Appendix 6.1 Methodology for human health Risk Assessment
1.1 The Human Health Risk Assessment (HHRA) was conducted with the following phases:
· Problem Formulation
· Hazard Identification, which consists of
l Contaminant of Potential Concern (COPC) Identification and Selection of Contaminant of Concern (COC)
l Potential Human Receptors Identification
· Exposure Assessment
· Dose-response Assessment
· Risk/hazard Characterization
1.2 Problem Formulation phase is added to cater the suggested approach in the Study Brief. The remaining phases of the proposed assessment approach is very similar to the model developed by the National Academy of Sciences (NAS) in the USA in 1983, which is widely used and accepted in the human health risk assessment for the impact due to chemicals. The NAS model also consists of four steps: hazard identification, dose-response assessment, exposure assessment and risk characterization.
1.3 The following tasks were accomplished in this phase:
· Establish objective of the assessment
· Establish scope of the assessment
· Establish focus of the assessment
· Construct Site Conceptual Model
· Define assessment endpoint(s)
1.4 The objective, scope and focus of the HHRA have been discussed in Section 6 of the EIA Report.
Site Conceptual Model
1.5 The SCM adopted in the HHRA was presented graphically in Figures 6.1. As seen in the figure, there are 3 types of exposure pathway in terms of completeness and significance, namely “exposure pathway complete and significant”, “exposure pathway complete, but insignificant or significance unknown” and “exposure pathway incomplete”. For the exposure pathway “complete and significant”, it means that contaminants can be up-taken by receptors through that pathway and the amount of uptake can be considerable to contribute to the risk level. This type of exposure pathway was considered in the risk assessment.
1.6 For the exposure pathway “complete, but insignificant or significance unknown”, it means that contaminants can be up-taken by receptors through that pathway but the amount of uptake is not sufficiently large to affect the risk level or the amount of uptake through that pathway is uncertain for determining the risk level. This type of exposure pathway was not considered in the risk assessment. For the “incomplete exposure pathway”, it means that the contaminants cannot be up-taken by the receptor through that pathway because there is no complete route for the contaminants to reach the receptor. This type of exposure pathway was not considered in the risk assessment.
1.7 The SCM was presented in text as shown in Table 1.
Table 1 SCM for Human Health Risk Assessment
|
Contaminant Source: |
Effluent from the outfall of SCISTW |
|
Receptor: |
Humans (children and adult) |
|
Complete and Significant Exposure Media and Pathway[1]: |
· Incidental ingestion of seawater · Ingestion of seafood (contaminated) · Dermal contact of seawater |
1.8 For most of the contaminants, the exposure via direct contact (i.e. dermal exposure) is considered to be very low due to their low permeability coefficients from water. Therefore, dermal exposure for most of the contaminants can be considered as a complete but insignificant pathway. However, the fastest penetrating contaminants may pose hazards similar to or greater than direct consumption (ingestion of water) for prolonged dermal exposure time (USEPA 1992). For the sake of conservatism, the risk contributed by dermal exposure was assessed in the HHRA.
Assessment Endpoint
1.9 The assessment endpoint for the HHRA is defined as protection of human health at individual level from chronic exposure of contaminants produced in disinfection process via the incidental ingestion and dermal contact of diluted effluent from SCISTW, and the dietary ingestion of seafood over a relatively long period of time. The measurement endpoint for the HHRA is to evaluate chemical doses that are unlikely to result in significant incremental chronic systematic or carcinogenic effects.
Identification of COPC and Selection of COC
Identification of COPC
1.10 A total number of 35 chemicals were identified as COPCs in the risk assessments. The COPCs included 9 chlorination by-products (CBPs) regulated by USEPA National Primary Drinking Water Standards; 25 priority pollutants[2] (which may contain potential CBPs) regulated by the USA National Pollutant Discharge Elimination System (NPDES)[3]; and total residual chlorine (as disinfectant residue). The list of COPCs was presented in Table 2.
