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Appendices of the Screening Assessment

Acetone
Chemical Abstracts Service Registry Number
67-64-1

Environment Canada
Health Canada
September 2014

Table of Contents

Appendix A: Concentrations of Acetone in Environmental Media and Food

Table A1-1: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, Ambient air; National Air Pollution Surveillance (NAPS)Program 2000–2009 (Environment Canada 2011b)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range
(μg/m3)		 Concentration 95th percentile (μg/m3)
Outdoors, all stations 24 h 3688 2.895 0.007 - 35.167 6.55
Outdoors, all stations 4 h 5754 2.931 0.003 - 80.228 12.39
Outdoors, Egbert, ON – agricultural 4 h 494 5.679 0.600 - 80.228 18.2
Outdoors, Windsor, ON – rural 24 h 285 2.829 0.800 - 22.206 6.617
Outdoors, Winnipeg, MB –commercial 24 h 460 3.101 0.025 - 13.678 5.854
Outdoors, Port Moody, Metro Vancouver, BC – industrial 24 h 299 3.873 0.05 - 14.202 8.946
Table A1-2: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, Residential homes, non-smoking participants, adults, 2005; Windsor Ontario Exposure Assessment Study (WOEAS) (Health Canada 2010a)
Season Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range (μg/m3) Concentration 95th percentile (μg/m3)
Winter Personal 24 h 225 34.8 9.7 - 814.5 135.8
Winter Indoor 24 h 232 29.3 5.9 - 673.3 134.5
Winter Outdoor 24 h 200 3.8 1.5 - 18.3 9.4
Summer Personal 24 h 206 116.1 18.2 - 1871.9 475.9
Summer Indoor 24 h 217 173.8 0.01 - 3755.5 647.2
Summer Outdoor 24 h 216 10.1 3.9 - 51.6 19.8
Table A1-3: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, Residential homes, non-smoking participants, children, 2006; Windsor Ontario Exposure Assessment Study (WOEAS) (Health Canada 2010a)
Season Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range/
(μg/m3)		 Concentration 95th percentile (μg/m3)
Winter Indoor 24 h 224 48.0 8.6 - 1380.7 194.3
Winter Outdoor 24 h 215 3.0 1.2 - 27.2 7.4
Summer Indoor 24 h 211 134.8 9.5 - 1977.5 538.9
Summer Outdoor 24 h 214 10.4 3.2 - 544.1 71.0
Table A1-4: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, residential homes – smoking/non-smoking participants, 2007, Regina Indoor Air Quality Study (RIAQS) (Health Canada 2010b)
Season Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range (μg/m3) Concentration 95th percentile (μg/m3)
Winter Indoor – all houses 24 h 104 36.5 8.6 - 436.9 120.3
Winter Indoor – all houses 5 days 89 45.2 7.5 - 451.9 127.5
Winter Indoor – smoker 24 h 21 37.0 11.5 - 436.9 113.1
Winter Indoor – smoker 5 days 19Footnote Appendix A Table A1-4[a] 45.2 10.1 - 451.9 451.9
Winter Indoor – non-smoker 24 h 83 35.4 8.6 - 192.6 120.3
Winter Indoor – non-smoker 5 days 70 45.2 7.5 - 202.9 127.5
Winter Outdoor – all houses 24 h 94 3.4 0.6 - 36.0 9.6
Winter Outdoor – smoker 24 h 17[a] 3.1 1.2 - 13.8 13.8
Winter Outdoor – non-smoker 24 h 77 3.5 0.6 - 36.0 9.6
Summer Indoor – all houses 24 h 105 41.1 11.3 - 1451.7 156.5
Summer Indoor – all houses 5 days 101 51.7 13.0 - 867.9 318.2
Summer Indoor – smoker 24 h 13[a] 32.4 14.0 - 101.8 101.8
Summer Indoor – smoker 5 days 13[a] 52.7 23.5 - 124.1 124.1
Summer Indoor – non-smoker 24 h 91 42.4 11.3 - 1451.7 241.3
Summer Indoor – non-smoker 5 days 88 51.7 13.0 - 867.9 327.6
Summer Outdoor – all houses 24 h 108 8.6 3.0 - 33.0 21.1
Summer Outdoor – all houses 5 days 97 11.0 4.7 - 303.4 106.4
Summer Outdoor – smoker 24 h 12[a] 7.2 3.4 - 18.4 18.4
Summer Outdoor – smoker 5 days 14[a] 12.9 4.7 - 245.9 245.9
Summer Outdoor – non-smoker 24 h 95 8.6 3.0 - 33.0 22.2
Summer Outdoor – non-smoker 5 days 82 10.8 5.3 - 303.4 102.2
Table A1-5: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, residential homes –non-smoking participants, 2009, Halifax Indoor Air Quality Study (HIAQS) (Health Canada 2011)
Season Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range (μg/m3) Concentration 95th percentile (μg/m3)
Winter Indoor 24 h 312 21.8 4.0 - 2188.0 108.7
Winter Outdoor 24 h 286 2.8 1.2 - 25.3 6.0
Summer Indoor 24 h 331 26.5 less than 0.06 - 1285.0 288.5
Summer Outdoor 24 h 324 4.7 2.1 - 50.2 9.9
Table A1-6: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, residential homes – smoking/non-smoking, Winter 2002-2003, Ottawa – (Zhu et al. 2005)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range
(μg/m3)		 Concentration 95th percentile (μg/m3)
Indoor 100 min 75 28.5 0.015 - 455.9 90th: 76.4
Outdoor 100 min 74 0.2 0.015 - 15.3 90th: 3.6
Table A1-7: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, residential homes, 1999-2001, Texas, Los Angeles, New Jersey – (Relationship of Indoor, Outdoor and Personal Air [RIOPA] study; Weisel et al. 2005)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range
(μg/m3)		 Concentration 95th percentile (μg/m3)
Indoor – passive 48 h 398 8.25 less than 0.4 - ns 45.8
Outdoor – passive 48 h 395 4.39 less than 0.4 - ns 19.6
Personal – passive, adult 48 h 409 8.36 less than 0.4 - ns 57.7
Personal – passive, child (15–19 years) 48 h 169 11.5 less than 0.4 - ns 81.0
In-vehicle 55–459 min 115 4.08 less than 13.38 - ns 45.0
Table A1-8: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, residential homes, 1997-2003; New York – (NYSDOH 2005)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range (μg/m3) Concentration 95th percentile (μg/m3)
Indoor 2 h 227 21   less than 0.25 - ns 90th: 110
Outdoor 2 h 114 6.4 less than 0.25 - ns 90th: 44
Table A1-9: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, suburban and rural homes, 2003-2006; New Jersey – (Weisel et al. 2008)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range (μg/m3) Concentration 95th percentile (μg/m3)
Indoor (94/100 detected) 24 h 100 34.5 less than 12 - 2900 190
Table A1-10: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, residential homes and workplaces, fall 1992; New Jersey, Pennsylvania – (Heavner et al. 1996)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range
(μg/m3)		 Concentration 95th percentile (μg/m3)
Indoor – non-smoking home 14 h 60 33.88 2.81 - 389.71 ns
Indoor – smoking home 14 h 29 39.33 19.73 - 664.99 ns
Indoor – non-smoking work 7 h 51 28.53 5.48 - 414.30 ns
Indoor – smoking work 7 h 28 60.53 8.26 - 21 083.81 ns
Table A1-11: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, Office buildings, 1995–1998 summer and winter; United States – (Building Assessment Survey and Evaluation [BASE] study; Girman et al. 1999)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range
(μg/m3)		 Concentration 95th percentile (μg/m3)
Indoor 8–10 h 56 29 7.1 - 220 ns
Table A1-12: Ambient, indoor and personal air concentrations of acetone in Canada and elsewhere, 2003–2008, 11 cities (European Indoor Air Monitoring and Exposure Assessment [AIRMEX] study; 2011 email Geiss 2011to Existing Substances Risk Assessment Bureau, unreferenced; Geiss et al. 2011)
Study, location and type of sample    Sample duration No. of samples Concentration Median
(μg/m3)		 Concentration Range
(μg/m3)		 Concentration 95th percentile (μg/m3)
Outdoor – passive 7 days 66 4.5 0.3 - 12.8 9.3
Indoor – passive, residential homes 7 days 88 31 10.4 - 165.1 94.2
Indoor – passive, public buildings/schools 7 days 129 19.5 1.4 - 336.8 59.6
Personal – passive 3 days 45 31 11.8 - 225.9 66.7
Table A2-1: Concentrations of acetone in water in Canada and elsewhere, drinking water
Location Sampling period No. of samples Mean (μg/L) Range (µg/L) Reference
Ottawa, Ontario Fall 2002 71 11.0

less than 2–131

P95 = 48

 2003 personal communication from J. Zhu Health Canada Chemistry Research Division to Existing Substances Risk Assessment Bureau, unreferenced
24 US communities 2002–2005 150 ns less than 6–11.73 USGS 2007
Lower Rio Grande Valley, TX, USA 1993 8 nd nd–10.7 US EPA 1994
Private and community wells in Wisconsin, USA 1980–1984 ns nd less than nd Krill and Sonzogni 1986
Canada (potable water treatment facilities) 1979 30 plants nd nd ( less than 1000) Otson et al. 1982
Seattle, Washington, USA 1975 ns ns Detected – 1 US EPA 1975
Table A2-2: Concentrations of acetone in water in Canada and elsewhere, surface water
Location Sampling period No. of samples Mean (μg/L) Range (µg/L) Reference
9 US communities 2002–2005 241 -- less than 7 USGS 2007
Streams in New York and New Jersey, USA January 1997 42 2.6 median estimated Max: 6.6 O’Brien et al. 1997
Seawater ns ns ns 5–53 Corwin 1969
Storm water runoff, 20 industrial sites, North Carolina, USA 1993–1994 20 ns

less than 100 (7 sites)

greater than 100 (2 sites)

