to ground level concentrations and deposition rates. This remains the best mechanism to forecast future distributions of emissions in built environments. The air dispersion models used to provide data for the current assessment are approved by the MOECC and the US EPA for use on these types of emission studies. Refer to the Air Quality study for further discussion of this uncertainty (Novus, 2014).

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Risk Assessment


Maximum predicted short term (i.e., for 1-hour, 8-hour, and 24-hour exposure durations) ground level air concentrations at each receptor location were used to evaluate all acute inhalation risk estimates.

In reality, the frequency with which the maximum would occur at any one receptor location varies with respect to the COC and the receptor location. Individual exposure to a 1-hour or 24-hour maximum ground-level air concentration requires that a receptor (person) be present at the same time and duration of the maximum predicted air concentration anywhere around the proposed project.

Worst-case project related emissions of a given COC are not likely to occur at the same time as worst-case regional background conditions occur.

When discussing predicted cumulative risks from 1-hour or 24-hour exposures, it is also important to realize that these predictions inherently assume that the worst-case measured background concentration of that chemical occurs at the exact same time as the worst-case maximum emission from the proposed project. Given the effects of local meteorology on predicted ground-level air concentrations and the differing emission sources, this is a very unlikely occurrence and leads to an overestimation of potential cumulative local concentrations of the COC, and related predicted health risk.

For the purpose of the current assessment, it was assumed that the historic ambient air quality will be the same into the future.

As provincial air quality has been shown to have dramatically improved over the past few decades due to a number of provincial and federal initiatives, one would expect this trend to continue into the future to some degree. As such, it is expected that this assumption would lead to an overestimation of potential regional background contributions into the future.

Toxicity Assessment

Toxicity reference values (TRVs) have been developed by regulatory agencies with sufficient conservatism assure protection of the sensitive and more susceptible individuals within the general population (e.g., infants and young children, the elderly, individuals with compromised health).

A considerable amount of conservatism is incorporated in the TRVs. These benchmarks are deliberately set by regulatory agencies with the protection of sensitive individuals in mind. Typically, the benchmarks used in the current assessment were derived from the most sensitive health-related endpoints, and then adjusted to account for differences in sensitivity to chemicals among individuals. The use of uncertainty factors is directed, in part, toward the protection of sensitive individuals. The most sensitive toxicological endpoint (for example, decreased growth, body weight loss/gain, reproductive effects) was selected for each chemical from the available scientific literature to represent the exposure limit (TRV).

For genotoxic carcinogens, it was assumed that no repair of genetic lesions occurs, and therefore, no threshold can exist for chemicals that produce self-replicating lesions.

The existence of enzymes and biological pathways that routinely repair damage to genetic material (DNA) is well documented in the scientific literature. The potential adverse health outcomes arising from damage to DNA is usually observed only when the ability of these repair enzymes to "fix" the damage is blocked or exceeded.

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Risk Assessment


Uncertainty factors were applied at exposure levels reported in animal or human studies where no adverse effects were observed (i.e., NOAEL). Thus, exceeding the toxicological criterion should not mean that adverse health outcomes would occur. Rather, it means that the uncertainty factor beyond the no-effect exposure is somewhat reduced.

Large uncertainty factors (i.e., 100-fold or greater) were used in the estimation of the TRVs for threshold type chemicals.

Humans were assumed to be the most sensitive species with respect to toxic effects of the COC.

For obvious reasons, toxicity assays are not generally conducted on humans, so toxicological data from the most sensitive laboratory species were used in the estimation of toxicological criteria for humans.