Table 2 List of Contaminants of Potential Concern
|
CBPs regulated by USEPA National Primary Drinking Water Standards |
Priority Pollutants listed in NPDES Permit Application Testing Requirements (40 CFR 122, Appendix D, Tables II to V), which may contain CBPs |
Disinfectant Residue |
|
Chloroform |
Methylene chloride |
Total residual chloride |
|
Bromodichloromethane |
Carbon tetrachloride |
|
|
Dibromochloromethane |
Chlorobenzene |
|
|
Bromoform |
1,1-dichloroethane |
|
|
Chloroacetic acid |
1,2-dichloroethane |
|
|
Bromoacetic acid |
1,1-dichloroethylene |
|
|
Dibromoacetic acid |
1,2-dichloropropane |
|
|
Dichloroacetic acid |
Tetrachloroethylene |
|
|
Trichloroacetic acid |
1,1,1-trichloroethane |
|
|
|
1,1,2-trichloroethane |
|
|
|
Trichloroethylene |
|
|
|
2-chlorophenol |
|
|
|
2,4-dichlorophenol |
|
|
|
p-chloro-m-cresol |
|
|
|
Pentachlorophenol |
|
|
|
2,4,6-trichlorophenol |
|
|
|
Bis(2-chloroethoxy)methane |
|
|
|
1,4-dichlorobenzene |
|
|
|
Hexachlorobenzene |
|
|
|
Hexachlorocyclopentadiene |
|
|
|
Hexachloroethane |
|
|
|
1,2,4-trichlorobenzene |
|
|
|
Alpha-benzene hexachloride |
|
|
|
Beta-benzene hexachloride |
|
|
|
Gamma-benzene hexachloride |
|
1.11 Unlike other conventional human health risk assessments for air pollution source (e.g. incinerator) and contaminated land/groundwater, a look-up table of contaminants/list of possible COPC for CBPs risk assessment in effluent was not identified from local and overseas authorities. Moreover, according to the review of local and overseas practice, list of “regulated CBPs in sewage effluent” was not identified.
1.12 Hence, a conservative approach was adopted in this Study to include all the regulated CBPs in drinking water plus the 25 priority pollutants (may contain potential CBPs) regulated by NPDES as COPCs, although these pollutants are not regulated due to the concern of generation during chlorination process.
1.13 The NPDES practice was adopted because it contains the most comprehensive list of regulated pollutants for effluent discharge, based on the review of practice in the USA, the United Kingdom, Australia, Canada, China and Hong Kong. Moreover, the purpose of NPDES is to ensure the US National Water Quality Criteria are complied by regulating pollutant concentrations in effluent discharge directly to surface water, in order to protect the human health and aquatic life.
1.14 Therefore, the 35 COPCs identified for the risk assessment include all documented potential CBPs/disinfectant residue which are regulated due to their potential to cause impact to human health and/or ecological resources. The list of identified COPCs (which the COCs for risk calculation were selected from the list) was considered sufficiently comprehensive to assess the potential risk to human health due to chronic exposure to the contaminants produced in the disinfection process in the effluent discharges.
1.15 Concerning the chemical species (sodium, bisulphite, sulphite and sulphate) associated with the dechlorination agent - sodium bisulphite, none of them was regulated by the current National Primary Drinking Water Regulations. Therefore, it was considered that the application of the dechlorination agent would not cause significant impact to human health and the related chemical species were not identified as COPCs in the HHRA.
1.16 The concentrations of the identified COPCs in chlorinated/dechlorinated (C/D) CEPT effluent from SCISTW (for assessment scenarios 1 to 4), secondary treated effluent from Shatin/Tai Po Sewage Treatment Works (for assessment scenario 5) and ambient seawater (2 sampling locations) were determined by chemical analysis works. The COC selection and determination of COC effluent concentrations for risk assessments were based on the chemical analysis results and the following rules.
Rules of COC Selection
Rule A – COPCs without relevant toxicity values, standards or criteria were not selected as COCs for risk assessments.
Rule B - COPCs detected in the C/D effluent were selected as COCs for risk assessment. The highest value from the replicates of analysis was chosen as the effluent concentrations to use in the risk assessment calculations.
Rule C – Non-detected COPCs with detection limit (for C/D effluent samples) exceeds the Concentration of Interest[4] (COI) were selected as COCs. For these COCs, effluent concentrations used in the risk assessments are one-half of the detection limit, which is a standard approach accepted by USEPA.
Rule D – COPCs with concentration in C/D effluent lower than the ambient seawater concentration were not selected as COCs.
Rules of COC Ambient Seawater Concentration Determination
Rule E – The highest COC concentrations found in the replicates of ambient seawater analysis were used to represent the background concentrations in the risk assessment calculations.
Rule F – For COCs that were not detected in the ambient seawater samples, the background concentration was set as zero.
1.17 Based on the chemical analysis results and above rules, COCs were selected for the risk assessments for Scenarios 1 to 4 and Scenario 5 and presented in Tables 3 and 4 respectively.
