Appendices of the Screening Assessment Report

Ethylbenzene

Chemical Abstracts Service Registry Number:
100-41-4

Environment and Climate Change Canada
Health Canada
April 2016

Table of Contents

Appendix A: Summary of Canadian Outdoor Air Studies

A1. Concentrations of Ethylbenzene in Ambient (Outdoor) Air in Canada.
DetailsMean concentration (µg/m3)Maximum concentration Footnote Table A1[a](µg/m3)Reference
42 locations, suburban and urban across all provinces (2005-2009)0.103-1.2835.84
(4.40* 95th percentile)
Environment Canada 2011a
Northeast Edmonton, Alberta. Eight continuous ambient air locationsN/A87.7FAP 2010
Three Creeks area, Alberta. Community and industrial source sites0.29-4.03
(1-hour average)
0.93
(maximum 1-hour average)
Alberta Environment 2010
Champlain Heights, New Brunswick, 20071.0
(annual average)
3.65
(maximum 24-hour average)
New Brunswick Department of Environment 2009
Edmonton East, Alberta, 1993-20030.97
(24-hour average)
21.82Alberta Environment 2005
Industrialized zone in Fort Saskatchewan, Alberta, September 2004-March 20060.33-0.362.14-6.49Mintz and McWhinney 2008
Alberta, northeastern British Columbia, and central and southern Saskatchewan, April 2001-December 20020.0546.21You et al. 2008
37 locations in Sarnia, Ontario0.46
(for 2-week average)
1.06Atari and Luginaah 2009
37 locations in Sarnia, Ontario0.48N/AMiller et al. 2009
Three urban locations: mechanics garage, storm drain of industrial waste landfill, two-lane street in industrial area10-13N/ABadjagbo et al. 2009
Clarkson Airshed: Oakville and Mississauga, Ontario0.40-1.46
(annual average)
9.63OMOE 2006
Residential homes in Windsor, Ontario
Winter 2005, Non-smokers, 201 samples (~47 homes)
0.43
(average of five 24-hr samples)
2.4
(0.90 95th percentile)
Health Canada 2010a
Residential homes in Windsor, Ontario Summer 2005, Non- smokers, 216 samples (~47 homes)0.75
(average of five 24-hr samples)
10.9
(1.7 95th percentile)
Health Canada 2010a
46-47 Residential homes in Windsor, Ontario
Winter 2006, Non-smokers, 214 samples (~47 homes)
0.37
(average of five 24-hr samples)
4.8
(0.81 95th percentile)
Health Canada 2010a
Residential homes in Windsor, Ontario Summer 2006, Non-smokers, 214 samples (~47 homes)0.74
(average of five 24-hr samples)
13.8
(1.7 95th percentile)
Health Canada 2010a
Residential homes in Regina, Saskatchewan
Winter 2007
Smokers, 17 samples (34 homes)
0.17
(single 24-hr sample)
0.38
(0.38 95th percentile)
Health Canada 2010b
Residential homes in Regina, Saskatchewan
Winter 2007
Non-smokers, 77 samples (~112 homes)
0.28
(single 24-hr sample)
1.2
(0.97 95th percentile)
Health Canada 2010b
Residential homes in Regina, Saskatchewan
Summer 2007
Smokers, 12 samples (34 homes)
0.17
(single 24-hr sample)
0.47
(0.47 95th percentile)
Health Canada 2010b
Residential homes in Regina, Saskatchewan
Summer 2007
Non-smokers, 95 samples (~34 homes)
0.36
(single 24-hr sample)
16.6
(0.46 95th percentile)
Health Canada 2010b
Residential homes in Halifax, Nova Scotia
Winter 2009, Non-smokers, 287 samples (50 homes)
0.13
(24-hr sample collected for 7 days)
1.4
(0.31 95th percentile)
Health Canada 2012
Residential homes in Halifax, Nova Scotia
Summer 2009, Non-smokers, 287 samples (50 homes)
0.28
(24-hr sample collected for 7 days)
8.3
(0.53 95th percentile)
Health Canada 2012
Residential homes in Edmonton, Alberta
Winter 2010, Non-smokers, 332 samples (50 homes)
1.139
(24-hr sample collected for 7 days)
146.51
(1.998 95th percentile)
Health Canada 2013
Residential homes in Edmonton, Alberta
Summer 2010, Non-smokers, 324 samples (50 homes)
0.407
(24-hr sample collected for 7 days)
14.99
(0.724 95th percentile)
Health Canada 2013
Residential homes in Ottawa, Ontario
Winter 2003, Smokers and Non-smokers, 74 samples (74 homes)
0.58
(24-hr sample 10L every 100 minutes)
9.4Zhu et al. 2005
Footnote Table A1

Abbreviations: N/A, not available;

Footnote Table A1 a

Values in bold denoted with an asterisk (*) were selected as predicted environmental concentrations
(PECs) for the calculation of risk quotients (RQs) later in this report.

Return to footnote Table A1[a] referrer

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Appendix B: Summary of Canadian Indoor Air Studies

Table B1. Indoor air concentrations of ethylbenzene in Canada
City, Season and Participant TypeLocation and Type of SampleNumber of SamplesMinimum
(μg/m3)
Maximum
(μg/m3)
Mean
(μg/m3)
95th Percentile
(μg/m3)
WindsorFootnote Table B1[a]
2005 Winter
Non-smoking
Personal backpack (avg of five 24 hr samples)2250.335658.39.8
Windsora
2005 Winter
Non-smoking
Indoor stationary (avg of five 24 hr samples)2320.226107.711.3
Windsora
2005 Summer
Non-smoking
Personal backpack (avg of five 24 hr samples)2070.5539210.627.3
Windsora
2005 Summer
Non-smoking
Indoor stationary (avg of five 24 hr samples)2170.4191315.339.7
Windsora
2006 Winter
Non-smoking
Indoor stationary (avg of five 24 hr samples)2240.27119910.710.2
Windsora
2006 Summers
Non-smoking
Indoor stationary (avg of five 24 hr samples)2110.2930810.354.3
ReginaFootnote Table B1[b]
2007 Winter
Smoking
Indoor stationary (24 hour)210.2713.51.85.0
Reginab
2007 Winter
Non-smoking
Indoor stationary (24 hour)840.2314.31.95.8
Reginab
2007 Summer
Smoking
Indoor stationary (24 hour)130.3611.42.411.4
Reginab
2007 Summer
Non-smoking
Indoor stationary (24 hour)910.1033.63.815.6
HalifaxFootnote Table B1[c]
2009 Winter
Non-smoking
Indoor stationary (24 hour)3120.141074.211.0
Halifaxc
2009 Summer
Non-smoking
Indoor stationary (24 hour)3310.0682106.923.1
EdmontonFootnote Table B1[d]
2010 Winter
Non-smoking
Indoor stationary (avg of 7 24-hr samples)3370.18551.910.517.4
Edmontond
2010 Summer
Non-smoking
Indoor stationary (avg of 7 24-hr samples)3280.1025.82.07.9
OttawaFootnote Table B1[e]
2003 Winter
Smoking / non-smoking
Indoor stationary750.0052014.7No data
Quebec CityFootnote Table B1[f]
2005 Winter and early Spring
Indoor stationary960.4019.502.69No data
Various locations across CanadaFootnote Table B1[g]
1991
Indoor stationary754No data539.318.2No data
Footnote Table B1 a

Health Canada 2010a.

Return to footnote Table B1[a] referrer

Footnote Table B1 b

Health Canada 2010b.

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Footnote Table B1 c

Health Canada 2012.

Return to footnote Table B1[c] referrer

Footnote Table B1 d

Health Canada 2013.

Return to footnote Table B1[d] referrer

Footnote Table B1 e

Zhu et al. 2005.

Return to footnote Table B1[e] referrer

Footnote Table B1 f

Héroux et al. 2008.

Return to footnote Table B1[f] referrer

Footnote Table B1 g

Fellin et al. 1992.

Return to footnote Table B1[g] referrer

Table B2. Sampling details for Canadian indoor air studies
Location/Reference and Measured ParameterSampling PeriodSampling DurationSampling EquipmentTotal Number of SamplesMethod Detection Limit (MDL) in µg/m3% of samples greater than MDL
Windsor, ON/Health Canada 2010a
Indoor, outdoor and personal air
Winter and Summer 20051-week (5 consecutive 24 hour samples) in each seasonSUMMA canisters
(active sampling)
12980.046100
Windsor, ON/Health Canada 2010a
Indoor and outdoor air
Winter and Summer 2006Five consecutive 24 hour samples in each seasonSUMMA canisters
(active sampling)
8630.03899.5 to 100
Regina, SK/Health Canada 2010b
Indoor and outdoor air (smoking and non-smoking homes)
Winter and Summer 200724 hour sample and a 5-day sample in each seasonSUMMA canisters
(active sampling)
699 (Full-set)
(smoking homes: 587)
(non-smoking homes: 109)
0.02998.9 to 100
Halifax, NS/Health Canada 2011b
Indoor and outdoor air
Winter and Summer 200924 hour samples collected for 7 consecutive daysSUMMA canisters
(active sampling)
12540.00299.7 to 100
Edmonton, AB/Health Canada 2013
Indoor and outdoor air
Winter and Summer 201024 hour samples collected for 7 consecutive daysSUMMA canisters
(active sampling)
13210.015 (Winter)
0.035 (Summer)
99.1 to 100
Ottawa, ON/Zhu et al. 2005
Indoor and outdoor air
November 2002 to March 200324 hour sample10 L over 100 minAdsorbent tubes
(active sampler)
750.173 to 83
Québec City, QC/Héroux et al. 2008
Indoor air
January to April 20057-day continuous samplingPassive monitors960.2100
Canadian National Study (ON, AB, QC, NFLD, BC, NB, SK, MB, NS)/Fellin et al. 1992
Indoor air
199124 hour samplePassive samplers
(organic vapour monitors)
7540.66Not specified