 Line et al. 1997
Table A2-3: Concentrations of acetone in water in Canada and elsewhere, groundwater
Location Sampling period No. of samples Mean (μg/L) Range (µg/L) Reference
15 US communities 2002–2005 223 ns less than 6–68.36 USGS 2007
In vicinity of 34 disposal sites from 8 American regions ns 254 ns

Detected

(not quantified)

 Plumb 1991
New Jersey, USA ns ns ns Max: 3000 US EPA 1980
Residential well water in vicinity of a landfill site, Delaware, USA 1977 6 ns 0.2–0.7 DeWalle and Chian 1981
Groundwater from landfill sites in Minnesota, USA, with good water quality ns 7 ns nd–25 Sabel and Clark 1984
Groundwater from sites in Minnesota, USA, contaminated with landfill leachate ns 13 ns nd–3000 Sabel and Clark 1984
Table A2-4: Concentrations of acetone in water in Canada and elsewhere, wastewater
Location Sampling period No. of samples Mean (μg/L) Range (µg/L) Reference
Industrial wastewater, 4000 sites, USA ns ns 2500 (highest median value, printing and publishing plants) 138–37 709 OECD 1999
Industrial and municipal landfill leachate from sites in the USA 1982, 1984 ns ns 50–62 000 Brown and Donnelly 1988
Landfill leachate, Delaware, USA 1977 1 43 700 na DeWalle and Chian 1981
Leachate from sites in Minnesota, USA ns 6 ns 140–13 000 Sabel and Clark 1984
Septic tank effluent from septic tank serving 97 homes in Tacoma, Washington, USA 1982 7 (24 h composite samples) 70 300 (one measurement only) ns DeWalle et al. 1985
Table A3-1: Concentrations of acetone detected in foods in Canada and elsewhere, dairy Footnote Appendix A Table A3-1 [a]
Item sampled Sampling period No. of samples Mean concentration (µg/kg) Concentration range (µg/kg) Reference
Whole, 1% and 2% commercial milk samples from Las Vegas, Nevada, USA January–February 2002

19 (whole)

8 (2%)

5 (1%)

29

30

30

5–42

22–36

25–36

 Hiatt and Pia 2004
Raw (unpasteurized) milk from cows in southern Ontario dairy herds January–December 1999 10 375 cows

1280

(raw milk basis)

0–269 900

(raw milk basis)

 Wood et al. 2004
Raw milk from hyperketonemic cows in SwedenFootnote Appendix A Table A3-1 [b] 26 h Samples from 8 cows ns 18 048–219 351 Andersson and Lundstrom 1984
Butter from Oregon, USA ns 1 130 ns Siek and Lindsay 1970
Cheddar cheese from USA ns 3

8500

(approximate)

 ns Day et al. 1960
Cheese ns ns ns 100–8500 Maarse and Visscher 1989
Yoghurt ns ns ns 300–58 000 Maarse and Visscher 1989
Table A3-2: Concentrations of acetone detected in foods in Canada and elsewhere, fruit
Item sampled Sampling period No. of samples Mean concentration (µg/kg) Concentration range (µg/kg) Reference
Strawberries ns ns ns 1300–3000 van Straten and Maarse 1983
Currants ns ns ns Max: 1200 Maarse and Visscher 1989
Black currants from Sweden Harvested in 1962; stored until 1964 ns 2000 ns Andersson and von Sydow 1966
Mangos from Sri Lanka ns 3 cultivars Trace ns MacLeod and Pieris 1984
Apples from Belgium ns ns 600 (dry weight) ns Feys et al. 1980
Apples ns ns ns 130 Maarse and Visscher 1989
Table A3-3: Concentrations of acetone detected in foods in Canada and elsewhere, vegetables
Item sampled Sampling period No. of samples Mean concentration (µg/kg) Concentration range (µg/kg) Reference
Canned and frozen sweet corn from Oregon, USA ns 7 1500 300–2400 Bills and Keenan 1968
Carrots from Oregon, USA 1969 growing season 3 240 200–310 Heatherbell et al. 1971
Carrots ns ns ns 100–800 Maarse and Visscher 1989
Common, lima and mung beans and soybeans (country of origin not specified) ns ns 880 260–2000 Lovegren et al. 1979
Split peas (country of origin not specified) ns ns 530 ns Lovegren et al. 1979
Lentils (country of origin not specified) ns ns 230 ns Lovegren et al. 1979
Soybean ns ns ns 4–1600 Maarse and Visscher 1989
Potato chips from USA  ns ns

110 (fresh)

255 (stale)

 ns Mookherjee et al. 1965
Tomatoes from Indiana, USA ns 3 varieties 810 640–1030 Nelson and Hoff 1969
Tomatoes ns ns ns 600–16 000 van Straten and Maarse 1983
Table A3-4: Concentrations of acetone detected in foods in Canada and elsewhere, cereal products
Item sampled Sampling period No. of samples Mean concentration (µg/kg) Concentration range (µg/kg) Reference
Bread ns ns ns 680–10 100 Maarse and Visscher 1989
Rice ns ns ns 400 van Straten and Maarse 1983
Table A3-5: Concentrations of acetone detected in foods in Canada and elsewhere, beverages
Item sampled Sampling period No. of samples Mean concentration (µg/kg) Concentration range (µg/kg) Reference
Beer ns ns ns 20–1700 van Straten and Maarse 1983
Beer from USA ns ns ns 600–1400 Rosculet and Rickard 1968
Cider apple juice from Britain 1971–1974 4 cultivars 109.5 µg/L 6–200 µg/L Williams et al. 1980
Brandy ns ns ns 4000 Maarse and Visscher 1989
Table A4: Concentration of acetone in soil outside Canada
Location Sampling period No. of samples Detection limit (ng/g) Mean concentration (ng/g) Reference
Vega Alta Public Supply well sites, Puerto Rico ns ns ns 9500 ATSDR 1988
Summit National Site, Ohio, USA (toxic waste site) ns ns ns 9484 US EPA 1988

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Appendix B: Upper-bounding Estimates of Daily Intake of Acetone by the General Population of Canada

Table B1: Upper-bounding estimates of daily intake of acetone by the general population of Canada, birth to 4 years of age
Route of exposure 0–6 monthsFootnote Appendix B Table B1[a],Footnote Appendix B Table B1[b],Footnote Appendix B Table B1 [c]Breast fed 0–6 months[a],[b],[c]Formula fed 0–6 months[a],[b],[c]Not formula fed 0.5–4 yearsFootnote Appendix B Table B1[d] 5–11 years[a] 12–19 years[b] 20–59 years[c] 60+ years[d]
AirFootnote Appendix B Table B1 [e] 133.3 133.3 133.3 285.5 222.6 126.6 108.7 94.5
Drinking waterFootnote Appendix B Table B1[f] Not applicable 5.1 1.3 0.6 0.6 0.3 0.3 0.3
Food and beveragesFootnote Appendix B Table B1[g] Not applicable 5.1 396.2 363.8 276.5 173.8 148.4 126.0
SoilFootnote Appendix B Table B1[h] 0.04 0.04 0.04 0.06 0.02 4.8 × 10−3 4.0 × 10−3 4.0 × 10−3
Total intake 133.3 138.4 530.7 650.0 499.7 300.7 257.4 220.8

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Appendix C: Estimates of Intake to Acetone from the Use of Cosmetic Products and Household Products

Table C1: Concentrations of acetone in air and inhalation intake estimates to acetone via the use of household products
Product Acetone concentration (%) Peak event Time
(min)		 Peak event Concentration (mg/m3) Mean event Time
(min)		 Mean event Concentration (mg/m3) 4 h TWAFootnote Appendix C Table C1 [a]Concentration (mg/m3) Estimated intake for adult CanadianFootnote Appendix C Table C1 [b]
(mg/kg-bw per event)
Spray paint 60 15 4415 20 2788 232 9
Concrete sealant 25 60 3830Footnote Appendix C Table C1[c] 60 2105 526 20
Cleaner/ degreaser 100 10 1500 10 762 32 1.2
Table C2: Estimated intake of acetone for an adult Canadian via the use of acetone as a cleaner
Product Acetone concentration (%) Dermal
(mg/kg-bw per event)		 Inhalation
(mg/kg-bw per event)		 Total
(mg/kg-bw per event)
Cleaner/ degreaser 100 0.4 1.2 1.6
Table C3: Concentrations of acetone in air from the use of cosmetic products
Product Acetone concentration (%) Peak event Time
(min)		 Peak event Concentration (mg/m3) Mean event Time (min) Mean event Concentration (mg/m3) 4 h TWAFootnote Appendix C Table C3 [a]Concentration (mg/m3)
Nail remover 100 30 123 30 64 8.4
Hairspray 30 0.25 209 25 141 15
Face mask 100 0.33 117 25 79 8.7
Table C4: Estimated intake of acetone for an adult Canadian via the use of cosmetic products
Product Acetone concentration (%) DermalFootnote Appendix C Table C4 [a]12–19 years (mg/kg-bw per event) Dermal[a] 20–59 years (mg/kg-bw per event) InhalationFootnote Appendix C Table C4 [b]12–19 years (mg/kg-bw per event) Inhalation[b] 20–59 years (mg/kg-bw per event) Total 12–19 years (mg/kg-bw per event) Total 20–59 years (mg/kg-bw per event)
Nail remover 100 0.58 0.56 0.37 0.32 0.95 0.88
Hairspray 30 N/A N/A 0.67 0.58 0.67 0.58
Face mask 100 N/A 0.04 N/A 0.33 N/A 0.37
Face cleanser 10 0.03 0.06 N/A N/A 0.03 0.06
Face Moisturizer 0.3 0.11 0.09 N/A N/A 0.11 0.09
Table C5: Detailed algorithms for intake estimatesFootnote Appendix C Table C5[a]
Product type Assumptions Estimated concentrations and daily intakes
Spray paint