Table 3 Results of COCs Selection for Scenarios 1 to 4
|
COPC |
HHRA |
Max. Conc. in C/D CEPT Effluent (mg/L) |
Max. Conc. in Ambient Seawater (mg/L) |
Note |
|
Total residual chloride |
Yes |
100 |
0 |
|
|
Chloroform |
Yes |
7 |
0 |
|
|
Bromodichloromethane |
Yes |
<5 |
0 |
A |
|
Dibromochloromethane |
Yes |
<5 |
0 |
A |
|
Bromoform |
|
<5 |
0 |
|
|
Chloroacetic acid |
Yes |
4 |
0 |
|
|
Bromoacetic acid |
|
<2 |
0 |
B |
|
Dibromoacetic acid |
Yes |
4 |
0 |
|
|
Dichloroacetic acid |
Yes |
45.9 |
0 |
|
|
Trichloroacetic acid |
Yes |
22 |
0 |
|
|
Methylene chloride |
|
<20 |
55 |
|
|
Carbon tetrachloride |
|
<0.5 |
0 |
|
|
Chlorobenzene |
|
<0.5 |
0 |
|
|
1,1-dichloroethane |
|
<0.5 |
0 |
|
|
COPC |
HHRA |
Max. Conc. in C/D CEPT Effluent (mg/L) |
Max. Conc. in Ambient Seawater (mg/L) |
Note |
|
1,2-dichloroethane |
|
<0.5 |
0 |
|
|
1,1-dichloroethylene |
|
<0.5 |
0 |
|
|
1,2-dichloropropane |
|
<0.5 |
0 |
|
|
Tetrachloroethylene |
Yes |
1.3 |
0 |
|
|
1,1,1-trichloroethane |
|
<0.5 |
0 |
|
|
1,1,2-trichloroethane |
|
<0.5 |
0 |
|
|
Trichloroethylene |
Yes |
2 |
0 |
|
|
2-chlorophenol |
|
<0.5 |
0 |
|
|
2,4-dichlorophenol |
|
<0.5 |
0 |
|
|
p-chloro-m-cresol |
|
<0.5 |
0 |
B |
|
Pentachlorophenol |
Yes |
<2.5 |
0 |
A |
|
2,4,6-trichlorophenol |
Yes |
2 |
0 |
|
|
Bis(2-chloroethoxy)methane |
|
<0.5 |
0 |
B |
|
1,4-dichlorobenzene |
|
<0.5 |
0 |
|
|
Hexachlorobenzene |
|
<0.5 |
0 |
|
|
Hexachlorocyclopentadiene |
|
<2.5 |
0 |
|
|
Hexachloroethane |
|
<0.5 |
0 |
|
|
1,2,4-trichlorobenzene |
|
<0.5 |
0 |
|
|
Alpha-benzene hexachloride |
Yes |
<0.5 |
0 |
A |
|
Beta-benzene hexachloride |
Yes |
<1 |
0 |
A |
|
Gamma-benzene hexachloride |
Yes |
<1 |
0 |
A |
Note: A) Detection limit exceeds the concentration of interest for human health
B) No available toxicity data for human health
Table 4 Results of COCs Selection for Scenario 5
|
COPC |
HHRA |
Max. Conc. in Secondary Treated Effluent (mg/L) |
Max. Conc. in Ambient Seawater (mg/L) |
Note |
|
Total residual chloride |
|
<20 |
0 |
|
|
Chloroform |
Yes |
<5 |
0 |
A |
|
Bromodichloromethane |
Yes |
<5 |
0 |
A |
|
Dibromochloromethane |
Yes |
8 |
0 |
|
|
Bromoform |
Yes |
49 |
0 |
|
|
Chloroacetic acid |
|
<2 |
0 |
|
|
Bromoacetic acid |
|
<2 |
0 |
B |
|
Dibromoacetic acid |
Yes |
10 |
0 |
|
|
Dichloroacetic acid |
Yes |
3 |
0 |
|
|
Trichloroacetic acid |
Yes |
7 |
0 |
|
|
Methylene chloride |
|
<20 |
55 |
|
|
Carbon tetrachloride |
|
<0.5 |
0 |
|
|
Chlorobenzene |
|
<0.5 |
0 |
|
|
1,1-dichloroethane |
|
<0.5 |
0 |
|
|
1,2-dichloroethane |
|
<0.5 |
0 |
|
|
1,1-dichloroethylene |
|
<0.5 |
0 |
|
|
1,2-dichloropropane |
|
<0.5 |
0 |
|
|
Tetrachloroethylene |
|
<0.5 |
0 |
|
|
1,1,1-trichloroethane |
|
<0.5 |
0 |
|
|
1,1,2-trichloroethane |
|
<0.5 |
0 |
|
|
Trichloroethylene |
|
<0.5 |
0 |
|
|
2-chlorophenol |
|
<0.5 |
0 |
|
|
2,4-dichlorophenol |
|
<0.5 |
0 |
|
|
p-chloro-m-cresol |
|
<0.5 |
0 |
B |
|
Pentachlorophenol |
Yes |
<2.5 |
0 |
A |
|
2,4,6-trichlorophenol |
|
<0.5 |
0 |
|
|
Bis(2-chloroethoxy)methane |
|
<0.5 |
0 |
B |
|
1,4-dichlorobenzene |
|
<0.5 |
0 |
|
|
COPC |
HHRA |
Max. Conc. in Secondary Treated Effluent (mg/L) |
Max. Conc. in Ambient Seawater (mg/L) |
Note |
|
Hexachlorobenzene |
|
<0.5 |
0 |
|
|
Hexachlorocyclopentadiene |
|
<2.5 |
0 |
|
|
Hexachloroethane |
|
<0.5 |
0 |
|
|
1,2,4-trichlorobenzene |
|
<0.5 |
0 |
|
|
Alpha-benzene hexachloride |
Yes |
<0.5 |
0 |
A |
|
Beta-benzene hexachloride |
Yes |
<1 |
0 |
A |
|
Gamma-benzene hexachloride |
Yes |
<1 |
0 |
A |
Note: A) Detection limit exceeds the concentration of interest of human health
B) No available toxicity data for human health
Identification of Potential Human Receptors
1.18 As presented in the SCM for HHRA above, the completed and significant COC exposure pathways are incidental ingestion and dermal contact of seawater, and ingestion of contaminated seafood. Therefore, the potential human receptors (children and adult) are:
· People who swim or engage in other water related activities in the sea area which is contaminated by the selected COCs discharged from the outfall of SCISTW
· People who consume seafood which is contaminated by the selected COCs discharged from the outfall of SCISTW
Human Health Risk Assessment
1.19 This phase of HHRA comprised the following tasks:
· Water quality modelling
· Exposure setting characterization, which consists of the following tasks:
o Determine exposure points
o Characterize potential human receptors
o Calculate the COC exposure
Water Quality Modelling
1.20 The water quality modelling has been conducted in this assignment and the results obtained were used for the risk assessment.
Exposure Setting Characterization
Exposure Points Determination
1.21 For the pathway of incidental ingestion of seawater, three exposure points were identified: (1) the edge of the zone of initial dilution (ZID), which caters the individuals who accidentally drop into the harbour from ships; (2) the edge of the mixing zone and (3) the nearest beach from the SCISTW[5], which caters the individuals frequently bath or swim in the beach, having a potentially higher exposure to contaminated seawater. The identified exposure points are consistent with the previous studies.
1.22 There was no specific exposure point for the contaminated seafood consumption pathway.
Potential Human Receptors Characterization
1.23 The following parameters were characterized for both children and adult human receptors:
· Exposure time, duration and frequency for each exposure pathway
· Contaminated water/seafood ingestion rate
· Body weight
· Averaging time
1.24 Table 5 presented the parameter values of human receptors
Table 5 Parameter Values of Human Receptors
|
Parameter |
Value |
Unit |
|
Exposure time for dropping from ships[6] |
5 |
hr/d |
|
Exposure frequency for dropping from ships7 |
1 |
d/yr |
|
Swimming exposure time |
2.6 |
hr/d |
|
Swimming exposure frequency |
124 |
d/yr |
|
Swimming exposure duration - adult and adult fishermen |
52 |
yr |
|
Swimming exposure duration - children and fishermen children |
18 |
yr |
|
Body weight – adult and adult fishermen |
60 |
kg |
|
Body weight – children and fishermen children |
32 |
kg |
|
Incidental water ingestion rate |
50 |
ml/hr |
|
Averaging time – adult and adult fishermen |
52 |
yr |
|
Averaging time – children and fishermen children |
18 |
yr |
|
Seafood consumption rate – adult |
148 |
g/d |
|
Seafood consumption rate – children |
79 |
g/d |
|
Seafood consumption rate – adult fishermen[7] |
300 |
g/d |
|
Seafood consumption rate – fishermen children[8] |
160 |
g/d |
|
Seafood exposure duration – adult and adult fishermen |
52 |
yr |
|
Seafood exposure duration – children and fishermen children |
18 |
yr |
|
Seafood consumption frequency |
350 |
d/yr |
|
Skin surface area available for contact – adult[9] |
20,000 |
cm2 |
|
Skin surface area available for contact – children[10] |
11,600 |
cm2 |
|
Lifetime (for cancer risk calculation) |
70 |
yr |
COC Exposure Calculation
1.25 The COC exposure would be calculated by the following equations, which Equations 1 to 4 are adopted from HATS EEFS Ecological and Health Risk Assessment (2004), Equation 5 is adopted from USEPA (1999b), Equations 6 and 7 are based on the daily dermal intake equation documented in USEPA (1998). It is considered that swimming would be the water related activity with the highest rate of incidental water ingestion and dermal exposure, therefore swimming would be considered to be the representative water related activity for the exposure pathway of incidental ingestion and dermal contact of seawater.