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Appendix C: Ethylbenzene in Various Food Items

Table C1. Summary of Ethylbenzene Concentrations in Various Food Items (US FDA 2006)
Food itemMean
(μg/kg)
Minimum
(μg/kg)
Maximum
(μg/kg)
Number of analysesNumber of results greater than or equal to LOQFootnote Table C1[a],Footnote Table C1[b]Number of trace resultsFootnote Table C1[c]
Dairy products
Cheese, American, processed
0.642124416
Dairy products
Cheese, cheddar, natural (sharp/mild)
0.732124414
Dairy products
Ice cream, light, vanilla
0.16234403
Dairy products
Cheese, Swiss, natural
0.23244404
Dairy products
Ice cream, regular, vanilla
0.09224402
Dairy products
Sour cream
0.05224401
Fats
Margarine, regular (salted)
2.3922044413
Fats
Butter, regular (salted)
4.45216441111
Fats
Olive/safflower oil
12234015
Fats
Salad dressing, creamy/buttermilk type, low-calorie
1.7577401
Fats
Olive oil
11.5418431
Fruits and fruit products
Apple (red), raw (with peel)
1.235254422
Fruits and fruit products
Banana, raw
0.05224401
Fruits and fruit products
Strawberries, raw/frozen
0.514184311
Fruits and fruit products
Avocado, raw
0.2244403
Fruits and fruit products
Orange juice, frozen concentrate, reconstituted
0.553114413
Fruits and fruit products
Sherbet, fruit-flavored
0.11234402
Fruits and fruit products
Cranberry juice cocktail, canned/bottled
1.566401
Vegetables
Corn, cream style, canned
0.05224001
Vegetables
Tomato, raw
0.912294413
Vegetables
Potato chips
2.272264457
Vegetables
BFa, carrots
0.05224401
Vegetables
Potato, french-fried, fast-food
2.322244313
Vegetables
Potato salad, mayonnaise-type, from grocery/deli
1.524402
Vegetables
Coleslaw, mayonnaise-type, from grocery/deli
3.538403
Vegetables
Popcorn, popped in oil
0.35244005
Vegetables
Popcorn, microwave, butter-flavored
42.755129421
Cereal products
Bread, white, enriched
1.252284423
Cereal products
Muffin, fruit or plain
1022244469
Cereal products
Corn/tortilla chips
0.32244405
Cereal products
Fruit-flavoured cereal, presweetened
0.43274405
Cereal products
Macaroni and cheese, prepared from box mix
0.3415154410
Cereal products
Cake, chocolate with icing
1.9821344116
Cereal products
Sweet roll/Danish pastry
1.3621244112
Cereal products
Chocolate chip cookies
1.72334429
Cereal products
Sandwich cookies with crème filling
0.48284406
Cereal products
Apple pie, fresh/frozen
1.8621444312
Cereal products
Pumpkin pie, fresh/frozen
0.6629294410
Cereal products
Crackers, graham
1.392234419
Cereal products
Crackers, butter-type
0.8384406
Cereal products
Cheese pizza, regular crust, from pizza carry-out
1.382224025
Cereal products
Pizza, cheese and pepperoni, regular crust, from pizza carry-out
0.982744012
Cereal products
Doughnut, cake-type, any flavour
2.0221644310
Cereal products
Brownie
1.8621444410
Cereal products
Sugar cookies
1.6821944211
Cereal products
Breakfast tart/toaster pastry
1.2555401
Cereal products
Macaroni salad, from grocery/deli
5.25312412
Meat and poultry
Beef, ground, regular, pan-cooked
0.36244406
Meat and poultry
Beef roast, chuck, oven-roasted
0.482144413
Meat and poultry
Pork bacon, oven-cooked
1.162164427
Meat and poultry
Liver (beef/calf), pan-cooked with oil
0.4821214410
Meat and poultry
Frankfurter (beef/pork), boiled
0.912944010
Meat and poultry
Bologna (beef/pork)
1.2722044110
Meat and poultry
Salami, luncheon-meat type (not hard)
0.68284409
Meat and poultry
Quarter-pound hamburger on bun, fast food
2.4323844211
Meat and poultry
Meatloaf, beef, homemade
0.43294405
Meat and poultry
BF, beef and broth/gravy
0.09444401
Meat and poultry
Chicken nuggets, fast-food
2.8222344414
Meat and poultry
Chicken, fried (breast, leg, and thigh), fast-food
1.252224026
Meat and poultry
Quarter-pound cheeseburger on bun, fast food
0.772114419
Meat and poultry
BF, veal and broth/gravy
1.524402
Meat and poultry
BF, turkey and broth/gravy
0.522401
Meat and poultry
Chicken breast, fried, fast-food (with skin)
5.75215412
Meat and poultry
Chicken leg, fried, fast-food (with skin)
1.566401
Meat and poultry
Chicken filet (broiled) sandwich on bun, fast-food
2.537402
Fish
Tuna, canned in oil, drained
0.18234003
Fish
Fish sticks or patty, frozen, oven-cooked
3.3421944712
Fish
Fish sandwich on bun, fast-food
0.2310104410
Fish
Catfish, pan-cooked with oil
12.5622422
Fish
Tuna, canned in water, drained
1.2523402
Eggs
Eggs, scrambled with oil
0.39254406
Food primarily sugar
Candy bar, milk chocolate, plain
2.321544314
Food primarily sugar
Candy, caramels
0.15244002
Food primarily sugar
Candy bar, chocolate, nougat, and nuts
4.5612411
Mixed dishes and soups
Taco/tostada with beef and cheese, from Mexican carry-out
1.8422844113
Mixed dishes and soups
Burrito with beef, beans and cheese, from Mexican carry-out
2.546402
Nuts and seeds
Peanut butter, creamy
2.6121444513
Nuts and seeds
Mixed nuts, no peanuts, dry roasted
4.7533840711
Nuts and seeds
Sunflower seeds (shelled), roasted, salted
141421430
Soft drinks and alcohol
Carbonated beverage, cola, regular
0.27574402
Soft drinks and alcohol
Coffee, from ground
0.3917174410
Soft drinks and alcohol
Bottled drinking water (mineral/spring), not carbonated or flavored
0.522401
Footnote Table C1 a

Abbreviations: LOQ: limit of quantification; BF: baby food.

Return to footnote Table C1[a] referrer

Footnote Table C1 b

These data represent samples of approximately 285 foods collected and analysed in 44 market baskets between 1991 and 2003.

Return to footnote Table C1[b] referrer

Footnote Table C1 c

Trace: number of results that were greater than or equal to the limit of detection but less than the LOQ.

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Appendix D: Summary of Ethylbenzene Concentrations in Various Food Items (US FDA 2006)

Table D1. Upper-bound estimates of daily intake of ethylbenzene by the general population in Canada
Route of exposure0-6 monthsFootnote Table D1[a],Footnote Table D1[b],Footnote Table D1[c] Breast fed
(μg/kg-bw per day)
0-6 monthsa,b,c
Formula fed
(μg/kg-bw per day)
0-6 monthsa,b,c
Not formula fed
(μg/kg-bw per day)
6 months-4 yearsFootnote Table D1[d]
(μg/kg-bw per day)
5-11 yearsFootnote Table D1[e]
(μg/kg-bw per day)
12-19 yearsFootnote Table D1[f]
(μg/kg-bw per day)
20-59 yearsFootnote Table D1[g]
(μg/kg-bw per day)
60+ yearsFootnote Table D1[h]
(μg/kg-bw per day)
Ambient airFootnote Table D1[i]0.150.150.150.330.260.150.130.11
Indoor airFootnote Table D1[j]131313282213119
Total intake via inhalation13.213.213.228.322.313.111.19.1
Drinking waterFootnote Table D1[k]N/A0.170.060.070.060.030.030.03
Food and beveragesFootnote Table D1[l]0.057NI2.82.41.60.970.880.72
SoilFootnote Table D1[m]3.0 × 10-43.0 × 10-43.0 × 10-45.0 × 10-42.0 × 10-44.0 × 10-53.0 × 10-53.0 × 10-5
Total intake via ingestion0.0570.172.92.51.71.00.910.75
Footnote Table D1

N/A, not applicable; NI, data not identified in the literature

Footnote Table D1 a

Human breast milk data was available from one study conducted in Baltimore, Maryland. The maximum ethylbenzene concentration reported in the study was 0.58 µg/L with a mean concentration of 0.232 µg/L. Assumed that infants consume 0.742 L/day of breast milk (Health Canada 1998).

Return to footnote Table D1[a] referrer

Footnote Table D1 b

Assumed to weigh 7.5 kg, breathe 2.1 m3 of air per day, drink 0.8 L of water per day (formula fed) or 0.3 L/day (not formula fed), and ingest 30 mg of soil per day (Health Canada 1998).

Return to footnote Table D1[b] referrer

Footnote Table D1 c

For exclusively formula-fed infants, intake from water is synonymous with intake from food. The concentration of ethylbenzene in water used to reconstitute formula was based on the Canadian Drinking Water Aesthetic Objective of 1.6 μg/L (Health Canada 2014a). Data on concentrations of ethylbenzene in formula were not identified. Approximately 50% of not-formula-fed infants are introduced to solid foods by 4 months of age and 90% by 6 months of age (NHW 1990).

Return to footnote Table D1[c] referrer

Footnote Table D1 d

Assumed to weigh 15.5 kg, breathe 9.3 m3 of air per day, drink 0.7 L of water per day, and ingest 100 mg of soil per day (Health Canada 1998).