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8.0 DISCUSSION AND CONCLUSIONS The results of the SLHHRA indicate that the projected emissions from the proposed bus garage alone would not result in any unacceptable health risk, either on an acute or chronic basis. However, in some cases, cumulative concentrations (i.e., existing background plus the additional contribution from the proposed facility and associated roadway contributions) have been predicted to exceed the health-based benchmarks under worst-case conditions. For example, the predicted cumulative risks for NO2 during the worst-case 1-hour exposure period marginally exceeded the health benchmark (i.e., a CR of 1.7) with the majority of the risk related to pre-existing background concentrations under worst-case conditions (i.e., existing regional background concentrations result in a predicted CR of 0.8). However, it is important to realize the background concentration evaluated in the SLHHRA (i.e., 156 µg/m3) represents the one worst-case 1-hour concentration observed at the worst-case monitoring station within the last five year period. The average 1-hour NO2 concentrations measured during that same five year period was 29.4 µg/m3 (i.e., more than five-fold less than the maximum), with a 90th percentile of 53.4 µg/m3 (3-fold less). The 90th percentile concentration provides a reasonable upper-bound estimate of typical background conditions, and if used would result in an overall cumulative concentration for 1-hour NO2 that was just marginally above the corresponding health-based standard (i.e., a CR of 1.1). One of the significant elements of conservatism built into this SLHHRA is the assumption that the worst-case background concentration occurs at the same time as the worst-case facility emissions. Given the effects of local meteorology on predicted ground-level air concentrations and the differing emission sources, this is a very unlikely occurrence and leads to an overestimation of potential health risk. Furthermore, it is important to understand how frequently exceedances of the health-based standard may occur. To provide further information on these two aspects, hourly 1-hour monitoring regional background NO2 concentrations were matched with the modelled 1-hour NO2 concentrations from predicted facility-related emissions for that exact same hour to provide a more accurate reflection of predicted worst-case cumulative NO2 expected around the proposed facility. Figure 8-1 provides a sorted (from highest to lowest) hourly depiction of predicted cumulative NO2 exposures for the year 2010, if the proposed facility were operating (2010 was the most recent year that had both regional background air quality data and project-specific modelling results available). The results of this enhanced analysis indicated that when one temporally matches regional background concentrations with predicted concentrations arising from Project-related emissions on an hour-by-hour basis, only one hour in the entire modelled year (i.e., 2010) showed predicted cumulative NO2 concentration that would have marginally exceeded the health-based benchmark (206 versus 200 µg/m3). This correlated to less than 0.011% of the time. As can be observed in this figure, in fact most of the time the predicted cumulative NO2 concentrations at the worst-case receptor location is significantly below the health-based benchmark. In fact, cumulative NO2 concentrations were predicted to be less than 100 µg/m3 (i.e., 50% of the health-based 1-hour benchmark) more than 98.5% of the time, and less than 50 µg/m3 (i.e., 25% of the health-based 1-hour benchmark) more than 80% of the time.

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Figure 8-1 Predicted Hourly Cumulative NO2 Concentrations at the Worst-case Receptor Location in 2010

The only other acute exceedances noted in the SLHHRA were the predicted 24-hour CRs for cumulative concentrations of PM10 and PM2.5. In both cases, the cumulative risk was entirely driven by the worst-case 24-hour regional background concentrations of these contaminants. For example, the worst-case PM2.5 concentration contribution from the Project was 12% of the regulatory health-based benchmark, and represented only 7.7% of the overall worst-case cumulative concentration. A similar pattern was observed for PM10 cumulative concentrations and predicted risks. As such, though worst-case regional background concentrations do occasionally result in a predicted health risk (i.e., as observed with health warnings around “bad air” days), the contribution from the proposed facility to local air quality result in negligible health risk. For the chronic exposure period, the air quality assessment indicated that emissions from the proposed facility resulted in no COCs having annual average cumulative concentrations that exceeded their corresponding health-based benchmark for non-carcinogenic health effects. Furthermore, emissions of potentially carcinogenic chemicals from the proposed facility resulted in predicted incremental lifetime cancer risks that were well below the provincial benchmark for acceptable incremental lifetime cancer risk of one-in-one-million (i.e., 1.0 x 10-6). Finally, it is also important to note that there is conservatism and safety build into the development of many of the regulatory benchmarks used in the SLHHRA. As such, though predicted risks for some projected worst-case cumulative concentrations may exceed a given regulatory benchmark, it is not necessarily indicative that an adverse health outcome will occur. There is significant conservatism built into not only the regulatory benchmarks, but the assumptions used in the current screening level risk assessment, to ensure that predicted exposures and related health risks are not under-estimated.

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For example, the 1-hour regulatory benchmark of 200 µg/m3 for NO2 was derived by the WHO based on the lowest level of exposure associated with health effects in sensitive subpopulations, which was estimated at approximately 400 μg/m3 (WHO, 2005). This level is also the 24-hour AAQC for NO2 in the Province of Ontario. These adverse health effects were slight, statistically significant, reversible effects on the pulmonary function (less than 5% decrease of the maximum expiratory volume per second, and increased reactivity of the pulmonary pathways) in sensitive individuals (asthmatics and subjects suffering to chronic obstructive pulmonary disease (“COPD”)). The WHO added a 2-fold safety factor to further protect sensitive individuals. If one compared the worst-case predicted NO2 concentrations, none of the predicted 1-hour cumulative concentrations modelled over a five year period exceeded the level of 400 µg/m3 where potential effects can be observed. Based on the results of the assessment, and given the considerable conservatism built into both the Air Quality Assessment and the SLHHRA itself, no unacceptable health risks related to emissions from the proposed bus garage would be expected. In fact, estimated emissions from the proposed Project represent a minimal to negligible contribution to the overall cumulative exposures for each of the COCs predicted for the sensitive receptor locations around the proposed facility.

FINAL REPORT


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