Non-carcinogen exposure via incidental ingestion of seawater (children or adult)
ADIiw = (Ciw x IRw x ET x EF x ED x 0.001L/ml) / (BW x AT x 365 d/yr) Equation 1
Where
ADIiw = average daily COC i intake via incidental ingestion of seawater (mg/kg-d)
Ciw = COC i concentration in water (mg/L)
IRw = incidental water ingestion rate (ml/hr)
ET = exposure time (hr/d)
EF = exposure frequency (d/yr)
ED = exposure duration (yr)
BW = body weight (kg)
AT = averaging time (yr)
Non-carcinogen exposure via consumption of seafood (children or adult)
ADIis = (Cis x IRs x EF x ED x FI x 0.001kg/g) / (BW x AT x 365 d/yr) Equation 2
Where
ADIis = average daily COC i intake via consumption of seafood (mg/kg-d)
Cis = COC i concentration in seafood (mg/kg)
IRs = seafood consumption rate (g/d)
EF = exposure frequency (d/yr)
ED = exposure duration (yr)
FI = fraction of seafood from ZID (unitless) = ZID area / 1800km2 (total area for fishing)[11]
BW = body weight (kg)
AT = averaging time (yr)
Carcinogen exposure via incidental ingestion of seawater
|
|
[(Ciw x IRw x ET x EF x ED x 0.001L/ml)adult] |
+ |
[(Ciw x IRw x ET x EF x ED x 0.001L/ml)child] |
|
LADDiw = |
BWadult |
|
BWchild |
|
|
LT x 365 d/yr |
||
Equation 3
Where
LADDiw = lifetime average daily COC i dose via incidental ingestion of seawater (mg/kg-d)
Ciw = COC i concentration in water (mg/L)
IRw = incidental water ingestion rate (ml/hr)
ET = exposure time (hr/d)
EF = exposure frequency (d/yr)
ED = exposure duration (yr)
BW = body weight (kg)
LT = lifetime (yr)
Carcinogen exposure via consumption of seafood (children or adult)
|
|
[(Cis x IRs x EF x ED x FI x 0.001kg/g)adult] |
+ |
[(Cis x IRs x EF x ED x FI x 0.001kg/g)child] |
|
LADDis = |
BWadult |
|
BWchild |
|
|
LT x 365 d/yr |
||
Equation 4
Where
LADDis = lifetime average daily COC i dose via consumption of seafood (mg/kg-d)
Cis = COC i concentration in seafood (mg/kg)
IRs = seafood consumption rate (g/d)
EF = exposure frequency (d/yr)
ED = exposure duration (yr)
FI = fraction of seafood from ZID (unitless)
BW = body weight (kg)
LT = lifetime (yr)
COC Concentration in Contaminated Seafood
1.26 With reference to HATS EEFS Ecological and Health Risk Assessment (2004), it is assumed that all seafood consumed by human receptor is fish and the same assumption is adopted in this HHRA. Therefore, water-to-fish bioconcentration factor is used in the below equation for calculation of COC concentration in seafood.
Cis = Ciw x BCFi x FCMi Equation 5
Where
Cis = COC i concentration in seafood (mg/kg)
BCFi = water-to-fish bioconcentration factor for COC i (L/kg)
FCMi = food chain multiplier of COC i (unitless)
Non-carcinogen exposure via dermal contact of seawater (children or adult)
DDIid = (Dievent x EF x ED x As) / (BW x AT x 365 d/yr) Equation 6
Where
DDIid = average daily COC i intake via dermal contact of water (mg/kg-d)
Dievent = dermally absorbed dose per event for COC i (mg/cm2-event)
EF = exposure frequency (d/yr)
ED = exposure duration (yr)
As = skin surface area available for contact (cm2)
BW = body weight (kg)
AT = averaging time (yr)
Carcinogen exposure via dermal contact of seawater
|
|
[(Dievent x EF x ED x As)adult] |
+ |
[(Dievent x EF x ED x As)child] |
|
LADDid = |
BWadult |
|
BWchild |
|
|
LT x 365 d/yr |
||
Equation 7
Where
LADDid = lifetime average daily COC i dose via dermal exposure of seawater (mg/kg-d)
Dievent = dermally absorbed dose per event for COC i (mg/cm2-event)
EF = exposure frequency (d/yr)
ED = exposure duration (yr)
As = skin surface area available for contact (cm2)
BW = body weight (kg)
LT = lifetime (yr)
For organic substances, Dievent will be calculated using the equations below:
If tevent < t*, then Dievent = 2x Kp x Ciw(6 x T x tevent)1/2 / 1000 Equation 8a
If tevent > t*, then Dievent = Kp x Ciw x [(tevent / (1+B)) + 2 x T (1+3B / 1+B)] / 1000 Equation 8b
Where
Kp = permeability coefficient from water for contaminant (cm/hr)
Ciw = contaminant i concentration in water (mg/L)
tevent = duration of event (hr/event)
T = lag time (hr)
T* = time to reach steady-state (hr)
B = parameter to describe relative contribution of permeability coefficients in stratum corneum and viable epidermis
For inorganic substances, Dievent will be calculated using the equation below:
Dievent = (2 x Kp x Ciw x tevent) / 1000 Equation 8c
1.27 A number of variables in the above equations needed to be defined for the exposure assessment. For COC concentrations at exposure points, they were determined by water quality modelling. The simulation periods for water quality modelling covered two 15-day full spring-neap cycles for dry and wet seasons respectively. The dry and wet seasons results were averaged to represent the annual mean results, which were used for exposure calculation.