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Footnote Table D1 e

Assumed to weigh 31.0 kg, breathe 14.5 m3 of air per day, drink 1.1 L of water per day, and ingest 65 mg of soil per day (Health Canada 1998).

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Footnote Table D1 f

Assumed to weigh 59.4 kg, breathe 15.8 m3 of air per day, drink 1.2 L of water per day, and ingest 30 mg of soil per day (Health Canada 1998).

Return to footnote Table D1[f] referrer

Footnote Table D1 g

Assumed to weigh 70.9 kg, breathe 16.2 m3 of air per day, drink 1.5 L of water per day, and ingest 30 mg of soil per day (Health Canada 1998).

Return to footnote Table D1[g] referrer

Footnote Table D1 h

Assumed to weigh 72.0 kg, breathe 14.3 m3 of air per day, drink 1.6 L of water per day, and ingest 30 mg of soil per day (Health Canada 1998).

Return to footnote Table D1[h] referrer

Footnote Table D1 i

Outdoor air quality measurements are available nationwide through The National Air Pollution Surveillance Inventory (NAPS). The upper-bound intake estimation was based on the highest 95th percentile measured 24-hour concentration recorded across all monitoring stations with a value of 4.40 μg/m3. The maximum 24-hour concentration occurred in the Burnaby area of British Colombia with a value of 35.84 μg/m3 (Environment Canada 2011a). Measured values below the detection limit (0.009 ug/m3) were replaced with half the detection limit (0.0045 ug/m3). Canadians are assumed to spend 3 hours outdoors each day (Health Canada 1998).

Return to footnote Table D1[i] referrer

Footnote Table D1 j

Six recent Canadian residential studies were identified that measured the indoor air concentrations of various chemicals (Zhu 2005; Health Canada 2010a,b; Health Canada 2012; Health Canada 2013a; Héroux et al. 2008). The highest 95th percentile value reported among the six studies was deemed appropriate to estimate the chronic upper-bounding estimate for exposure. The highest 95th percentile value (54 μg/m3) was reported during the 2006 survey of 46 Windsor homes. Canadians are assumed to spend 21 hours indoors each day (Health Canada 1998).

Return to footnote Table D1[j] referrer

Footnote Table D1 k

The concentration of ethylbenzene in water used to estimate the upper-bound exposure was based on the Canadian Drinking Water Aesthetic Objective of 1.6 μg/L (Health Canada 2014a). Concentrations of ethylbenzene above this level would result in taste and odour problems that would probably be addressed before continuing to consume.

Return to footnote Table D1[k] referrer

Footnote Table D1 l

Estimates of intake from food are based upon concentrations in foods that are selected to represent the 12 food groups addressed in calculating intake (Health Canada 1998). Lockhart et al. (1992) analyzed fish samples from northern Manitoba and the Northwest Territories, observing a maximum concentration of 273 µg/kg in whitefish muscle. This value was not used to estimate the "fish" component for the food intake calculation as the source of ethylbenzene may have been industrial and therefore not representative of exposures to the general population of Canada. Estimates of intake from food are based upon concentrations of ethylbenzene identified in the total diet study conducted in the United States from 1991 to 1993 and from 2003 to 2004 and are shown in Appendix C (US FDA 2006). The maximum concentrations identified for each food category were selected except for the vegetable and cereal categories. The maximum concentrations in these food categories (popcorn for vegetable category and muffins for cereal products category) were quite a bit higher than the other items in the category and did not represent a typical maximum daily value for the category. More typical maximum values listed below were selected for the vegetable and cereal product categories.
Dairy products: maximum concentration value of 12 µg/kg of ethylbenzene identified in cheddar cheese.
Fats: maximum concentration value of 23 µg/kg of ethylbenzene identified in olive/safflower oil.
Fruits and fruit products: maximum concentration value of 25 µg/kg of ethylbenzene identified in apples.
Vegetables: maximum concentration value of 29 µg/kg of ethylbenzene in vegetables identified in tomatoes.
Cereal products: maximum concentration value of 33 µg/kg of ethylbenzene identified in chocolate chip cookies (similar to concentration identified in white bread).
Meat and poultry: maximum concentration value of 38 µg/kg of ethylbenzene identified in a fast-food quarter-pound hamburger.
Fish: maximum concentration value of 22 µg/kg of ethylbenzene identified in pan-cooked catfish.
Eggs: maximum concentration value of 5 µg/kg of ethylbenzene identified in eggs.
Foods, primarily sugar: maximum concentration value of 15 µg/kg of ethylbenzene in a plain, milk chocolate bar.
Mixed dishes: maximum concentration value of 28 µg/kg of ethylbenzene in a take-out taco with beef and cheese.
Nuts and seeds: maximum concentration value of 38 µg/kg of ethylbenzene in mixed nuts (dry roasted).
Beverages (soft drinks/alcohol/coffee/tea): maximum concentration value of 17 µg/L of ethylbenzene in coffee.
Amounts of foods consumed on a daily basis by each age group are described by Health Canada (Health Canada 1998).

Return to footnote Table D1[l] referrer

Footnote Table D1 m

The highest concentration of ethylbenzene found in 122 soil samples collected from typical urban, residential, and parkland locations in Ontario was below the study detection limit (2 ng/g). The Canadian Council of Ministers of the Environment (CCME) published Canadian Soil Quality Guidelines for ethylbenzene. The limits for coarse and fine soil are 0.082 and 0.018 mg/kg, respectively, and are identical across all land uses. The upper-bound intake calculation was based on the guidance value of 0.082 mg/kg.

Return to footnote Table D1[m] referrer

Table D2. Upper-bound estimates of daily intake of ethylbenzene by individuals living in northern Canada that may consume fish with high concentrations of ethylbenzene
Route of exposure0-6 monthsFootnote Table D2[a],Footnote Table D2[b],Footnote Table D2[c] Breast fed
(μg/kg-bw per day)
0-6 monthsa,b,c
Formula fed
(μg/kg-bw per day)
0-6 monthsa,b,c
Not formula fed
(μg/kg-bw per day)
6 months-4 yearsFootnote Table D2[d]
(μg/kg-bw per day)
5-11 yearsFootnote Table D2[e]
(μg/kg-bw per day)
12-19 yearsFootnote Table D2[f]
(μg/kg-bw per day)
20-59 yearsFootnote Table D2[g]
(μg/kg-bw per day)
60+ yearsFootnote Table D2[h]
(μg/kg-bw per day)
Drinking waterFootnote Table D2[k]N/A0.170.060.070.060.030.030.03
Food and beveragesFootnote Table D2[l]0.057NI2.83.32.31.41.31.0
SoilFootnote Table D2[m]3.0 × 10-43.0 × 10-43.0 × 10-45.0 × 10-42.0 × 10-44.0 × 10-53.0 × 10-53.0 × 10-5
Total intake via ingestion0.0570.172.93.42.41.41.31.0
Footnote Table D2

N/A, not applicable; NI, data not identified in the literature

Footnote Table D2 a

See description of footnotes in Table D1.

Return to footnote Table D2[a] referrer

Footnote Table D2 b

See description of footnotes in Table D1.

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Footnote Table D2 c

See description of footnotes in Table D1.

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Footnote Table D2 d

See description of footnotes in Table D1.

Return to footnote Table D2[d] referrer

Footnote Table D2 e

See description of footnotes in Table D1.

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Footnote Table D2 f

See description of footnotes in Table D1.

Return to footnote Table D2 [f] referrer

Footnote Table D2 g

See description of footnotes in Table D1.

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Footnote Table D2 h

See description of footnotes in Table D1.

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Footnote Table D2 k

See description of footnotes in Table D1.

Return to footnote Table D2[k] referrer

Footnote Table D2 l

Estimates of intake from fish are based upon the maximum concentration of ethylbenzene identified in fish samples from northern Manitoba and the Northwest Territories. The maximum concentration was 273 μg/kg measured in whitefish muscle (Lockhart et al. 1992).

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Footnote Table D2 m

See description of footnotes in Table D1.

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Appendix E: Consumer Product Information

Table E1. Information on Consumer Products in the United States and Denmark
Product categoryType of productNumber of productsConcentration (%)
Arts and craftsFootnote Table E1[a]Spray paint730.01 to 15
Arts and craftsaThinner (liquid)115 to 25
Arts and craftsaRubber coating (aerosol)74
Arts and craftsaCleaner (aerosol)1less than 1
Arts and craftsaGlue (aerosol)1less than 1
Automotive productsaSpray Paint140.01 to 20
Automotive productsaCleaner (aerosol and liquid)8less than 1 to 25
Automotive productsaLiquid paint100.6 to 6.87
Automotive productsaOil (liquid)10.005 to 0.006
Automotive productsaFuel related products10less than 0.1 to 5
Home maintenanceaSpray paint770.01 to 10
Home maintenanceLiquid paint39less than 0.1 to 3
(wood paint up to 20)
Home maintenanceaSealant (paste or liquid)140.1 to less than 5
Home maintenanceaStain (liquid or aerosol)80.118 to 1
Home maintenanceaCleaner (liquid)3less than 1 to 20
Home maintenanceaVarnish (liquid)20.6 to 3
Home maintenanceaStain stripper (aerosol)1less than 12
Home maintenanceaThinner (liquid)15 to 15
Home maintenanceaAdhesive (paste)50.1 to less than 3
Other inside home productsaSpray coatings650.1 to 15
Other inside home productsaArt spray11 to 3
Other inside home productsaStain (aerosol)2less than 5
Other inside home productsaSnow spray1less than 1
Consumer productsFootnote Table E1[b]paint (aerosol and liquid), paint remover, stains, furniture polish and cleaners, and insecticides200less than 0.1 to 23% (two products were reported to contain approximately 70% ethylbenzene; however, the details of these two products were not given as the information was classified as confidential)
AutomotiveFootnote Table E1[c]Not specified157/6587.2%
Household cleaners and polishescNot specified157/6580.1%
PaintcNot specified157/6582.4%
Fabric and leathercNot specified157/6581%
Spray paintsFootnote Table E1[d]Not specified5"not present" to 1.83%
Footnote Table E1 a

US Household Products Database (HPD, 2011), United States.