Concentration of acetone in spray paint: 60%, maximum concentration of acetone found in spray paint (HPD 1993– )

Applied amount: 300 g, entire can (Bremmer and van Engelen 2007)

Room volume: 34 m3 (Bremmer and van Engelen 2007), similar to small garages in Canada (reported sizes range from 26 m3 in northern Canada to 102 m3 in southern Canada) (contractor report prepared for Existing Substances Risk Assessment Bureau, 2011, unreferenced)

Ventilation rate: 1.5/h, well ventilated (Bremmer and van Engelen 2007)

Emission rate = (300 g/15 min) × 0.6 fraction acetone = 12 g/min

Room supply air exchange rate (AER) = (1.5/h × 34 m3)/60 min = 0.85 m3/min

Estimated TWA concentration in air using Industrial Hygiene Model (IHMod) “Well-mixed Room Model with a Constant Emission Rate” (AIHA 2009a):

  • contaminant mass emission rate: 12 000 mg/min
  • room supply AER: 0.85 m3/min
  • room volume: 34 m3
  • release duration: 15 min (Bremmer and van Engelen2007)
  • exposure duration: 20 min (Bremmer and van Engelen2007)
  • percentage losses through sorption or chemical degradation: 0
  • initial concentration of acetone in air: 0 mg/m3
  • concentration of acetone in inflow air: 0 mg/m3

Model output:

Peak concentration, 15 min

= 4415 mg/m3

Mean event concentration, 20 min

= 2788 mg/m3
Concrete sealant

Concentration of acetone in concrete sealant: 25% weight/weight basis, maximum value found (Deco-Crete Supply 2010a)

Applied amount: 3.8 L, based on product application directions (400 ft2/gallon; Deco-Crete Supply 2010b)

Density of paint: 0.92 g/mL (Deco-Crete Supply 2010a)

Application duration: 60 min (professional judgment)

Ventilation rate: 0.6/h (standard room; Bremmer and van Engelen 2007)

Mass acetone applied = 3.8 L × 0.92 g/mL × 0.25 wt. fraction = 874 g

Emission rate = mass applied ÷ drying time = 874 g/120 min = 7300 mg/min

Room supply AER = (0.6/h × 86 m3)/60 min = 0.86 m3/min

Estimated TWA concentration in air using IHMod “Well-mixed Room Model with a Constant Emission Rate” (AIHA 2009a):

  • contaminant mass emission rate: 7300 mg/min
  • room supply AER: 0.86 m3/min
  •  room volume: 86 m3 (37.5 m2  × 2.3 m high) (professional judgment)
  • release duration (time to dry): 120 min (product application directions)
  • exposure duration: 60 min (professional judgment)
  • percentage losses through sorption or chemical degradation: 0
  • initial concentration of acetone in air: 0 mg/m3
  • concentration of acetone in inflow air: 0 mg/m3

Model output:

Peak event concentration, 60 min

= 3830 mg/m3

Mean event concentration,

60 min

= 2105 mg/m3

Peak concentration, 120 min

= 5931 mg/m3
Cleaner/ degreaser

Concentration of acetone: 100%, maximum value (HPD 1993– )

Exposure duration: 10 min (Bremmer and van Engelen 2007)

Density of acetone: 0.790 g/mL (West and Lide 1989)

Air exchange rate: 0.2 m3/min (derived from 0.6/h ventilation rate for an unspecified room in Bremmer et al. 2006)

Amount used: 40 mL (professional judgment)

Room volume: 20 m3 (volume of unspecified room in Bremmer et al. 2006)

Maximum dermal absorption rate (flux): 0.687 mg/(cm2·h) (AIHA 2009c)

One-half surface area of one hand, 20–59 years: 228 cm2 (Health Canada 1995)

Body weight, 20–59 years: 70.9 kg (Health Canada 1998)

Absorbed(Dermal) = Absorption rate × Surface area × Duration = 0.687 mg/(cm2·h) × 228 cm2 × 1/6 h = 26 mg

Intake(Dermal) = Absorbed(Dermal) ÷ Body weight = 26 mg ÷ 70.9 kg = 0.4 mg/kg-bw

Emission rate = (Amount used – Amount absorbed dermally) ÷ Time of use × Density = [(40 mL × 0.790 g/mL × 1000 mg/g) – 26 mg] ÷ 10 min = 3150 mg/min

Room supply AER = (0.6/h × 20 m3)/60 min = 0.2 m3/min

Estimated TWA concentration in air using IHMod “Well-mixed Room Model with a Constant Emission Rate” (AIHA 2009a):

  • contaminant mass emission rate: 3150 mg/min
  • room supply AER: 0.2 m3/min
  • room volume: 20 m3
  • release duration: 10 min
  • exposure duration: 10 min
  • percentage losses through sorption or chemical degradation: 0
  • initial concentration of acetone in air: 0 mg/m3
  • concentration of acetone in inflow air: 0 mg/m3

Calculated intake from dermal exposure on day of event

= 0.4 mg/kg-bw

Model output:

Peak concentration, 10 min

= 1500 mg/m3

Mean event concentration, 10 min

= 762 mg/m3
Artificial nail remover

Concentration of acetone: 100% 2011 emails from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced)

Exposure duration: 30 min (Bremmer and van Engelen 2007)

Air exchange rate: 0.2 m3/min (derived from 0.6/h ventilation rate for

an unspecified room in Bremmer et al. 2006).

Room volume: 20 m3 (volume of unspecified room in Bremmer et al. 2006)

Maximum dermal absorption rate: 0.687 mg/(cm2·h) (AIHA 2009c)

Body weight, 12–19 years: 59.4 kg (Health Canada 1998)

Body weight, 20–59 years: 70.9 kg (Health Canada 1998)

Surface area fingertips, 1/8th surface area of hands, 12–19 years: 100 cm2 (Health Canada 1995)

Surface area fingertips, 1/8th surface area of hands, 20–59 years: 115 cm2 (Health Canada 1995)

12–19 years:

Absorbed(Dermal) = Absorption rate × Surface area × Duration ÷ Body weight = 0.687 mg/(cm2·h) × 100 cm2 × 0.5 h ÷ 59.4 kg = 0.58 mg/kg-bw per day

20–59 years:

Absorbed(Dermal) = Absorption rate × Surface area × Duration ÷ Body weight = 0.687 mg/(cm2·h) × 115 cm2 × 0.5 h ÷ 70.9 kg = 0.56 mg/kg-bw per day

Room supply AER = (0.6/h × 20 m3)/60 min = 0.2 m3/min

Estimated evaporation rate using IHMod “Estimating Contaminant Generation Rate from Small Spills” model (AIHA 2009a):

  • system pressure: 1 atm
  • velocity of air: 2 cm/s (2009 email from Toxicology Excellence for Risk Assessment to Existing Substances Risk Assessment Bureau, Health Canada; unreferenced)
  • surface temperature of pool: 25°C
  • surface area of pool: 9 cm2 (assuming approximately 20 g of substance and a depth of liquid of 2 cm to ensure full coverage of the nail bed)
  • length of pool: 3 cm

Mass emission rate of acetone from pool: 95.1 mg/min

Estimated TWA concentration in air using IHMod “Well-mixed Room Model with a Constant Emission Rate” (AIHA 2009a):

  • contaminant mass emission rate: 95.1 mg/min
  • room supply air exchange rate: 0.2 m3/min (derived from 0.6/h)
  • room volume: 20 m3
  • release duration: 1 min
  • exposure duration: 30 min
  • percentage losses through sorption or chemical degradation: 0
  • initial concentration of acetone in air: 0 mg/m3
  • concentration of acetone in inflow air: 0 mg/m3

Calculated:

12–19 years internal dermal dose, 30 min

 = 0.58 mg/kg-bw per day

20–59 years internal dermal dose, 30 min

 = 0.56 mg/kg-bw per day

Model output:

Peak concentration, 30 min

= 123 mg/m3

Mean event concentration, 30 min

= 64 mg/m3
Face mask

Concentration of acetone: 100%  (2011 emails from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced).