1.28 Other defined variables were presented in Tables 6 and 7.
Table 6 Bioconcentration Factor and Food Chain Multiplier of COC
|
COC |
Water-to-fish Bioconcentration Factor |
FCMa |
|
Total residual chlorine |
N/A |
N/A |
|
Bromoform |
13.3b |
1.0 |
|
Bromodichloromethane |
8.26b |
1.0 |
|
Chloroform |
6.92b |
1.0 |
|
Dibromochloromethane |
10.4b |
1.0 |
|
Chloroacetic acid |
0.26c |
1.0 |
|
Dibromoacetic acid |
0.82c |
1.0 |
|
Dichloroacetic acid |
1.13c |
1.0 |
|
Trichloroacetic acid |
5.75c |
1.0 |
|
Tetrachloroethylene |
82.8b |
1.0 |
|
Trichloroethylene |
14.1b |
1.0 |
|
Pentachlorophenol |
671b |
3.2 |
|
2,4,6-trichlorophenol |
56.1b |
1.0 |
|
Alpha-BHC |
168b |
1.0 |
|
Beta-BHC |
168b |
1.0 |
|
Gamma-BHC |
168d |
1.0 |
N/A: Not Available
Note: a FCMs were developed using Kow values reported in USEPA (1995), as in USEPA (1999b).
b BCF values documented in USEPA (2005).
c No recommended BCF value identified. Regression equation was used to calculate the BCF values (Bintein et al. (1993), as in USEPA (1999b)).
d Same BCF adopted from isomer.
Table 7 Parameters related to Dermal Exposure
|
COC |
Kp (cm/hr) |
T (hr) |
t* (hr) |
B |
|
Total residual chlorinea |
1E-3 |
- |
- |
- |
|
Bromoforma |
2.6E-3 |
3 |
7.3 |
2.3E-2 |
|
Bromodichloromethanea |
1.3E-1 |
4.7E-1 |
1.1 |
9.3E-3 |
|
Chloroforma |
5.8E-3 |
8.7E-1 |
2.1 |
1.2E-2 |
|
Dibromochloromethanea |
3.9E-3 |
1.6 |
3.9 |
1.7E-2 |
|
Chloroacetic acidb |
7.24E-4 |
3.3E-1 |
0.8 |
1.7E-4 |
|
Dibromoacetic acidb |
3.15E-4 |
1.89 |
4.5 |
5.9E-4 |
|
Dichloroacetic acidb |
1.40E-3 |
5.3E-1 |
1.3 |
8.3E-4 |
|
Trichlroacetic acidb |
3.09E-3 |
8.9E-1 |
2.1 |
5E-3 |
|
Tetrachloroethylenea |
3.7E-1 |
9E-1 |
4.3 |
2.5E-1 |
|
Trichloroethylenea |
2.3E-1 |
5.5E-1 |
1.3 |
2.6E-2 |
|
Pentachlorophenola |
6.5E-1 |
3.7 |
1.7E+1 |
7.2E+1 |
|
2,4,6-trichlorophenola |
5.9E-2 |
1.4 |
9.2 |
4.9E-1 |
|
Alpha-BHCb |
0.016 |
5.19 |
36.7 |
0.60 |
|
Beta-BHCb |
0.015 |
5.19 |
34.8 |
0.52 |
|
Gamma-BHCa |
0.014 |
5.20 |
35.0 |
0.52 |
Note: a parameter values were adopted from USEPA (1992).
b No recommended values documented, values were calculated using equations documented in USEPA (1992).