Return to footnote Table E1[a] referrer

Footnote Table E1 b

US EPA's Source Ranking Database (SRD, 2004), United States.

Return to footnote Table E1[b] referrer

Footnote Table E1 c

Sack et al. (1992), United States.

Return to footnote Table E1[c] referrer

Footnote Table E1 d

Nielsen et al. (2003), Denmark.

Return to footnote Table E1[d] referrer

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Appendix F: Estimates of Exposure to Ethylbenzene

Table F1. Estimates of exposure to Ethylbenzene from Consumer Products by CanadiansFootnote Table F1[a],Footnote Table F1[b]
Consumer product typeAssumptionsEstimated concentrations and daily intakes
Mouthing plastic

Based on the results from VCCEP (2007) report for young children mouthing plastic toys

  • Assume all non-pacifying objects mouthed by young children are made of styrene-containing polymers, and
  • Migration rate of ethylbenzene from toys does not decrease over age interval for which exposure is estimated.
  • Assume mouthable toy contains 108 ppm (µg/g) ethylbenzene (concentration from disposable HIPS food-contact materials) (PWSG 1997 cited in VCCEP 2007), and assume a density of 1 g/cm3 to give an initial residual ethylbenzene in the polymer of 108 µg/cm3 (Cp0)
  • Assume that general diffusion of ethylbenzene is expected to be similar to that of styrene, based on their structural similarities, at body temperature, therefore, the estimated diffusion coefficient of ethylbenzene is 1.08 × 10-13 cm2/s (Dp)
  • Assume the toy is 2 months old at time of purchase
  • Based on these assumptions, daily migration rate (DMR) of ethylbenzene is 0.00075 µg/cm2-day using following equations:

DMR = Mt (2 months + 1 day) - Mt (2 months)

Mt = 2 x Cp0 x [(Dp x t)/π]1/2

  • Assume for 2- to 12-month olds: average mouthing time (ET) of 35 min/day (maximum of 350 min/day), mean body weight (BW) of 8.5 kg, oral surface area (SAoral) of 24.4 cm2.
  • Assume for 13- to 24-month olds: average mouthing time of 35 min/day (maximum of 350 min/day), mean body weight of 12.2 kg, oral surface area of 31.0 cm2.
  • Assume for 25- to 36-month olds: average mouthing time of 2 min/day (maximum of 220 min/day), mean body weight of 34.1 kg, oral surface area of 34.1 cm2.

Ethylbenzene intake = DMR x ET x SAoral x conversion factor
1440 min/day x BW

Refer to VCCEP 2007 for more details

2 to 12 months of age:
5.2 × 10-8 to 5.2 × 10-7 mg/kg-bw per day

13 to 24 months of age:
4.6 × 10-8 to 4.6 × 10-7 mg/kg-bw per day

25 to 36 months of age:
2.5 × 10-9 to 2.8 × 10-7 mg/kg-bw per day

2.5 × 10-9 to 5.2 × 10-7 mg/kg-bw per day

Range covers calculations using average and maximum mouthing times.
Aerosol spray paintFootnote Table F1[c] (ConsExpo model - using spray paint scenario but evaporation model since EB is volatile) Assume use entire can or approximately 300 g)Reported weight fractions ranging from 0.01 to 5% were used (HPD 2011, Home Hardware 2013, Rust-Oleum 2013a, Health Canada 2013b, 2014b).

Frequency of 2 times/year (RIVM 2007a).

Inhalation: evaporation from an increasing area

Exposure duration of 20 min, application duration of 15 min, applied amount of 300 g, room volume of 34 m3, ventilation rate of 1.5/hour (well ventilated), release area of 2 m2, use Langmuir method for mass transfer rate, molecular weight matrix of 300 g/mol since compound of interest is not the main solvent (RIVM 2007a).

Dermal: contact rate
Contact rate of 100 mg/min, release duration of 15 min (RIVM
2007a)
Inhalation - Mean concentration on day of event = 0.006 to 3 mg/m3

Dermal -
Acute applied dose = 0.002 to 1.1 mg/kg-bw per event
Liquid paint (high solid paint - painting wood lathed wall)Reported weight fractions ranging from 0.1 to 1% were used (HPD 2011, Rust-Oleum 2013b, ICI Paints 2010, Health Canada 2013b, 2014b). The maximum concentration of 20% was not used as it was for a specialized product that no longer appears to be available.

Frequency of 1 time/year (RIVM 2007a).

Inhalation: evaporation from an increasing area

Exposure duration of 132 min, application duration of 120 min, room volume of 20 m3, ventilation rate of 1.5/hour (well ventilated), applied amount of 1300 g, release area of 10 m2, molecular weight matrix of 550 g/mol (compound of interest is not the main solvent), use Langmuir method for mass transfer rate (RIVM 2007a).

Dermal: constant rate
Contact rate of 30 mg/min, release duration of 120 min (RIVM 2007a)
Inhalation - Mean concentration on day of event = 1.3 to 13 mg/m3

Dermal - Acute applied dose = 0.051 to 0.51 mg/kg-bw per event
Paint remover (liquid spot remover)Assume a weight fraction of 4%, (IPCS 1996; SRD 2004; WM Barr 2012, Health Canada 2013b, 2014b)

Frequency of 1 time/year (RIVM 2007b).

Inhalation: evaporation from an increasing area
Exposure duration of 60 min, application duration of 60 min, room volume of 20 m3, ventilation rate of 1.5/hour (well ventilated), release area of 2 m2, molecular weight matrix of 300 g/mol (compound of interest is not the main solvent), use Langmuir method for mass transfer rate (RIVM 2007b), applied amount of 106 g (assuming use entire bottle (133 mL) of spot remover in one application (use density from msds (0.797 g/mL) and volume of product (133 mL) = 106 g) (WM Barr 2012),

Dermal: instant application
Exposed surface area of 430 cm2 (palms of both hands), applied amount of 0.5 g (RIVM 2007b).
Inhalation - Mean concentration on day of event = 2.8 mg/m3

Dermal - Acute applied dose = 0.28 mg/kg-bw per event
Lacquer/Stain/varnish (use solvent-rich paint scenario)Reported weight fractions ranging from 0.1 to 2% were used (HPD 2011; Rust-Oleum 2011, Performance Coatings 2013, Sherwin-Williams 2010, Health Canada 2013b, 2014b)

Frequency of 4 times/year, based on mean frequency (US EPA 1997).

Inhalation: evaporation from an increasing area

Exposure duration of 132 min, application duration of 120 min, room volume of 20 m3, ventilation rate of 1.5/hour (well ventilated), release area of 10 m2, molecular weight matrix of 300 g/mol (compound of interest is not the main solvent), use Langmuir method for mass transfer rate (RIVM 2007a), applied amount of 460 g, based on mean amount of product used (US EPA 2009)

Dermal: constant rate
Contact rate of 30 mg/min, release duration of 120 min (RIVM 2007a)
Inhalation - Mean concentration on day of event = 0.5 to 9.4 mg/m3

Dermal - Acute applied dose = 0.051 to 1.0 mg/kg-bw per event
Caulking/SealantReported weight fractions of 0.1 to 5% were used (Henkel 2008, 2009; Sherwin-Williams 2008; HPD 2011, Health Canada 2013b, 2014b)
Frequency of 3 times/year (RIVM 2007b).

Inhalation: evaporation from an increasing area (use weight fractions 0.1 to 1% (products used indoors) as 5% was reported in a product meant for exterior use only)

Exposure duration of 45 min, application duration of 30 min, room volume of 10 m3, ventilation rate of 1.5/hour, applied amount of 75 g, release area of 30 m2, molecular weight matrix of 300 g/mol (compound of interest is not main solvent), use Langmuir method for mass transfer rate (RIVM 2007b).

Dermal: constant rate (use weight fractions of 0.1 to 5%)
Contact rate of 50 mg/min, release duration of 30 min, exposed surface area of 2 cm2 (RIVM 2007b)
Inhalation - Mean concentration on day of event = 0.09 to 5.2 mg/m3

Dermal - Acute applied dose = 0.021 to 1.1 mg/kg-bw per event
Footnote Table F1 a

Since these products are used primarily by adults (20-59 years old), estimated exposures have been derived for this age group only unless otherwise stated.

Return to footnote Table F1[a] referrer

Footnote Table F1 b

Assume 100% absorption across the lungs.

Return to footnote Table F1[b] referrer

Footnote Table F1 c

Exposure to an aerosol spray paint was considered representative of exposures to aerosol paint removers as well.

Return to footnote Table F1[c] referrer

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Appendix G: Estimates of Potential Exposure to Ethylbenzene from Gasoline

Table G1. Estimates of Potential Exposure to Ethylbenzene from Gasoline
Consumer product typeAssumptionsEstimated concentrations and daily intakes
GasolineFootnote Table G1[a]

Dermal exposure while refuelling a vehicle
Reported weight fractions range from 1.0 to 5.4% were used (CONCAWE 1997)

  • Use thin-film thickness to derive mass of gasoline on the skin, and assume that the thin-film on skin measures 0.002 cm (value for mineral oil, immersion with partial wipe scenario) (US EPA 2011)
  • Assume gasoline has a density of 0.79 g/cm3 (CONCAWE 1992)
  • Assumethat gasoline gets onto one-eighth of one hand (57 cm2) (Health Canada 1995).