Amount used: 1.2 g (Loretz et al. 2005)

Air exchange rate: 0.333 m3/min (derived from 2/h ventilation rate for bathroom in Bremmer et al. 2006)

Room volume: 10 m3 (volume of unspecified room in Bremmer et al. 2006)

Surface area one-half head, 20–59 years: 638 cm2(Health Canada 1995)

Bathroom supply AER = (2/h × 10 m3)/60 min = 0.333 m3/min

IH SkinPerm model

Input parameters:

  • instantaneous deposition: 1200 mg
  • surface area: 638 cm2
  • chemical: default acetone data
  • start deposition: 0 h
  • end observation time: 1 h
  • calculation intervals/h: 10 000
  • report intervals/h: 1000

Output:

  • Fraction absorbed: 0.2%
  • Amount absorbed: 2.7 mg

Dermal estimated daily intake:

Daily intake = Event dose × Use frequency ÷ Body weight = 2.7 mg × 1 time/day ÷ 70.9 kg = 0.04 mg/kg-bw per day

Emission rate to air = (Amount used – Amount absorbed dermally) ÷ Time to evaporate × 

= (1200 mg – 2.7 mg) ÷ 1/3 min = 3530 mg/min

Estimated TWA concentration in air using IHMod “Well-mixed Room Model with a Constant Emission Rate” (AIHA 2009a):

  • contaminant mass emission rate: 3530 mg/min
  • room supply air exchange rate: 0.333 m3/min (derived from 2/h)
  • room volume: 10 m3
  • release duration: 1/3 min
  • exposure duration: 25 min (50th percentile for time spent in bathroom, for adult 18–64 years; US EPA 2011)
  • percentage losses through sorption or chemical degradation: 0
  • initial concentration of acetone in air: 0 mg/m3
  • concentration of acetone in inflow air: 0 mg/m3

Calculated:

Internal dermal dose

 = 0.04 mg/kg-bw

Model output:

Peak concentration, 0.33 min

= 117 mg/m3

Mean event concentration, 25 min

= 79 mg/m3
Hairspray

Concentration of acetone: 30%  (2011 emails from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced).

Spray duration: 0.24 min (Bremmer et al. 2006)

Emission rate: 28 000 mg/min (Bremmer et al. 2006)

Air exchange rate: 0.333 m3/min (derived from 2/h ventilation rate for bathroom in Bremmer et al. 2006)

Room volume: 10 m3 (Bremmer et al. 2006)

Exposure duration: 25 min (US EPA 2011)

Bathroom supply AER = (2/h × 10 m3)/60 min = 0.333 m3/min

Estimated TWA concentration in air using IHMod “Well-mixed Room Model with a Constant Emission Rate” (AIHA 2009a):

  • contaminant mass emission rate: 8400 mg/min (based on emission rate of 28 000 mg/min, 30% acetone concentration and spray duration of 0.24 min)
  • room supply air exchange rate: 0.333 m3/min (derived from 2/h)
  • room volume: 10 m3
  • release duration: 0.24 min
  • exposure duration: 25 min (50th percentile for time spent in bathroom, for adult 18–64 years; US EPA 2011)
  • percentage losses through sorption or chemical degradation: 0
  • initial concentration of acetone in air: 0 mg/m3
  • concentration of acetone in inflow air: 0 mg/m3

Model output:

Peak concentration, 0.25 min

= 209 mg/m3

Mean event concentration, 25 min

= 141 mg/m3
Face moisturizer

Concentration of acetone: 0.3% (2011 emails from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced).

Amount used: 1.2 g (Loretz et al. 2005)

Frequency: 1.8/day (Loretz et al. 2005)

Body weight, 12–19 years: 59.4 kg (Health Canada 1998)

Body weight, 20–59 years: 70.9 kg (Health Canada 1998)

Retention factor: 1 (Health Canada 2012b)

Absorbed fraction: 1

Dermal event dose = Concentration × Product amount

= 0.3% × 1200 mg = 3.6 mg acetone applied per event

Daily intake = Event dose × Use frequency ÷ Body weight

12–19 years:

Daily intake = 3.6 mg × 1.8 times/day ÷ 59.4 kg = 0.11 mg/kg-bw per day

20–59 years:

Daily intake = 3.6 mg × 1.8 times/day ÷ 70.9 kg = 0.09 mg/kg-bw per day

Calculated:

Internal daily dermal dose, 12–19 years

 = 0.11 mg/kg-bw per day

Internal daily dermal dose, 20–59 years

 = 0.09 mg/kg-bw per day
Face cleanser

Concentration of acetone: 10% (2011 emails from the Consumer Product Safety Directorate, Health Canada, to the Existing Substances Risk Assessment Bureau, Health Canada; unreferenced).

Amount used: 2.6 g (Loretz et al. 2008)

Frequency of use, 12–19 years: 0.7/day (Health Canada 2012b)

Frequency of use, 20–59 years: 1.7/day (Loretz et al. 2008)

Body weight, 12–19 years: 59.4 kg (Health Canada 1998)

Body weight, 20–59 years: 70.9 kg (Health Canada 1998)

Retention factor: 0.01 (Health Canada 2012b)

Absorbed fraction: 1

Dermal event dose = Concentration × Retention factor × Product amount

= 10% × 0.01 × 2600 mg = 2.6 mg acetone applied per event

Dermal daily intake = Event dose × Use frequency ÷ Body weight

12–19 years:

Daily intake = 2.6 mg × 0.7 times/day ÷ 59.4 kg = 0.03 mg/kg-bw per day

20–59 years:

Daily intake = 2.6 mg × 1.7 times/day ÷ 70.9 kg = 0.06 mg/kg-bw per day

Calculated:

Internal daily dermal dose, 12–19 years

 = 0.03 mg/kg-bw per day

Internal daily dermal dose, 20–59 years

 = 0.06 mg/kg-bw per day

Top of Page

Appendix D: Summary of Animal Effects Data for Acetone

Table D1-1: Summary of data on acute effects of acetone
Route of Entry / Reference Species Protocol Results
Inhalation / Safronov et al. 1993 Male rats, (number per group not specified) Exposure to varying (unspecified) concentrations for 15, 30, 60, 120 or 240 min

15 min LC50 = 724 000 mg/m3

4 h LC50 = 71 000 mg/m3

Other LC50 values not available in the secondary source
Inhalation / Safronov et al. 1993 Male mice (no other details available from secondary source) Exposure to varying (unspecified) concentrations for 15, 30, 60, 120 or 240 min

15 min LC50 = 604 000 mg/m3

4 h LC50 = 44 000 mg/m3

Other LC50 values not available in the secondary source
Oral / Kimura et al. 1971 Sprague-Dawley rats, newborn, 14 days old, younger adult and older adult (6 males each in young and older adult groups, 6–12 of both sexes in newborn and 14-day-old groups) Single exposure via gavage to 2.2–9.1 mL/kg (1700- mg/kg-bw)

LD50 = 1700 mg/kg-bw (newborn)

LD50 = 4400 mg/kg-bw (14-day-old)

LD50 = 7100 mg/kg-bw (younger adult)

LD50 = 6700 mg/kg-bw (older adult)
Oral / Freeman and Hayes 1985 Rats (strain and number not reported) Exposure to varying (unspecified) doses LD50 = 5800 mg/kg-bw
Oral / Tanii et al. 1986 Male ddY mice (4 animals per dose group) Exposure to four (unspecified) doses; animals pretreated with intraperitoneal injection of olive oil 24 h prior to acetone administration LD50 = 5200 mg/kg-bw
Oral / Krasavage et al. 1982 Rabbits Detailed information not available LD50 = 5300 mg/kg-bw
Dermal / Roudabush et al. 1965 Male and female White rabbits (4 animals per dose group) Exposure to a minimum of 3 doses up to 9.4 mL/kg (7400 mg/kg-bw); other doses not specified LD50 greater than 7400 mg/kg-bw
Dermal / Roudabush et al. 1965 Male Hartley guinea pigs, (4 animals per dose group) Exposure to a minimum of 3 doses up to 9.4 mL/kg (7400 mg/kg-bw); other doses not specified LD50 greater than 7400 mg/kg-bw
Dermal / Smyth et al. 1962 Rabbits Exposure to doses up to 20 mL/kg (15 800 mg/kg-bw) LD50 greater than 15 800 mg/kg-bw
Table D1-2: Summary of data on irritation and sensitization effects of acetone
Route of Entry / Reference Species Protocol Results
Inhalation / Kane et al. 1980 Male Swiss Webster mice (4 per group) Exposure to unspecified concentrations for 10 min RD50 = 184 136 mg/m3 (sensory irritation)
Inhalation / De Ceaurriz et al. 1984 Male Swiss OF1 mice Exposure to unspecified concentrations for 15 min RD50 = 55 776 mg/m3 (sensory irritation)
Inhalation / Schaper and Brost 1991 Male Swiss Webster mice (4 per group) Exposure for 30 min once or on 5 consecutive days to 6000 ppm (14 253 mg/m3) No change in respiratory cycle (time of inspiration/expiration, time of pause between breaths) or thoracic volume displacement (tidal volume)
Dermal and ocular / Smyth et al. 1962 Albino rabbits (5 per group) Uncovered application of 0.01 mL of acetone to clipped skin No irritation to the skin
Dermal and ocular / Carpenter and Smyth 1946; Smyth et al. 1962 Rabbits (no other details provided) Instillation of various volumes and concentrations of acetone to the cornea Severe burn to the cornea from 0.005 mL of acetone (grade 5 on a scale of 10 for grading degree of corneal necrosis)
Dermal and ocular / Iversen et al. 1988 CD-1 mice (no other details in secondary sources) 0.2 mL of acetone to shaved skin Increased DNA synthesis and moderate hyperplasia after 24 h; considered signs of slight irritation
Dermal and ocular / Descotes 1988 Male and female mice, various strains Topical application of acetone 100% on both sides of ear on days 0 and 2, and scapular subcutaneous injection of 0.05 mL acetone 100% on day 2 Mouse ear sensitization assay; no change in ear thickness
Dermal and ocular / Nakamura et al. 1994 Female albino guinea pigs, Hartley strain (2–10 per group) Initial intradermal injection and topical application of acetone 100%, followed by intradermal injection of 0.01 mL acetone 21 days later Guinea pig maximization test; no erythema or edema formation was observed
Dermal and ocular / Montelius et al. 1996 Mice, unspecified strain (4 per group) Daily topical application of 25 µg of acetone or of a mix of acetone and olive oil in various proportions according to local lymph node assay protocol Acetone induced a non-significant increase in cell proliferation; proliferative response increased only as the proportion of olive oil increased
Table D1-3: Summary of data on short-term effects of acetone
Route of Entry / Reference Species Protocol Results
Oral /
NTP 1991		 Male and female F344 rats (5 per sex per group) Exposed to 0, 5000, 10 000, 20 000, 50 000, 100 000 ppm (intakes reported by authors: males: 0, 714, 1616, 2559, 4312, 6942 mg/kg-bw per day; females: 0, 751, 1485, 2328, 4350, 8560 mg/kg-bw per day) of acetone in drinking water for 14 days