1.29 This stage of HHRA involved determination of the relationship between the contaminant doses from exposure and corresponding response in humans (risk of cancer development, in terms of cancer slope factor and/or non-cancer health impact, in terms of reference dose). This relationship for various contaminants is documented in database/publications in authorities such as US Environmental Protection Agency (USEPA) and World Health Organization (WHO).
1.30 The Cancer Slope Factor (CSF) and reference dose of the COCs adopted in World Health Organization (WHO) and USEPA[12] were presented in Table 8. More stringent value was typed in bold adopted. For the identified COCs, adjustment of oral toxicity data (cancer slope factor and/or reference dose) for calculation of the risk/hazard due to absorbed doses was not needed according to USEPA (2001b). Therefore, the oral cancer slope factor and reference dose selected for oral exposure were used for the risk calculation in dermal exposure pathway.
Table 8 Cancer Slope Factor and Reference Dose of COCs
|
COC |
Cancer Slope Factor (oral, (mg/kg/d)-1) |
Reference Dose (mg/kg/d) |
||
|
WHO |
USEPA |
WHO |
USEPA |
|
|
Bromoform |
N/A |
7.9E-3a |
25b |
20a |
|
Bromodichloromethane |
5.0E-3c |
6.2E-2a |
N/A |
20a |
|
Chloroform |
N/A |
Note d |
10b |
10a |
|
Dibromochloromethane |
N/A |
8.4E-2a |
30b |
20a |
|
Chloroacetic acid |
N/A |
N/A |
N/A |
2f |
|
Dibromoacetic acid |
N/A |
N/A |
20b |
N/A |
|
Dichloroacetic acid |
N/A |
5E-2a |
40b |
4a |
|
Trichloroacetic acid |
N/A |
N/A |
40b |
N/A |
|
Total residual chlorine |
N/A |
N/A |
150b |
100a |
|
Tetrachloroethylene |
N/A |
N/A |
14c |
10a |
|
Trichloroethylene |
N/A |
N/A |
23.8c |
N/A |
|
Pentachlorophenol |
N/A |
1.2E-1a |
N/A |
30a |
|
2,4,6-trichlorophenol |
N/A |
1.1E-2a |
N/A |
N/A |
|
Alpha-BHC |
N/A |
6.3a |
N/A |
N/A |
|
Beta-BHC |
N/A |
1.8a |
N/A |
N/A |
|
Gamma-BHC |
N/A |
N/A |
5c |
0.3a |
Note: N/A: Not Available
a Source: USEPA IRIS Database
b Source: WHO (2000)
c Source: WHO (2004b)
d According to Integrated Risk Information System (IRIS) database, a dose of 0.01mg/kg/d can be considered protective against cancer risk.
e According to WHO (2004a), the available data are inadequate to establish guideline values for the chemical.
f Health Effects Assessment Summary Tables (HEAST) as reported in The Risk Assessment Information System.
Risk/Hazard Characterization
1.31 There were 2 types of risk/hazard to be characterized in HHRA, as follows:
· Cancer risk, from exposure to identified carcinogenic COCs
o The lifetime individual excess cancer risk can be calculated by the following equation:
Cancer Riski = LADDi x CSForal(i) Equation 9
Where
Cancer Riski = incremental probability that an individual will develop cancer over a lifetime as a result of a specific exposure to carcinogenic COC i
CSForal(i) = oral cancer slope factor for COC i
Cancer RiskT = Σ Cancer Riski Equation 10
Where
Cancer RiskT = total cancer risk for exposure to all identified carcinogenic COCs via a specific exposure pathway
Total Cancer Risk = Σ Cancer RiskT Equation 11
Where
Total Cancer Risk = total cancer risk for exposure to all identified carcinogenic COCs via all identified exposure pathways
From Equations 9 to 11, the lifetime incremental cancer risk due to exposure of all identified carcinogenic COCs via the pathways “ingestion of seawater”, “dermal contact of water” and “consumption of contaminated seafood” can be calculated.
· Non-cancer effect health hazard, from exposure to identified COCs imposing non-carcinogenic health effects
o The Hazard Quotient (HQ) can be calculated by the following equation:
HQi = ADIi / RfDi Equation 12
Where
HQi = hazard quotient for COC i
ADIi = average daily COC i intake
RfDi = reference dose for COC i
HIi = Σ HQi Equation 13
Where
HIi = Hazard Index, total hazard attributable to exposure to all identified COCs through a single exposure pathway
Total HI = Σ HIi Equation 14
Where
Total HI = Total hazard index from multiple pathways
From Equations 12 to 14, the total hazard index for both children and adult human receptor due to exposure of all identified COCs imposing non-carcinogenic effect via the pathways “ingestion of seawater”, “dermal contact of water” and “consumption of contaminated seafood” can be calculated.