Mass of gasoline on skin = 0.002 cm × 0.79 g/cm3 × 57 cm2 = 0.09 g

Dose = 0.09 g × 0.054 = 6.85 × 10-5g/kg-bw = 0.0685 mg/kg-bw
70.9 kg

Estimated short-term dermal dose = 0.01 to 0.07 mg/kg-bw per event
Footnote Table G1 a

The highest 95th percentile concentration of 1461 µg/m3 identified in the PACE studies (1987, 1989) was used to estimate inhalation exposures to ethylbenzene while refuelling a vehicle.

Return to footnote Table G1[a] referrer

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Appendix H: Summary of Health Effects

Table H1. Information for Ethylbenzene in laboratory animals and in vitro
EndpointLowest effect levelsFootnote Table H1[a]/Results
Acute toxicityLowest oral LD50 = 3500 mg/kg-bw in rats (Wolf et al.1956)

[Additional studies: Smyth et al.1962; NTP 1986]

Lowest dermal LD50 = 1 354 mg/kg-bw in rabbits (Smyth et al.1962)

[Additional studies: Harton and Rawl 1976]

Lowest inhalation LC50 = 17 200 mg/m3 in rats (4 hours) (Smyth et al.1962)

[Additional studies: Ivanov 1962]

LowestinhalationLOEC (rats) greater than or equal to 1740 mg/m3 (400 ppm), based on arbitrary assessment of the authors that a moderate activation in motor behaviour was observed in male CFY rats (8 per group) exposed to ethylbenzene vapour at concentrations between 1740 to 6514 mg/m3(400 and 1500 ppm) for 4 hours, compared with other solvent-exposed rats. The minimum narcotic concentration for ethylbenzene was 9466 mg/m3 (2180 ppm ) (Molnar et al.1986)

[Additional studies: Yant et al.1930; Gerarde 1960; Ivanov 1962; Tegeris and Baltser 1994].
Short-term repeated-dose toxicityLowest inhalation LOEC (mice) = 326 mg/m3 (75 ppm), based on significant reductions in liver pentoxyresorufin O-dealkylase (PROD) and ethoxyfluorocoumarin-O-dealkylase activities and concentration-related, although not significant, reductions in lung ethoxyresorufin O-dealkylase and PROD activities in male and female mice exposed to 326 mg/m3 ethylbenzene for 1 week. In this study, six mice per group were exposed to ethylbenzene at 326 mg/m3 for 1 week or at 3260 mg/m3 (750 ppm) for 1 or 4 weeks (6 hours/day, 5 days/week). At higher concentration (3260 mg/m3)significantly increased relative liver weights, hepatic S-phase DNA synthesis and mitotic figures, hepatoenzyme activities, and hepatocellular hypertrophy were observed in both sexes of mice exposed to ethylbenzene for 1 week or 4 weeks. Significantly increased lung S-phase DNA syntheses were observed after exposure to ethylbenzene for 1 week in both sexes but decreased after 4 weeks exposure in males, while in females, no significant difference between exposed and control mice was observed after 4 weeks exposure. In addition, several mixed function oxygenases in mice lung altered after 1 or 4 week exposure (Stott et al.2003).

Lowest inhalation LOAEC (rats) = 1740 mg/m3 (400 ppm), based on ototoxicity.with a NOAEC identified at 1305 mg/m3 (300 ppm) (Cappaert et al. 2000). See Neurotoxicity/ototoxicity section below.

[Additional studies: Andersson et al.1981; Toftgård and Nilsen 1982; Elovaara et al.1985; EPA 1986 a, 1986b; Romanelliet al.1986; Mutti et al.1988; Cragg et al.1989; Cappaert et al.1999, 2001, 2002; Stott et al.2003 (rats); Saillenfait et al.2006; Li et al. 2010]

Lowest oral (gavage) LO(A)EL (rats) = 250 mg/kg per day, based on significantly increased absolute and relative liver weights, with centrilobular hepatocyte hypertrophy, relative kidney weights, and significantly increased numbers of granular and epithelial cell casts in the urine of exposed male rats. Increased incidence and severity of hyaline droplet nephropathy were also observed in the exposed male rats at this dose level. Although the authors speculate the nephropathy was α2u-globulin-associated, no further test has been conducted to confirm the α2u-globulin deposition in the animals. The NOAEL = 75 mg/kg-bw per day as defined by the authors. In this study, 5 rats/sex per group were administered 0, 75, 250, or 750 mg/kg per day ethylbenzene by gavage for 4 weeks. At highest dose level (750 mg/kg-bw per day), significantly increased absolute and relative liver weights and significantly increased serum alanine aminotransferase, serum urea, and cholesterol concentrations were observed in both sexes. In addition, significantly increased total bilirubin in females and the number of transitional epithelial cells in urinary sediment in males were observed. Histological results showed centrilobular hepatocyte hypertrophy in mid (males only) and high dose groups (male and females) and an increase incidence and severity of hyaline droplet nephropathy in mid and high dose males (Mellert et al. 2007).

[Additional study: Gagnaire and Langlais 2005]
Subchronic toxicityLowestinhalation LOEC (rat) = 435 mg/m3 (100 ppm), based on significantly decreased serum alkaline phosphatase levels in female rats exposed to ethylbenzene, 6 hours/day, 5 days/week for 13 weeks. In this study, 10 of each sex of F344 rats per group were exposed to ethylbenzene at 0, 435, 1087, 2175, 3263, or 4350 mg/m3(0, 100, 250, 500, 750, or 1000 ppm). Ten additional rats of each sex were included at each exposure level to provide blood samples for clinical pathology. Clinical chemistry data were collected on day 5, 23, and after 13 weeks. Toxicity data were analysed at 13 weeks. At higher concentrations ( greater than or equal to 1087 mg/m3), significantly decreased alkaline phosphatase levels were observed in both sexes of rats. In addition, significantly increased absolute kidney weights in both sexes and increased relative kidney weights in males were observed at greater than or equal to 2175 mg/m3; significantly increased absolute liver weights in both sexes and increased relative liver weights in males were observed at greater than or equal to 1087 mg/m3; significantly increased absolute lung weights were observed in females at greater than or equal to 1087 mg/m3. No effects on sperm, testicular morphology or the length of the oestrous cycle were observed. No histopathological changes were observed in an association with the liver or kidney weights changes. Lymphoid hyperplasia in the bronchial and mediastinal lymph nodes and inflammatory cell infiltrates around vessels with foci of inflammatory cells in septae and lumen of alveoli in lung were observed in rats exposed to ethylbenzene at greater than or equal to 1087 mg/m3; however, the severity of these lesions were not dose related and the characteristics of the lesions were more of a response to an infectious agent. The authors thus stated that the inflammatory lung lesions were probably unrelated to ethylbenzene exposure (NTP 1992).

[Additional studies: Wolf et al. 1956; Elovaara et al. 1985; NTP (mice) 1992; Gagnaire et al. 2007, described in the "neurotoxicity" section of this table; Zhang et al 2010]]

Lowestoral LO(A)EL (rats) = 250 mg/kg-bw per day, based on significantly increased absolute and relative liver weights and relative kidney weights in both sexes, and significantly increased absolute kidney weights in males, significantly increased alanine aminotransferase and gamma glutamyltransferase levels, significantly increased total bilirubin, number of transitional epithelial cells and granular and epithelial cell casts in urinary sediments, serum potassium and calcium concentrations in males, and significantly increased cholesterol and reduced prothrombin time in both sexes of rats. NOAEL = 75 mg/kg-bw per day as defined by the authors. In this study, 10 of each sex of Wistar rats were exposed to 0, 75, 250, or 750 mg/kg-bw per day ethylbenzene by gavage for 13 weeks (daily dosage was divided into two doses administered to each rat at approximately 8-hour intervals). In the high dose groups, significantly increased mean corpuscular volume, alanine aminotransferase and serum magnesium concentrations in both sexes, and significantly increased total serum protein and reduced platelet counts in females were observed. In addition, landing foot-splay was significantly decreased in high dose males and motor activity was significantly increased in high dose females. Histological results revealed significantly increased incidence of centrilobular hypertrophy of hepatocytes in both sexes of mid- and high-dose treated groups. A treatment-related increase in hyaline droplet storage in the male renal tubular epithelium was observed; however, no treatment-related effects were seen in the incidence of initial signs of chronic progressive neuropathy. Thymus weights were reduced in mid- and high-dose females without any histomorphological changes (Mellert et al. 2007). Significantly increased relative liver and kidney weights in male rats were also observed at 250 and 500 mg/kg-bw per day dose levels in another subchronic (13 weeks) study with Crl:CD(SD) rats (10-11/sex per dose. Rats were administered 0, 50, 250, or 500 mg/kg-bw per day ethylbenzene by gavage; daily dosage was divided into two doses administered to each rat at approximately 3-hour intervals). Significantly increased relative liver weights were observed at the 500 mg/kg-bw per day dose level in female rats. No treatment related histopathological changes were observed in livers or kidneys of rats in the 500 mg/kg-bw per day dosage group (Li et al. 2010)

[Additional study: Wolf et al. 1956; Barnett 2006]
Chronic toxicity/carcinogenicityCarcinogenicity bioassay via inhalation in rats and mice:
F344 rats and B6C3F1 mice were exposed to 0, 326, 1090, or 3260 mg/m3 (0, 75, 250, or 750 ppm) ethylbenzene, 6 hours/day, 5 days/week, for 104 and 103 weeks, respectively. In the rat study, at the highest concentration, significantly increased incidences of renal tubular neoplasms (3 out of 50 [3/50], 5/50, 8/50, 21/50; historical control ranged 0-4%), interstitial cell adenomas in the testis (36/50, 33/50, 40/50, 44/50; historical control ranged 54-83%), and bilateral testicular adenoma (27/50, 23/50, 32/50, 40/50) were observed in males, and significantly increased renal tubular neoplasms (0/50, 0/50, 1/50, 8/50) were observed in females. In the mouse study, at the highest concentration, significantly increased incidences of alveolar/bronchiolar neoplasms were observed in males (7/50, 10/50, 15/50, 19/50; historical control ranged 10-42%) and significantly increased hepatocellular neoplasms were observed in females (13/50, 12/50, 15/50, 25/50; historical control ranged 3-54%) (Chan et al. 1998; NTP 1999).