No deaths occurred greater than or equal to 2559/2328 mg/kg-bw per day: ↑ liver wt. (male/female), ↑ kidney wt. (female) (non-adverse) greater than or equal to 4312/4350 mg/kg-bw per day: ↓ bw, ↑ kidney wt. (male/female),↑ relative testis wt in male

  greater than or equal to 6942/8560 mg/kg-bw per day: bone marrow hypoplasia (male), ↓ bw (female)

LOAEL = 4312 mg/kg-bw per day, based on 13% decreased body weights in males relative to controls
Oral /
NTP 1991		 Male and female B6C3F1mice (5 per sex per group) Exposed to 0, 5000, 10 000, 20 000, 50 000, 100 000 ppm (intakes reported by authors: males: 0, 965, 1579, 3896, 6348, 10 314 mg/kg-bw per day; females: 0, 1569, 3023, 5481, 8804, 12 725 mg/kg-bw per day) of acetone in drinking water for 14 days

greater than or equal to 965/1569 mg/kg-bw per day: ↑ liver wt. (male)

greater than or equal to 3896/5481 mg/kg-bw per day: ↑ centrilobular hepatocellular hypertrophy (male), ↑ liver wt. (female)

greater than or equal to 6348/8804 mg/kg-bw per day: ↑ kidney wt. (male), ↑ centrilobular hepatocellular hypertrophy, ↑ kidney wt. (female)

LOAEL = 3896 mg/kg-bw per day, based on liver hypertrophy in males
Table D1-4: Summary of data on subchronic effects of acetone
Route of Entry / Reference Species Protocol Results
Inhalation / Bruckner and Peterson 1981b Male ARS/Sprague-Dawley rats (5 per group) Exposure to 0 or 45 100 mg/m3 (0, 19 000 ppm) for 3 h/day, 5 days/week, for 8 weeks, with additional group sacrificed after 2, 4 and 8 weeks of exposure and after 2-week recovery

No treatment-related effects on blood chemistry, enzymatic activity or histology of the heart, lung, brain and liver. Body weight gain was slightly lower throughout the experiment, but the difference was not statistically significant.

Decrease in absolute brain weight at 4 and 8 weeks at 45 100 mg/m3.

Decrease in absolute kidney weight at 4 weeks at 45 100 mg/m3, but not at 8 weeks.

No statistically significant change in organ weights compared with controls after 2-week recovery.Relative organ weights were consistently higher in exposed rats (data not provided).
Inhalation / Buron et al. 2009 Female OF-1 mice (10–20 per group)

Exposure to fresh air or 4 mL for 5 h/day, 5 days/week, for 4 weeks

(concentration reported by authors to rise during first 1.5 h to a constant level of 8000 ppm [19 000 mg/m3] for the remaining 3.5 h)

Behavioural effects:

Olfactory sensitivity (assessed by how the mice avoided acetone in a maze) increased (less time spent in the acetone compartment of maze) during exposure (weeks 2 and 4) through the end of the post-exposure period (weeks 6 and 8)

Histological examination:

  • Significant decrease in number of olfactory epithelial cells at week 2, an increase at week 4 that remained at week 6 and a recovery by week 8.
  • Thickness of olfactory epithelium remained stable at weeks 0 and 2, decreased at week 4, increased at week 6 and recovered by week 8.

Immunochemistry:

  • No change in olfactory marker protein
  • The number of cells positive for proliferating cell nuclear antigen decreased in the basal layer during week 2, but increased afterwards, recovering to near-baseline level by 4 weeks post-exposure.

(Other subchronic inhalation study :Christoph et al. 2003; listed under neurotoxicity).
Oral / Woolhiser et al. 2003 Male CD-1 mice (8 per group) Exposure to 0, 121, 621, 1144 mg/kg-bw per day (concentrations reported by authors: 0, 600, 3000, 6000 ppm acetone in drinking water) for 28 days

No deaths occurred, and no clinical signs of toxicity

No changes in body weight

No treatment-related effects on hematological parameters (total and differential white blood cells, red blood cells, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, platelets)

No effects on spleen or thymus weight or on total or differential white blood cell counts

No effects on SRBC antibody response

NOAEL = 1144 mg/kg-bw per day (highest dose tested)
Oral / American Biogenics Corporation 1986

Male and female Sprague-Dawley rats (30 per sex per group)

(10 for interim sacrifice and 20 evaluated at completion of the study)

 Exposure to 0, 100, 500, 2500 mg/kg-bw per day by gavage in water for 90 days

No effects on survival or food consumption

greater than or equal to 500 mg/kg-bw per day: ↑ kidney wt., ↑ liver wt. (female), ↓ body wt. (female), accentuation of renal proximal tubule generation and intracytoplasmic hyaline droplet accumulation (male)

greater than or equal to 2500 mg/kg-bw per day: ↑ kidney wt., ↑ liver wt., ↓ brain wt., ↑ ALT, ↑ mean corpuscular hemoglobin, mean corpuscular volume, ↓ platelets, glucose, potassium (male); ↑ relative heart wt. (female), ↑ hemoglobin, hematocrit (male/female), accentuation of renal proximal tubule generation and intracytoplasmic hyaline droplet accumulation (male), accentuation of renal proximal tubular degeneration (female)

LOAEL = 2500 mg/kg-bw per day, based on significant increase in absolute kidney weights supported by histopathological findings
Oral / NTP 1991 Male and female F344/N rats (10 per sex per group) Exposure to 0, 2500, 5000, 10 000, 20 000, 50 000 ppm (intakes reported by authors: males: 0, 200, 400, 900, 1700, 3400 mg/kg-bw per day; females: 0, 300, 600, 1200, 1600, 3100 mg/kg-bw per day) of acetone in drinking water for 13 weeks

No effects on survival, and no clinical signs of toxicity or ophthalmic irregularities

greater than or equal to 200/300 mg/kg-bw per day: ↑ mean corpuscular hemoglobin, mean cell volume (male)

greater than or equal to 400/600 mg/kg-bw per day: ↓ hematocrit, hemoglobin, erythrocytes, reticulocytes (female)

greater than or equal to 900/1200 mg/kg-bw per day: ↑↓ mean corpuscular hemoglobin, mean cell volume, reticulocytes (female)

greater than or equal to 1700/1600 mg/kg-bw per day: ↓ water consumption, ↑ severity of nephropathy, ↑↓ lymphocytes, leukocytes, hematocrit, hemoglobin, mean corpuscular hemoglobin, mean cell volume, erythrocytes, reticulocytes (female), ↓ platelets (male/female), ↑ spleen pigmentation (male), ↑ kidney wt. (female), ↑ liver wt. (male/female)

greater than or equal to 3400/3100 mg/kg-bw per day: ↑ kidney wt., ↑ liver wt. (male/female), ↑ testes wt. (male), ↑ abnormal sperm, ↓ sperm motility, epididymal wt., ↓ bw (male), ↑↓ lymphocytes, leukocytes, mean corpuscular hemoglobin, mean cell volume, platelets (male/female), ↓ hemoglobin, erythrocytes, reticulocytes

LOAEL = 1700 mg/kg-bw per day, based on hematological effects in female and renal effects in male rats
Oral / NTP 1991 B6C3F1 mice (10 per sex per group) Exposure to 0, 1250, 2500, 5000, 10 000, 20 000 ppm (males) (intakes reported by authors: 0, 380, 611, 1353, 2258, 4858 mg/kg-bw per day) and 0, 2500, 5000, 10 000, 20 000, 50 000 ppm (females) (intakes reported by authors: 0, 892, 2007, 4156, 5945, 11 298 mg/kg-bw per day) of acetone in drinking water for 13 weeks

Males:

No effects on survival, and no clinical signs of toxicity

No significant changes in body weight or water consumption

No significant changes in organ weights

greater than 892 mg/kg-bw per day: ↓ water consumption (female)

greater than 1353 mg/kg-bw per day: ↑ hemoglobin (male)

4858 mg/kg-bw per day: ↑ mean corpuscular hemoglobin (male)

greater than 5945 mg/kg-bw per day: ↑ hemoglobin (female)

11 298 mg/kg-bw per day: ↑ liver wt., ↓ spleen wt., centrilobular hepatocellular hypertrophy, ↑ hematocrit (female)

LOAEL = 11 298 mg/kg-bw per day, based on increased absolute liver weight coupled with liver histopathology in female mice
Oral / Ladefoged et al. 1989 Male Wistar rats (11 per group)

Exposure to 0%, 0.5% in drinking water for 6 weeks

(0, 700 mg/kg-bw per day)

No effect on nerve conduction velocity at weeks 3, 4, 5

 