Output of Risk Assessment
1.32 The output of the HHRA are listed as follows:
l Lifetime incremental cancer risk due to exposure of identified carcinogenic COCs (contributed by both HATS effluent and “background” COC concentrations existing in ambient seawater) by incidental exposure to seawater at edge of ZID and consumption of contaminated seafood
l Lifetime incremental cancer risk due to exposure of identified carcinogenic COCs (contributed by both HATS effluent and “background” COC concentrations existing in ambient seawater) by swimming activity at edge of mixing zone and consumption of contaminated seafood
l Lifetime incremental cancer risk due to exposure of identified carcinogenic COCs (contributed by both HATS effluent and “background” COC concentrations existing in ambient seawater) by swimming activity at the nearest beach from SCISTW outfall and consumption of contaminated seafood
l Total health hazard index due to exposure of identified COCs (contributed by both HATS effluent and “background” COC concentrations existing in ambient seawater) by incidental exposure to seawater at edge of ZID and consumption of contaminated seafood
l Total health hazard index due to exposure of identified COCs (contributed by both HATS effluent and “background” COC concentrations existing in ambient seawater) by swimming activity at edge of mixing zone and consumption of contaminated seafood
l Total health hazard index due to exposure of identified COCs (contributed by both HATS effluent and “background” COC concentrations existing in ambient seawater) by swimming activity at the nearest beach from SCISTW outfall and consumption of contaminated seafood
References
1. NHMRC (2004). Australian Drinking Water Guidelines 2004.
2. The Nation Academy of Science (1983). Risk Assessment in the Federal Government: Managing the Process.
3. The Risk Assessment Information System. Available online: http://risk.lsd.ornl.gov/tox/tox_values.shtml.
4. USEPA. Integrated Risk Information System (IRIS) Database. Available online at www.epa.gov/iris.
5. USEPA (1992). Dermal Exposure Assessment: Principles and Applications.
6. USEPA (1998). Methodology for Assessing Health Risks associated with Multiple Pathways of Exposure to Combustor Emissions.
7. USEPA (1999a). Risk Assessment Technical Background Document for the Chlorinated Aliphatics Listing Determination – Appendixes.
8. USEPA (1999b). Screening Level Ecological Risk Assessment Protocol for Hazardous Waste Combustion Facilities.
9. USEPA (2001b). Risk Assessment Guidance for Superfund, Volume 1: Human Health Evaluation Manual, Part E, Supplemental Guidance for Dermal Risk Assessment.
10. USEPA (2005). Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities – Final.
11. WHO (2000). International Programme on Chemical Safety – Environmental Health Criteria 216.
12. WHO (2004a). Brominated Acetic Acids in Drinking-water.
13. WHO (2004b). Guidelines for Drinking-water Quality (Third Ed.) – Volume 1.
[1] Exposure pathways not associated with the HATS discharge, including normal dietary food (non-seafood), potable water consumption, incidental ingestion of soil and inhalation of contaminants in air (under ambient, indoor or workplace conditions), are not considered in the assessment.
[2] The 25 pollutants are regulated in NPDES due to their presence in industrial effluent but not their possible generation in chlorination process. However, a conservative approach is adopted to study all these regulated chlorinated organic substances, which are documented as potential CBPs, in US drinking water and wastewater discharge.
[3] The NPDES permit program controls water pollution by regulating point sources that discharge pollutants into water of the United States. Industrial, municipal, and other facilities must obtain permits if their discharges go directly to surface waters.
[4] The COIs for human health were the standards for drinking/tap water. The list of COIs are presented in Annex A.
[5] In terms of lowest outfall dilution factor calculated by water quality modelling rather than the shortest geological distance.
[6] Conservative values are assumed for the purpose of risk assessment.
[7] Adopted from ERM (2005).
[8] Calculated based on the ratio of seafood consumption rate between adult and children and the seafood consumption rate of fishermen adult. Therefore, seafood consumption rate of fishermen children = (79/148 x 300) g/d
[9] Adopted from USEPA (1992).
[10] Adopted from USEPA (1992).
[11] Adopt from SSDS/EIAS DRA (1998) and HATS EEFS E&HRA (2004).
[12] In SSDS/EIAS DRA (1998), values adopted from National Health and Medical Research Council and Agricultural and Resource Management Council of Australia and New Zealand (NHMRC) were also compared. However, cancer slope factor and reference dose for the COCs were not identified in NHMRC (2004).