Carcinogenicity bioassay via oral exposure in rats
SD rats, 40 of each sex per group were exposed to 500 mg/kg-bw per day ethylbenzene in olive oil by stomach tube, 4-5 days/week for 104 weeks. Animals were examined after week 141. Total malignant tumours were increased in exposed rats (14/40 and 17/37 in exposed males and females, respectively, and 12/45 and 11/49 in control males and females, respectively). No further information was provided in the report (Maltoni et al. 1985). Additional information was published later (Maltoni et al. 1997) in which SD rats were also exposed to 800 mg/kg-bw ethylbenzene. Increased incidences in nasal cavity tumours, type not specified (2% in exposed females versus 0% in controls), neuroesthesioepitheliomas (2% in exposed females versus 0% in controls; 6% in exposed males versus 0% in controls), and oral cavity tumours (6% in exposed females versus 2% in controls; 2% in exposed males versus 0% in controls) were observed at 800 mg/kg-bw. Statistical analysis was not provided.

Non-cancer endpoints:
Lowest inhalation LOAEC
(rats) = 326 mg/m3 (75 ppm), based on significantly increased severity of nephropathy in female rats (104-week study). Nephropathy was characterized by a spectrum of changes, including dilation of renal tubules with hyaline or cellular casts, interstitial fibrosis and mononuclear inflammatory cell infiltration, foci of tubular regeneration, and transitional epithelial hyperplasia of the renal papilla. Details of the study were described above. The severities of nephropathy were significantly increased in all exposed female rats and in 3260 mg/m3 (750 ppm) male rats. At 3260 mg/m3, significantly increased incidences of renal tubule hyperplasia in exposed both male and female rats and significantly decreased survival of male rats were observed. Other pathological lesions, such as bone marrow and parathyroid gland hyperplasia, prostate gland inflammation, cystic degeneration of the liver, oedema, congestion and haemorrhage in the lungs, haemorrhage in mesenteric and slightly increased renal lymph nodes, were also observed in exposed male rats; the authors considered that the biological significance of these effects was unclear and their relationship to ethylbenzene exposure was uncertain,
LOAEC (mice) = 1090 mg/m3(250 ppm), based on significantly increased incidences of hyperplasia of the pituitary gland pars distalis in exposed female mice and significantly increased incidences of synctyial alteration of hepatocytes in exposed males. NOAEC (mice) = 326 mg/m3 (75 ppm). At 3260 mg/m3, significantly increased incidences of synctyial alteration of hepatocytes, hepatocellular hypertrophy and hepatocyte necrosis in males and significantly increased incidences of eosinophilic foci of the liver and pituitary gland pars distalis hyperplasia in females were observed. Significantly increased thyroid gland follicular cell hyperplasia and alveolar epithelial metaplasia in both males and females were observed at 3260 mg/m3 (Chan et al. 1998; NTP 1999).
Genotoxicity and related endpoints: in vivoChromosomal aberrations
Negative results:
Rat bone marrow cells collected from rats exposed to a dose equivalent to 239 mg/m3 of xylene containing 18.3% ethylbenzene (300 ppm), 6 hours/day, 5 days/week, for 9, 14, and 18 weeks (no further details available) (Donner et al. 1980)

Micronuclei test
Negative results:
Mouse peripheral lymphocytes collected from male and female B6C3F1 mice exposed to ethylbenzene vapour for 13 weeks (details of this study were described above in the subchronic data set) (NTP 1992, 1999),

Mouse bone marrow cells collected from male NMRI mice exposed to ethylbeneze by intraperitoneal injection of two similar doses, 2 mL/kg-bw (equivalent to 1.74 mg/kg-bw), 24 hours apart. Mice were sacrificed 30 hours after the first injection (Mohtashamipur et al. 1985)

[Additional study: negative results were observed in mouse bone marrow cells with 1-phenylethanol, the major phase I metabolite of ethylbenzene, in NMRI male mice, five per group, administered a single gavage dose of 187.50, 375, or 750 mg/kg of 1-phenylethanol. Animals were sacrificed 24 or 48 hours post-treatment and bone marrow was sampled (Engelhardt 2006)]

Unscheduled DNA synthesis
Negative results:
Mouse liver cells collected from B6C3F1 males exposed to 2175 or 4350 mg/m3 (500 or 1000 ppm ) and females exposed 1631 or 3263 mg/m3 (375 or 750 ppm) of ethylbenzene vapour for 6 hours (Clay 2001).

Non-mammalian sex-linked recessive lethal assay
Negative results:
Drosophila (Donner et al. 1980)
Genotoxicity and related endpoints: in vitroMutagenicity
Positive results:
Gene mutation assay in mouse lymphoma cells without metabolic activation, only at higher dose level (80 µg/mL) that elicited cytotoxicity (McGregor et al. 1988; NTP 1992, 1999)

Negative results:
Ames assays in Salmonella typhimurium strains TA97, TA98, TA100, TA1535 with and without metabolic activation (NTP 1992, 1999; Zeiger et al. 1992); Salmonella typhimurium strains TA98, TA100, TA1535, TA 1537, and TA 1538, Escherichia coli WP2, Wp2uvrA, and Saccharomyces cerevisiae JD1 with and without metabolic activation (Dean et al. 1985); Saccharomyces cerevisiae D7 and XV185-14C without metabolic activation (Nestmann and Lee 1983)

Chromosomal aberrations
Negative results:
Chinese hamster ovary with and without metabolic activation (NTP 1992, 1999); rat liver (RL4) epithelial type cells, with and without metabolic activation (Dean et al.1985)

Micronuclei test
Positive results:
Syrian hamster embryo cells without metabolic activation (Gibson et al. 1997)

Sister chromatid exchange
Positive results:
Marginal effects in human lymphocytes without metabolic activation, at the highest dose (10 mM) that elicited cytotoxicity (Norppa and Vainio 1983)

Negative results:
Chinese hamster ovary cells with and without metabolic activation (NTP 1992. 1999)

Cell transformation assay
Positive results:
Syrian hamster embryo (SHE) cells after exposure to ethylbenzene for 7 days (the results were negative after the cells were exposed to ethylbenzene for 24 hours) (Kerckaert et al. 1996)

Negative results:
Syrian hamster embryo (SA7/SHE) cells after exposure to ethylbenzene for 24 hours and the transformed foci were scored after 6 weeks (Casto and Hatch 1977)

DNA damage (Comet assay)
Positive results:
Single DNA strand breaks in human peripheral blood lymphocytes (Chen et al. 2008)

[Additional studies: Oxidative DNA damage in human p53 tumour suppressor gene fragments (in vitro test) and DNA adducts, 8-oxo-7,8-dihydro-2′dexyguanosine, formation in calf thymus DNA (in vitro test) after exposure to sunlight-irradiated ethylbenzene and in the presence of Cu2+ (Toda et al. 2003) or after exposure to ethylbenzene metabolites, including ethylhydroquinone and 4-ethylcatechol, in the presence of Cu2+ in a dose-dependent manner (Midorikawa et al. 2004)]

Gene conversion
Negative results:
Pseudomonas putida (Leddy et al. 1995)
Developmental toxicityLowest inhalation LOEC = 435 mg/m3(100 ppm), based on significantly increased incidence of extra ribs in rats that were exposed to ethylbenzene during gestation period. Significantly reduced number of live foetuses per litter was observed in rabbits; however, the implantation number and resorption number did not differ significantly from the controls in rabbits. In this study, female Wistar rats (29-33 per group) were exposed to 435 mg/m3 or 4350 mg/m3 (1000 ppm)ethylbenzene via inhalation for 7 hours/day, 5 days/week for 3 weeks. The control group rats were exposed to air. The rats were then mated and exposed daily through 19 days of gestation. The rats that were exposed to air during pregestation period were divided into three groups during gestation exposure period: control (air), 435 mg/m3, and 4350 mg/m3 groups. The rats that were exposed to a low or high concentration of ethylbenzene during pregestation were divided into two groups, respectively, during the gestation exposure period: control (no further exposure during gestation) and exposure group (at the same exposure level as they had before gestation). Female New Zealand white rabbits (21-24 per group) were artificially inseminated and exposed to 0, 435 mg/m3, and 4350 mg/m3 ethylbenzene via inhalation during gestation days 1-24. Maternal toxicity was observed at 4350 mg/m3 in rats, including significantly increased relative and absolute liver, kidney, and spleen weights without pathological changes. A possible reduction in fertility, indicated by the reduction in the percent of sperm-positive rats that were pregnant following pregestational exposure to either concentration, was observed in rats at both exposure levels; however, there was no significant difference in response at 435 and 4350 mg/m3. No significant exposure-related maternal toxicity was observed in exposed rabbits. The significantly increased incidence of extra ribs were also observed in rats that were exposed to a high concentration of ethylbenzene during both pregestation and gestation periods, or during the gestation period only, but not in the rats that were exposed to a low concentration of ethylbenzene during both pregestation and gestation periods. Therefore, the authors considered that the dose-repsonse relationship for this effect at 435 mg/m3 was not consistent. In addition, the authors considered the increased incidence of extra ribs is not a teratogenic response, but rather an indication for teratogenesis at higher exposure levels (Hardin et al. 1981; NIOSH 1981)