No effect on balance time on rotorod
Oral / Spencer et al. 1978 Sprague-Dawley rats (3 per group; sex not reported) Exposure to 0%, 0.5% in drinking water (for 8 weeks; 700 mg/kg-bw per day) or 1% in drinking water (for 4 weeks; 1400 mg/kg-bw per day)

No evidence of peripheral neuropathy

No clinical signs of toxicity
Oral / Sollman 1921 Rats (3 in total) Exposed to 2.5% (3500 mg/kg-bw per day) acetone in drinking water for 18 weeks

Decrease in food and water consumption and body weights

Histopathology was not conducted
Dermal / Rengstorff et al. 1972 Guinea pigs (8 per group) Dermal exposure to 0 or 0.5 mL acetone 5 days/week for 8 weeks Cataracts in 2/8 treated animals and 0/8 controls
Dermal / Rengstorff et al. 1976 New Zealand White rabbits (8 per group) 1 mL acetone on clipped back, 3 times/week, for 3 weeks; saline was used in the control group No lens abnormalities were observed at end of exposure or after 6 months of follow-up
Dermal / Taylor et al. 1993 Albino guinea pigs, Hartley hairless (20 animals) Topical exposure to 0.5 mL acetone for 5 days/week for 6 months No cataracts observed
Table D1-5: Summary of data on carcinogenicity and chronic effects of acetone
Route of Entry / Reference Species Protocol Results
Inhalation Not available Not available Not available
Oral Not available Not available Not available
Dermal / Barr-Nea and Wolman 1972 ICR mice (sex and number per group not specified) Dermal exposure to unspecified amounts of acetone for 5 or 7 months; untreated group included

0/9 and 2/18 animals diagnosed with amyloid deposition after 5 and 7 months of exposure, respectively, but none in unspecified number of untreated animals

Significant increase in amyloid deposition in the heart, liver, kidney, skin, pancreas and adrenals in 12/23 acetone-treated animals compared with 1/18 untreated animals
Dermal / DePass et al. 1989 Male C3H/HeJ mice (40 exposed) Dermal exposure to approximately 670 mg/kg-bw (amount reported by authors: 25 µL of a 100% solution), 3 times/week for “their complete lifespan; average daily dose of 290 mg/kg-bw per day”; no untreated group included

No skin tumours noted

Subcutaneous mesenchymal neoplasms (a fibrosarcoma and a lymphosarcoma) in two animals, ulcerative dermatitis in two animals, epidermal hyperplasia and hyperkeratosis in 2/40, 2/40, 1/40 and 1/40 animals, respectively
Dermal / Ward et al. 1986 Female SENCAR mice (30 per group)

Dermal exposure to

5300 mg/kg-bw (amount reported by authors: 0.2 mL) of acetone, 2 times/week for 92 weeks; average daily dose of 1520 mg/kg-bw per day; another group dermally exposed to 0.2 mL of formalin once, followed 4 weeks later by dermal exposure to similar dose of acetone (1520 mg/kg-bw per day) for 88 weeks; no untreated group included

Authors reported that neoplastic and non-neoplastic lesions occurred with similar incidence, and survival was similar; therefore, results were combined for statistical analysis

Only 50% survived past 96 weeks of age; causes of death included non-neoplastic and neoplastic lesions

Glomerulonephritis and histiocytic sarcoma reported as the two major contributing causes of death

Other effects not regarded as contributors to death:

neoplastic lesions--lung tumours (adenomas and adenocarcinomas) and mammary gland tumours (primarily adenocarcinomas); non-neoplastic lesions--lymphoid and epithelial hyperplasia of the thymus, myeloid metaplasia and lymphoid hyperplasia of the spleen, lymphoid hyperplasia of the lymph nodes, cytomegaly and chronic cholangitis of the liver, amyloidosis of the nasal turbinates, cystic endometrial hyperplasia
Table D1-6: Summary of data on reproductive and developmental effects of acetone
Route of Entry / Reference Species Protocol Results
Inhalation / Mast et al. 1988 Sprague-Dawley rats (pregnant) (26–29 per group) Exposure to 0, 1045, 5200, 26 100 mg/m3 acetone vapour (concentrations reported by authors: 0, 440, 2200, 11 000 ppm) for 6 h/day, 7 days/week, for 14 days (days 6–19 of gestation)

No clinical signs of maternal toxicity

 

Statistically significant decrease in extragestational weight gain, uterine weight in the 26 100 mg/m3 group

Fetal weights were statistically decreased at 26 100 mg/m3

At 26 100 mg/m3, the percentage of litters with resorptions (77% vs. 50%) and percentage of litters with at least one malformation (11.5% vs. 3.8%) were higher than control

NTP concluded that acetone had not caused a teratogenic effect in rats

LOAEC (maternal toxicity) = 26 100 mg/m3, based on significant decreases in body weight gain and uterine weight

LOAEC (developmental toxicity) = 26 100 mg/m3, based on significant decrease in fetal weights, increased number of resorptions and increased malformations
Inhalation / Mast et al. 1988 CD-1 mice (pregnant) (28–31 per group) Exposure to 0, 1045, 5200, 15 670 mg/m3 acetone vapour (concentrations reported by authors: 0, 440, 2200, 6600 ppm) for 6 h/day, 7 days/week, for 12 days (days 6–17 of gestation); high exposure was initially 11 000 ppm (26 100 mg/m3), but reduced after 1st day due to severe narcosis

No clinical signs of maternal toxicity, and no significant effect on maternal body weights, absolute and relative kidney weights, or uterine weights

Significant increase in absolute and relative liver weights in pregnant mice at 15 670 mg/m3

Statistically significant decrease in fetal weights, increased incidence of litters with reduced sternebrae ossification, and a slight but statistically significant increase in the percentage incidence of late resorptions at 15 670 mg/m3

LOAEC (maternal toxicity) = 15 670 mg/m3based on increase in absolute and relative liver weights in pregnant mice

LOAEC (developmental toxicity) = 15 670 mg/m3 based on decrease in fetal weights and increase in the percentage incidence of late resorptions and retarded ossification
Oral / Larsen et al. 1991 Male Møllegard/ Wistar rats (10 per group) Exposure to 0 or 800 mg/kg-bw (0% or 0.5% in drinking water) for 6 weeks, and then mated with untreated females; other groups were exposed for 6 weeks, held for 10 weeks exposure-free, and then mated to untreated females No changes were observed in reproductive parameters or testicular measurements (number of matings, pregnancies, fetuses, testicular weight and testicular histopathology)
Oral / Dalgaard et al. 2000 Male Wistar rats (10 per group) 0 or 700 mg/kg-bw per day (0% or 0.5% acetone in drinking water) for 9 weeks; or 0 or 1400 mg/kg-bw per day (0% or 1% acetone in drinking water) for 4 weeks; and then mated with untreated females

No effect on body weight, male fertility, reproductive organ weights or testes histopathology

Acetone-exposed rats had reduced forelimb and hindlimb grip strength and blood glucose levels

(Other reproductive toxicity studies: American Biogenics Corporation 1986, NTP 1991; listed under short-term and subchronic toxicity studies)
Table D1-7: Summary of data on immunological effects of acetone
Route of Entry / Reference Species Protocol Results
Oral See subchronic section See subchronic section See subchronic section
Dermal / Singh et al. 1996 Female SSIN mice (6 per group) Dermal exposure to 0; 187 or 380; 375 or 750; 750 or 1500; 1125 or 2250 mg/kg-bw per day--reflecting dosing once or twice a week (concentrations reported by authors: 0, 50, 100, 200 or 300 µL) acetone once or twice weekly for 2 or 4 weeks

No changes in relative percentages of B cells, T cells or ratio of CD4+ to CD8+ T cells

Statistically significant suppression of SRBC antibody response at 2250 mg/kg-bw per day; responses at other doses were reported to be schedule dependent

Changes in plaque numbers in SRBC assay not accompanied by changes in splenic cellularity

No effect on the mixed lymphocyte response
Table D1-8: Summary of data on neurological effects of acetone
Route of Entry / Reference Species Protocol Results
Inhalation / Goldberg et al. 1964 Female CFE rats (8–10 per group) Exposure to 0, 3000, 6000, 12 000 or 16 000 ppm (calculated for this report to be 0, 7120, 14 240, 28 480 and 37 975 mg/m3) for 4 h/day, 5 days/week, for 10 total exposures

No effect on growth rate

Concentration-dependent increase in inhibition of avoidance response: 0%, 38%, 50% and 62% at 7120, 14 240, 28 480 and 37 975 mg/m3, respectively, after single exposure; this incidence decreased with repeated exposure

 

Ataxia at exposure to 28 480 or 37 975 mg/m3 after single exposure

LOAEC = 14 240 mg/m3, based on increase in inhibition of avoidance response
Inhalation / Christoph et al. 2003 Male Crl:CD BR rats (10 per group) Exposure to 0, 1000, 2000 or 4000 ppm acetone (0, 2400, 4800 or 9500 mg/m3) for 6 h/day, 5 days/week, for 13 weeks; exposures preceded by 9 weeks of operant training

No clinical signs at end of exposure or effect on response to auditory alerting stimulus, fixed ratio response rate, fixed interval response rate or fixed interval index of curvature

NOAEC = 9500 mg/m3 (highest concentration tested)
Inhalation / De Ceaurriz et al. 1984 Male Swiss OF1 mice (10 per group) Exposure to 4827, 6129, 6789, 7176 mg/m3(concentrations reported by authors: 2032, 2580, 2858 or 3021 ppm) for 4 h

Statistically significant decreases in mobility time at 6129 mg/m3 and above, but not at 4827 mg/m3, in the behavioural despair swimming test