[Additional studies: Ungvary and Tatrai 1985; Saillenfait et al. 2003, 2006, 2007; Faber et al. 2007]
Reproductive toxicityInhalation NOAEC for reproductive toxicity (rats) greater than 2174 mg/m3 (500 ppm, the highest concentration tested), based on no significant exposure-related reproductive effects, were observed in this study. In this two-generation study, Crl:CD(SD) IGS BR rats (F0 generation, 30/sex per group; F1 generation, 25/sex per group) were exposed to 0, 109, 435, and 2174 mg/m3 (0, 25, 100, or 500 ppm) ethylbenzene 6 hours/day, 7 days/week, started at least 70 consecutive days before mating. F0 and F1 females continued inhalation exposure throughout mating and gestation day 20. On lactation days 1-4, F0 and F1 females were given either corn oil or ethylbenzene via gavage at doses of 0, 26, 90, and 342 mg/kg per day. Inhalation exposure of these rats was continued on lactation days 5 to 21 (euthanasia time). For F1 animals, inhalation exposure was initiated on postnatal day 22. The F2 generation was not directly exposed. No significant changes in oestrous cycle length, pre-coital intervals, male and female mating and fertility indices, gestation length, spermatogenic endpoints, and reproductive organ weights were observed in exposed rats. The ovarian follicle counts for the F1 females in the 2174 mg/m3 group were similar to the control values. There were no exposure-related deaths or clinical observations in any test group in either generation of animals. The authors defined a NOEC of 435 mg/m3 (100 ppm)and a NOAEC of 2174 mg/m3 for parental systemic toxicity, based on transiently decreased body weight gain in F0 and F1 males at 2174 mg/m3and in F0, but not F1, females at 435 and 2174 mg/m3, significantly increased relative liver weights in both F0 and F1 males and females at 2174 mg/m3, and significantly increased relative kidney weights in both F0 and F1 males at 2174 mg/m3, without pathological changes. In addition, significantly increased absolute and relative thyroid weights in F0, but not F1, males, were observed at 435 and 2174 mg/m3, and significantly increased absolute lung and prostate weights in F0, but not F1, males were observed at 2174 mg/m3, without pathological findings. Although there were significant decreases in oestrous cycle length in F0 females at 2174 mg/m3, the results were not significant in F1 females and the oestrous cycle length in F0 rats was similar to those historical controls. The authors considered that these effects were not ethylbenzene exposure related. Neurobehavioral development of one F2 offspring was assessed in a functional observational battery (FOB) (PND 4, 11, 22, 45, and 60), motor activity sessions (PND 13, 17, 21, and 61), acoustic startle testing (PND 20 and 60), a Biel water maze learning and memory task (initiated on PND 26 or 62), and in evaluations of whole-brain measurements and brain morphometric and histologic assessments (PND 21 and 72). There were no alterations in FOB parameters, motor activity counts, acoustic startle endpoints, or Biel water maze performance in offspring attributed to parental ethylbenzene exposure at the highest exposure level tested (Stump 2004a; Faber et al. 2006, 2007).

[Addition studies: Hardin et al.1981; NIOSH 1981; Cragg et al. 1989; NTP 1992]

Oral LOEL = 500 mg/kg-bw, based on significantly decreased luteinizing hormone and 17 ß-estradiol levels accompanied by uterine changes such as increased stromal tissue with dense collagen bundles and reduced lumen. In this study, CFY rats were given 500 or 1000 mg/kg ethylbenzene orally in the morning of oestrus, two dioestruses, and pro-oestrus. (The study report is very limited. The test dosage was not clearly stated as the ratio of test material weight versus body weight or versus food weight, but was assumed to be the test maternal weight versus body weight.) The author concluded that ethylbenzene exposure blocked the ovarian cycle and this blocking occurs during dioestrus, based on the vaginal smears and the structure of the uterine wall (Ungváry 1986)
ImmunotoxicityInhalation NOAEC for immunotoxicity (rats) = 2174 mg/m3 (500 ppm, the highest concentration tested), based on no treatment-related effects on functional ability of the hormonal component of the immune system in rats as measured by splenic IgM antibody-forming cell response to the T-dependent antigen, sheep erythrocytes. In this study, SD rats were exposed to doses equivalent to 0, 109, 435, or 2174 mg/m3(0, 25, 100, 500 ppm) ethylbenzene vapour for 6 hours/day for 28 consecutive days. The rats then received a single intravenous immunization injection of sheep red blood cells approximately 4 days prior to the scheduled necropsy. No treatment-related effects on survival, clinical signs, body weight, feed consumption, haematology parameters, or IgM antibody-forming cell response were observed. Relative liver and kidney weights were increased in the 2174 mg/m3 group (Stump 2004b; Li et al. 2010)
Neurotoxicity/ototoxicityLowestacute inhalation LOEC for neurotoxicity (rats) greater than or equal to 1740 mg/m3(400 ppm), based on a moderate activation in motor behaviour in male CFY rats (8 per group) exposed to ethylbenzene vapour at concentrations between 1740 to 6514 mg/m3(400 and 1500 ppm) for 4 hours. The minimum narcotic concentration for ethylbenzene was 9466 mg/m3 (2180 ppm ) (Molnar et al. 1986)

[Additional studies: Yant et al. 1930; Gerarde 1960; Ivanov 1962; Tegeris and Baltser 1994].

Lowest short-term inhalation LOAEC for ototoxicity (rats) = 1740 mg/m3(400 ppm), based on ototoxic effects, defined as increased auditory thresholds and outer hair cell loss after exposure to ethylbenzene 8 hours/day for 5 days. In this study, rats were exposed to ethylbenzene at 0, 1305, 1740, 2393 mg/m3 (0, 300, 400, and 550 ppm) for 8 hours/day for 5 consecutive days. Three to six weeks after the exposure, auditory function was tested by measuring compound action potentials (CAP) in the frequency range of 1-24 kHz and 2f1-f2 distortion product otoacoustic emissions (DPOAEs) in the frequency range of 4-22.6 kHz. At 1740 mg/m3, auditory thresholds were increased by 15 and 16 dB at 12 and 16 kHz, respectively, and at 2393 mg/m3 by 24, 31, and 22 dB at 8, 12, and 16 kHz, respectively. DPOAE amplitude growth with stimulus level was affected only after exposure to 2393 mg/m3 at 5.6, 8, and 11.3 kHz. Outer hair cell (OHC) loss was found in two of the five examined locations in the cochlea. At 1740 mg/m3, 25% OHC loss was found at the 11- and 21-kHz region. The highest concentration evoked 40 and 75% OHC loss at the 11- and 21-kHz location, respectively. NOAEC for ototoxicity = 1305 mg/m3 (300 ppm) (Cappaert et al. 2000). In addition, ethylbenzene exposure induced significant depletion of striatal and tubero-infundibular dopamine levels in rabbits at concentration of 3260 mg/m3 (750 ppm) and above (Romanelli et al.1986; Mutti et al.1988)

[Additional studies: Andersson et al.1981; Frantik et al. 1994; Cappaert et al.1999, 2001, 2002].

Lowest short-term oral LOAEL for ototoxicity (rats, 2 weeks, gavage) = 900 mg/kg-bw per day, based on irreversible hearing loss measured by behavioural or electrophysiological methods and associated with damage to outer hair cells in cochlea (Gagnaire and Langlais 2005)

Lowestsubchronic inhalation LO(A)EC for ototoxicity (rats) = 870 mg/m3(200 ppm, the lowest concentration tested), based on dose-dependent outer hair cell losses (hearing loss) during the recovery period. In this study, SD rats were exposed to 0, 870, 1739, 2609, or 3478 mg/m3(0, 200, 400, 600, or 800 ppm) ethylbenzene vapour for 6 hours/day, 6 days/week for 90 days with an 8-week post-exposure recovery period. Outer hair cell losses with increasing severity (4% to nearly 100%, respectively) in the rats that received 870 to 3478 mg/m3 ethylbenzene were observed. Concentrations of 1739 mg/m3 and greater produced significantly higher audiometric thresholds that did not recover 8 weeks after exposure ceased (Gagnaire et al. 2007)

[Additional study: Faber et al., 2007, details included in the above Reproductive toxicity session]

Lowest subchronic oral LOEL for neurotoxicity (rats) = 750 mg/kg-bw per day, based on significantly decreased landing foot-splay in males and significantly increased motor activity in females (Mellert et al. 2007). Subchronic oral NOEL for neurotoxicity = 500 mg/kg per day, based on no treatment-related adverse neurotoxicological effects observed in SD rats administered 0, 50, 250, and 500 mg/kg-bw per day ethylbenzene by gavage daily for 90 days (Barnett 2006). Similarly, neurobehavioural changes, as measured by FOB, including acoustic reaction, and motor activity evaluations, were not observed in rats exposed to ethylbenzene up to 500 mg/kg-bw per day for 90 days (Li et al. 2010).
IrritationEthylbenzene is a mucous membrane irritant. Guinea pigs exposed to 0.2% ethylbenzene vapour for 1 minute experienced moderate eye and nasal irritation, while exposure to 0.1% ethylbenzene vapour caused slight basal irritation that ceased after 30 minutes (Lewis 1992). Instillation of undiluted ethylbenzene in rabbit eyes caused conjunctival irritation (Wolf et al.1956; Smyth et al.1962) and moderate corneal injury (Smyth et al. 1962).

Ethylbenzene is a moderate skin irritant. Uncovered application of undiluted ethylbenzene induced moderate irritation and necrosis in rabbit skin (Wolf et al.1956; Smyth et al. 1962)
Footnote Table H1 a

Definitions: LC50 = median lethal concentration; LD50 = median lethal dose; LOAEC = lowest-observed-adverse-effect concentration; NOAEC = no-observed-adverse-effect concentration; LOEC = lowest-observed-effect concentration; NOEC = no-observed-effect concentration; LO(A)EL = lowest-observed-(adverse)-effect level; NOEL = no-observed-effect level.

Return to footnote Table H1[a] referrer

Table H2. Information for Ethylbenzene in humans
EndpointLowest effect levelsFootnote Table H2[a]/Results
IrritationHuman volunteers exposed to ethylbenzene vapour reported severe eye irritation at 4348 mg/m3 (1000 ppm) and above (Yant et al. 1930; Cometto-Muñiz and Cain 1995) and nasal and throat irritation at 8696 mg/m3 (2000 ppm) and above (Yant et al. 1930). No eye irritation or other effects were observed at 870 mg/m3 (200 ppm) and below (Gerarde 1963; Bardodej and Bardodejova 1970; Moscato et al.1987).
SensitizationNo skin sensitization reaction occurred after dermal application of 10% ethylbenzene in 25 human volunteers (Kligman 1974)
Acute toxicityHumans incidentally exposed to ethylbenzene above the occupational limit value (100 ppm, equivalenet to 435 mg/m3) reported central nervous system depression, such as fatigue, sleepiness, and headache, in addition to eye and respiratory tract irritation (Bardodej and Bardodejova 1970). Dizziness was also reported in human subjects exposed to 8696 mg/m3 (2000 ppm) ethylbenzene for 6 minutes (Yant et al. 1930).
Repeated exposure toxicityA historical cohort was conducted in the United States among 560 styrene-production and polymerization workers who had been employed for at least 5 years on May 1, 1960. The workplace exposure included styrene, benzene, ethylbenzene, and other chemicals. Mortality was monitored from May 1, 1960 or the 10th anniversary in the plant through the end of 1975. Overall, 83 deaths were observed versus 106.41 expected from the general population; 17 died from cancer versus 21.01 expected, including nine from lung cancer (6.99 expected), one from leukaemia (0.79 expected), and one from lymphoma (1.25 expected) (Nicholson et al. 1978).

A cross-sectional study investigated the blood and urine samples of 35 spraymen at six workplaces in two plants in Germany. The workers were varnishing and priming vehicles and special metal pieces, and had been exposed to solvent mixtures, mainly containing o-, m-, p-xylene, ethylbenzene, and toluene, for 2 to 24 years. Altered blood cell counts were observed in the spraymen. On average, increased lymphocytes and decreased erythrocytes and haemoglobin levels were observed in 31 exposed workers compared with matched pairs (controls) (Angerer and Wulf 1985).

A biomonitoring study was conducted among 200 ethylbenzene production workers in Czechoslovakia for 20 years. The exposure levels were measured by the mandelic acid concentrations in urine samples, which never exceeded 3.25 mMol/L (500 mg/L). The biological limit for medanilic acid was established at 6.5 mMol/L (1000 mg/L). No altered haematological parameters or serum enzymes as an indication of liver function were detected in the workers. No case of malignancy has been recored over the last 10 years in this facility (Bardodej and Círek 1988).

A cross-section study was conducted among 105 German house painters employed for at least 10 years who were exposed to solvent mixtures in paints and lacquers, including ethylacetate (CMax, 50 ppm), toluol (CMax, 15 ppm), butylacetate (CMax, 11 ppm), methylisobutylketone (CMax, 11 ppm), xylene (CMax, 7 ppm), and ethylbenzene (CMax, 3 ppm, equivalent to 13.05 mg/m3). The control group comprised 53 non-painters, who were matched with age, training, and socio-economic status. The neurophysiologic examinations (electroencephalography and nerve conduction velocity) did not reveal any significant differences between the painters and the control group. As well, no changes in certain brain structures (ventricular diameter, cellar media index) or cerebral atrophy were observed in the painters. In the neurobehavioural tests, significant differences in the "change of personality" and "short term memory capacity" were observed in the painters with repeated prenarcotic symptoms at the workplace (Triebig et al. 1988).

A study reported nerve conduction effects in ethylbenzene workers. Minor changes in evoked potential and nerve conduction velocity were found in 22 workers exposed to ethlybenzene concentrations ranging from 0.43 to 17.2 mg/m3 (0.1 to 4 ppm) for 4 to 20 years. These workers also received exposure to styrene (about 1.5 ppm) (Lu and Zhen 1989).

A historical cohort study was conducted in a rubber factory in Mexico among 48 workers who were exposed to hydrocarbons for 2-24 years; 42 unexposed workers served as controls. The hydrocarbons included ethylbenzene (220.7-234 mg/m3), benzene (31.9 -47.8 mg/m3), toluene (189.7-212.5 mg/m3), and xylene (47-56.4 mg/m3). Significantly increased abnormalities in the semen of exposed workers, including increased normozoospermia, altered sperm viscosity, decreased sperm liquefaction, increased nonspecific sperm aggregation, decreased sperm counts, and motile sperms and normal sperm percentages were observed (De Celis et al. 2000).

A historical cohort study was conducted among 303 workers from four Polish paint and lacquer enterprises who were exposed to solvents for at least 6 months. The control group contained 214 unexposed workers. The exposed workers were further divided into two groups: solvent exposure only (207 workers) and solvent plus noise exposure (96 workers). The solvents contain xylene (1.0-110.0 mg/m3), ethyl acetate (0.0-120.0 mg/m3), white spirit (0.0-563.0 mg/m3), toluene (0.0-92.5 mg/m3), butyl acetate (0.0-285.5 mg/m3), and ethylbenzene (0.0-65.6 mg/m3). The relative risks (RR) of hearing loss in both exposed groups were significantly increased (RR 2.8, 95% CI 1.8-4.3 and RR 2.8, 95% CI 1.6-4.9, respectively) in a wide range of frequencies (2-8 kHz). No additional risk in the solvent plus noise exposure group was found. Hearing thresholds were also significantly increased in both exposed groups (Sliwinska-Kowalska et al. 2001).

A cross-sectional study was conducted from workers in two different petrochemical plants in China. From these two plants, 246 and 307 male workers were classified into two ethylbenzened-exposed groups: petrochemical group 1 and group 2. Two reference groups were used for comparison: a power station group (290 male workers from a power station exposed to noise level similar to petrochemical workers) and a control group (327 office personnel in these petrochemical plants). Air ethylbenzene concentrations were 122.83±22.86 mg/m3 and 134.64±31.97 mg/m3in petrochemical group 1 and 2, respectively. The levels of other volatile aromatic hydrocarbons (styrene, bezene, toluene and xylene) were below the limit of detection. The prevalence of hearing loss 25 dB or more was higher in petrochemical group 1 (78.4%) and group 2 (80.1%) than that in the power station (56.9%) and control (5.2%) groups, with age, cigarette smoking and alcohol drinking adjusted. Based on neurobehavioural core test battery, descending neurobehavoural function involving adverse alteration of short-term memory, quick hand movement and hand-eye coordination were observed in exposed workers compared to controls and these changes started in the third year of working age. Acetylcholinesterase activity in blood was signficiantly decreased compared to the control group (Zhang et al. 2013).
GenotoxicityDNA adduct formation, DNA single strand breaks, and sister chromatid exchange were not detected in 25 workers occupationally exposed to a mixture of styrene, benzene, ethylbenzene, xylenes, and toluene in a styrene production plant in the former German Democratic Republic. However, the kinetochore-positive micronuclei (suggestive of aneuploidy induction) in peripheral lymphocytes were significantly increased in exposed workers compared with the controls (25 age- and sex-matched unexposed healthy workers in the same company). The ethylbenzene levels in all areas of the factory ranged from 365 to 2340 µg/m3 (0.08-0.53 ppm). Biomonitoring data measured by the metabolites of these aromatic hydrocarbons in the urine samples of the exposed workers indicated that the workers were exposed mainly to xylene and ethylbenzene (Holz et al. 1995).

Significantly increased chromosomal aberrations were detected in 39 male workers occupationally exposed to ethylbenzene and benzene in a petrochemical plant. The concentrations of ethylbenzene and benzene in the workplaces ranged from 0.2 to 13.1 and from 0.4 to 15.1 mg/m3, respectively. The control group consisted of 55 matched subjects (Sram et al. 2004).

Levels of 8-hydroxydeoxyguanosine (8-OHdG) in urine were measured among 64 male workers (15 spray painters exposed to paint, two non-exposed groups: 19 sandblasting workers and 30 office staff). Urinary 8-OHdG was used as biomarker of oxidative DNA damage. Personal exposure to xylene and ethylbenzene (measured by urine levels of mandelic acid) in air were also collected using diffusive samplers. Urinary 8-OHdG levels displayed greater DNA damage in spray painters compared to other unexposed groups and their holiday leave samples. A significant correlation was found between urinary 8-OHdG and the exposure to ethylbenzene. Authors did acknowledge that ethylbenzene exposure could not explain all urinary 8-OHdG measured and that other components of paint could be involved in the increased levels (Chang et al 2011).
Footnote Table H2 a

See description of footnotes in Table H1.

Return to footnote Table H2[a] referrer

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