ID50 (concentration estimated to cause a 50% decrease in the duration of immobility) = 6650 mg/m3

LOAEC = 6129 mg/m3 for 4 h
Inhalation / Bruckner and Peterson 1981a Male ARS/Sprague-Dawley rats (5 per group) Exposure to 29 900, 45 100, 60 100, 120 200 mg/m3(concentrations reported by authors: 0, 12 500, 19 000, 25 300 or 50 600 ppm) for up to 3 h; the methods section noted control groups, but no data on the controls were reported

Concentration-related increase in depth of CNS depression and increase in rate of depression, based on five tests of unconditioned performance and reflexes (wire manoeuvre, visual placing, grip strength, tail pinch, righting reflex)

120 200 mg/m3 was lethal within 2 h

LOAEC = 45 100 mg/m3 for 1 h
Inhalation / Glowa and Dews 1987 Mice (strain and number not available in secondary sources) Exposure to six nominal concentrations ranging from 240 to 133 000 mg/m3 (concentrations reported by secondary sources: 100–56 000 ppm) for 1 day

No effect on the correct response rate at acetone concentrations less than 2380 mg/m3; the highest concentration tested (133 000 mg/m3) completely eliminated the response

EC50 = 25 000 mg/m3 for acetone-induced changes in schedule-controlled operant behavior (Morgott 2001)

NOAEC = 2380 mg/m3, with a LOAEC of 7130 mg/m3, based on a 10% decreased response to food presentation in a fixed interval operant behavioural test (ATSDR 1994)
Inhalation / Geller et al. 1979a Male juvenile baboon (n = 4) Exposed continuously to 500 ppm (1206 mg/m3) for 7 days Neurobehavioural effect (increased response time on match-to-sample operant behavioural test) in all four animals, and possible increased alerting response in two of four animals
Inhalation / Mashbitz et al. 1936 White mice (sex and number per exposure group not reported) Exposure to 40 000, 60 000, 80 000, 100 000, 120 000, 133 000 or 200 000 mg/m3 acetone for durations up to 4 h

Time to narcosis at 40 000, 60 000, 80 000, 100 000, 120 000, 133 000 and 200 000 mg/m3 was 158, 92, 59, 38, 33, 38 and 34 min, respectively

At greater than or equal to 100 000 mg/m3, drowsiness preceded period of excitement, with impaired coordination at 25–28 min, followed by deep narcosis at 33–38 min. Effects were accompanied by frequent rhythmical clonic movement of the hind legs and abdominal muscles. A similar pattern of effects was seen at lower concentrations, with a longer time to effect.

Mice remained in deep narcosis for 38–100 min post-exposure.
Inhalation / Haggard et al. 1944 Rats (no strain or sex reported) Exposure to 5000, 10 000, 25 000, 50 000, 100 000, 200 000 or 300 000 mg/m3 acetone for 45 min to 8 h

No intoxication (slight incoordination) less than or equal to 10 000 mg/m3 for durations up to 8 h, but intoxication observed at 25 000, 50 000, 100 000, 200 000 and 300 000 mg/m3 at durations of 100–250, 40–80, 15–35, 10–15 and 5–7 min of exposure, respectively

No loss of righting reflex at less than or equal to 10 000 mg/m3 for up to 8 h or at 25 000 mg/m3 for up to 6 h, but loss observed at 50 000, 100 000, 200 000 and 300 000 mg/m3 at durations of 130–160, 50–57, 22–25 and 10–15 min of exposure, respectively

No loss of corneal reflex at less than or equal to 10 000 mg/m3 for up to 8 h or at 25 000 and 50 000 mg/m3 for up to 6 h, but was observed at 100 000, 200 000 and 300 000 mg/m3 at durations of 105–155, 45–50 and 22–25 min of exposure, respectively

Slight incoordination at blood concentrations of approximately 1000–2000 mg/L, loss of righting reflex at about 3000 mg/L, loss of corneal reflex at 5000 mg/L and respiratory failure at 9100–9300 mg/L
Oral / Ladefoged et al. 1989 Male Wistar rats (11 per group) Exposure to 0%, 0.5% acetone (0, 700 mg/kg-bw per day) in drinking water for 6 weeks

No effect on nerve conduction velocity at weeks 3, 4, 5

 

No effect on balance time on rotarod
Table D2-1: in vitro genotoxicity studies with acetone for Prokaryotic organisms
Assay Indicator system Highest concentration tested Metabolic activation Results (with/ without S9) Reference
Reverse mutation (Ames assay) S. typhimurium TA98, TA100, TA1535 & TA1537 10 mg/plate Rat & hamster liver S9 −/− Zeiger et al. 1992
Reverse mutation (Ames assay) S. typhimurium TA98, TA100, TA1535, TA1537 & TA1538 73 mg/plate None NA/− De Flora et al. 1984
Reverse mutation (Ames assay) S. typhimurium TA92, TA94, TA98, TA100, TA1535 & TA1537 10 mg/plate Rat liver S9 −/NA Ishidate et al. 1984
Lambda prophage WP2s(λ) induction (Microscreen assay) Escherichia coli TH-008 10% (v/v) Rat liver S9 −/− DeMarini et al. 1991
Lambda prophage WP2s(λ) induction (Microscreen assay) E. coli SR714 10% (v/v) Rat liver S9 −/− Rossman et al. 1991
β-Galactosidase activation (SOS chromotest) E. coli PQ37 100 mM Rat liver S9 −/− Von der Hude et al. 1988
Colitis phage DNA transfection assay E. coli CR63 0.1 mL Rat liver S9 −/NA Vasavada and Padayatty 1981
DNA binding assay E. coli Q13 0.05% (v/v) Rat liver S9 −/− Kubinski et al. 1981
Recombination assay Bacillus subtilis H-17 & M-45 10 mg/well Rat liver S9 −/− McCarroll et al. 1981
β-Galactosidase activation (SOS chromotest) S. typhimurium TA1535/pSK1002 33 mg/mL Rat liver S9 −/− Nakamura et al. 1987
Table D2-2: in vitro genotoxicity studies with acetone for Eukaryotic organisms
Assay Indicator system Highest concentration tested Metabolic activation Results (with/without S9) Reference
Chromosomal malsegregation Saccharomyces cerevisiae D61.M 7.8% (v/v) None NA/+ Zimmermann et al. 1985
Point mutation and mitotic recombination S. cerevisiae D61.M 7.8% (v/v) None NA/− Zimmermann et al. 1985
Chromosomal malsegregation S. cerevisiae D61.M 50 mg/mL None NA/± Whittaker et al. 1989
Chromosomal malsegregation S. cerevisiae D61.M 8% (v/v) None NA/± Albertini 1991
Reverse mutation S. cerevisiae D7 10% (v/v) None NA/± Yadav et al. 1982
Forward mutation Schizosaccharomyces pombe P1 3.7% (v/v) Mouse liver S10 −/NA Abbondandolo et al. 1980
Forward mutation S. cerevisiae D4 5% (v/v) Rat liver S9 −/NA Barale et al. 1983
Cell transformation assay Syrian hamster embryo cells 135 μg/m3 None NA/− Hatch et al. 1983
Cell transformation assay Syrian hamster embryo cells 8% (v/v) None NA/− Pienta 1980
Cell transformation assay Rat embryo cells 100 μg/mL None NA/− Freeman et al. 1973
Cell transformation assay Rat embryo cells 0.1% (v/v) Rat liver S9 −/− Mishra et al. 1978
Transformation assay Asynchronous mouse embryo fibroblasts 0.5% (v/v) None NA/− Peterson et al. 1981
Cell transformation assay Mouse embryo fibroblasts 0.5% (v/v) None NA/− Lillehaug and Djurhuus 1982
Cell transformation assay Mouse prostate fibroblasts 0.5% (v/v) None NA/− Gehly and Heidelberger 1982
SCE Chinese hamster lung fibroblasts 100 mM Rat liver S9 −/− von der Hude et al. 1987
Chromosomal aberration Chinese hamster fibroblasts 5% (v/v) None NA/+ Ishidate et al. 1984
SCE Chinese hamster lung fibroblasts 8.6 mM None NA/− Latt et al. 1981
Chromosomal aberration & SCE Chinese hamster ovary cells 1 mg/mL Rat liver S9 −/− Tates and Kriek 1981
Chromosomal aberration & SCE Chinese hamster ovary cells 5 mg/mL Rat liver S9 −/− Loveday et al. 1990
Chromosomal aberration & SCE Human lymphocytesFootnote Appendix D Table D2-2[b] 20.9 mM None NA/− Norppa et al. 1981
Mouse lymphoma mutation assay L5178Y mouse lymphoma cells 470 mM None NA/− Amacher et al. 1980
Mouse lymphoma mutation assay L5178Y mouse lymphoma cells 1% (v/v) Rat liver S9 −/NA McGregor et al. 1988
Mouse lymphoma mutation assay S49 mouse lymphoma cells 140 mM Rat lvi −/NA Friedrich and Nass 1983
Reverse mutation ouabain resistance Chinese hamster lung fibroblasts 0.2% (v/v) None NA/− Lankas 1979
Forward mutation thioguanine resistance Chinese hamster lung fibroblasts 0.5% (v/v) Rat liver S9 −/NAFootnote Appendix D Table D2-2[a] Cheng et al. 1981
Micronucleus test Human lymphocytes[b] 5 mM Rat liver S9 − Zarani et al. 1999
Unscheduled DNA synthesis Bovine lymphocytes 0.4 mg/mL None − Targowski and Klucinski 1983
Unscheduled DNA synthesis Human skin cells[b] 10% (v/v) None − Lake et al. 1978
Metabolic cooperation assay Chinese hamster lung fibroblasts 5% (v/v) None + Chen et al. 1984
Alkaline elution assay Rat hepatocytes 1% (v/v) None − Sina et al. 1983
Two-stage cell transformation assay Mouse 3T3 cells 0.5% (v/v) None − Sakai and Sato 1989
Table D2-3: in vivo genotoxicity studies with acetone for Eukaryotic organisms
Assay Indicator system Highest concentration tested Metabolic activation Results (with/without S9) Reference
Micronucleus test Chinese hamster bone marrow cells 865 mg/kg-bw NA − Basler 1986
Micronucleus test Mouse bone marrow 5000–20 000 ppm in drinking water (1000–4000 mg/kg-bw per day)Footnote Appendix D Table D2-3 [a] for 13 weeks NA − Unpublished study cited in NTP 1991
Host-mediated assay Hamster fetal cells 2300 mg/kg-bw NA − Quarles et al. 1979

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Appendix E: Summary of Human Effects Data for Acetone

Table E1-1: Summary of volunteer exposure
Subjects Protocol Results Reference
31 acetone-exposed workers from a cellulose acetate production facility employed for 1.5–33 years and age- and sex-matched controls unexposed to acetone except for infrequent nail polish remover use Volunteers were presented with pairs of bottles with a blank solution or various dilutions of acetone, inserted the nose-piece in each nostril, sniffed and tried to identify the bottle containing acetone

Olfactory threshold was 855 ppm (2031 mg/m3) in exposed workers and 41 ppm (97 mg/m3) in unexposed controls

Lateralization threshold (to indicate sensory irritation) was 36 669 ppm (87 106 mg/m3) in exposed workers and 15 758 ppm (37 433 mg/m3) in unexposed controls

 Wysocki et al. 1997
8 subjects (4 anosmics, 4 normosmics) Volunteers were presented with pairs of bottles with a pop-up spout and squeezed the bottle to sniff varying dilutions of acetone or a blank into one nostril Odour threshold in normosmics was approximately 10 000 ppm (23 755 mg/m3). Nasal pungency threshold was 100 000 ppm (237 500 mg/m3) in anosmics. Cometto-Muñiz and Cain 1993
25 males Exposed to acetone vapour 240, 590, 1190 and 2400 mg/m3 (concentrations reported by authors: 100, 250, 500 and 1000 ppm) for 3 h in morning and 3 h in afternoon for 1 day or exposed to 590 or 1190 mg/m3 (250 or 500 ppm) for 6 h/day (with 45 min break) for 6 days

greater than or equal to 240 mg/m3: very mild nose, eye and throat irritation after 1 day of exposure; effects were inconsistent among exposed subjects

greater than or equal to 1190 mg/m3: irritating to nose, eyes, throat and trachea; very slight irritation at lower concentrations;

statistically significant increase in white blood cell counts and decrease in phagocytic activity of neutrophils at 1190 mg/m3 after single day exposure of 6 h (2×3h in same day) or repeated 6 h exposure for 6 days, possibly reflecting inflammatory response

1190 mg/m3 was considered the most appropriate LOEC

 Matsushita et al. 1969a, b
Average of 10 people per group of both sexes Exposed to acetone vapour 475, 713 and 1190 mg/m3(concentrations reported by authors: 200, 300 or 500 ppm) for 3–5 min Symptoms of eye and throat irritation were reported by the volunteers at concentrations greater than or equal to 713 mg/m3 Nelson et al. 1943
10 males Exposed to acetone vapour 551 mg/m3 (concentration reported by authors: 231 ppm) for 2 h No subjective symptoms of eye, nose, throat or airway irritation and no subjective CNS effects, based on ratings on an analogue scale; acetone smell was detected Ernstgård et al. 1999
9 males Exposed to acetone vapour 240 and 1190 mg/m3(concentrations reported by authors: 100 and 500 ppm) for 2 or 4 h No effect on clinical chemistry or hematology; no subjective symptoms DiVincenzo et al. 1973
Males or females (2–4 per group) Exposure to 0, 475, 2370 and 2970 mg/m3(concentrations reported by authors: 0, 200, 1000 and 1250 ppm) for 3 or 7.5 h/day for up to 4 days

No significant neurological abnormalities

Visual evoked response changes at 2970 mg/m3following repeated exposures

Premature menstruation in 3 of 4 women at 2370 mg/m3for 7.5 h/day for 4 days (early by 1 week or more), but not at same concentration for 3 h/day for 4 days

Pulmonary function testing showed no abnormalities at any concentration

 

No effect on complete blood count or clinical chemistry

Eye and throat irritation was present at all concentrations, but complaints were inconsistent from one week to the other; however, throat irritation at an incidence greater than controls was reported in subjects exposed to 2370 mg/m3 for 3 or 7.5 h

 Stewart et al. 1975
32 subjects, sex not specified Exposure to 2375 mg/m3 (concentration reported by author: 1000 ppm) for 4 or 8 h

Throat irritation at both durations

No increased reporting of subjective symptoms of tiredness, tension, complaints or annoyance

 Seeber et al. 1992
11 male and 11 female volunteers Exposure to 600 mg/m3 (concentration reported by authors: 250 ppm) for 4 h

Increase in response time and percentage of incorrect responses in dual auditory tone discrimination compensatory tracking test

Profile of Mood States test showed increase in anger-hostility score in males

 Dick et al. 1989
Table E1-2. Epidemiological studies
Subjects Protocol Results Reference
776 female university employees in laboratory work Exposure was evaluated through a questionnaire on type of work and substances handled, but was not quantified. Pregnancies and outcome of pregnancies were investigated through questionnaire, and information was verified in medical records.

Overall miscarriage rate was 11.1%. When divided by main occupation during pregnancy, miscarriage rates were 9.9%, 7.7% and 7.2% for laboratory work, laboratory study and work at home, respectively.

Outcome of pregnancy related to solvent exposure in the first trimester indicates that miscarriage was higher among women not engaged in laboratory work (11.5%) compared with those working with solvent (10.6%).

No dose–response trend was observed when comparing frequency of work with solvent with frequency of miscarriage.

No effects of solvent exposure were apparent on incidence of malformation.

Birth weight was not correlated with exposure to solvent.

Miscarriage rate was 12.5% among women exposed to acetone during the first trimester.

 Axelsson et al. 1984

Retrospective case–referent study of female laboratory workers

Spontaneous abortion study included 535 women (206 cases and 329 referents)

Malformation study included 141 women (36 cases and 105 referents)

Birth weight analysis included 500 referent women

 Solvent use was self- reported, with frequency of use per week specified on an individual chemical basis. An exposure index was calculated for each individual.

Odds ratio of spontaneous abortion for acetone was 1.2 (95% CI 0.7–1.8) in women exposed 1–2 days/week and 1.3 (95% CI 0.7–2.4) in women exposed 3–5 days/week.

Odd ratios for congenital malformations were not increased for any type of chemical exposure. Acetone was not assessed individually.

Birth weight was negatively associated with mothers employed in a laboratory (133 g decrease). Acetone was not assessed individually.

 Taskinen et al. 1994
25 males working in reinforced plastic production plant matched to male patients from a fertility clinic Average breathing zone acetone concentrations in workers were 224, 385 and 164 mg/m3 for 10, 15 and 28 weeks, respectively, before semen collection. Semen was collected within 3 weeks of closure of the plant. Workers were also exposed to high concentrations (294–552 mg/m3) of styrene.

No effects on serum concentration of follicle stimulating and luteinizing hormones or on sperm concentration.

Increased live sperm (80% vs. 68% in controls).

Decreased percentage of immobile sperm (30% vs. 40% in controls).

Decreased percentage of normal sperm morphology (47% vs. 60% in controls).

 Jelnes 1988

Cross-sectional study

110 exposed males (ages 18.7–56.8 years, mean 37.6 years)

67 unexposed males (ages 20.7 –57.5 years, mean 41.9 years)

 Exposure to concentrations ranging from 5 to 1212 ppm (12–2888 mg/m3); mean TWA exposure over the course of the workday was 361 ppm (858 mg/m3)

Exposure-related increase in 1) eye irritation, tearing and acetone odour at the end of the workshift and 2) heavy, vague or faint feeling in the head, nausea and loss of weight.

No changes in hematological parameters, serum biochemistry or phagocytic activity of peripheral neutrophils.

No changes in Manifest Anxiety Scale scores, Self-rating Depression Scale scores or R-R interval variation on ECG

 Satoh et al. 1996
Retrospective mortality study of 948 subjects; additional evaluation on 341 subjects: 188 men, 153 women

TWA acetone concentration was 1000 ppm (2400 mg/m3)

13.9% of the employees employed for less than 1 year and 55.1% employed for more than 5 years in a cellulose fibre plant; acetone used as only solvent

Mortality study found no significant excess risk of death from any cause compared with the general population in the USA

All hematological and clinical blood chemistry parameters were within normal limits

Study did not include control group.

Study conducted to use the acetone-exposed group as reference group to examine the hematopoietic effect of methylene chloride during co-exposure of methylene chloride, acetone and methanol.

 Ott et al. 1983a, b, c
120 volunteers (30 per exposed group, 60 controls) Exposure to TWA acetone concentrations ranging from 948 to 1048 ppm in high-exposure group and from 549 to 653 ppm in low-exposure group (2300–2500 mg/m3 and 1300–1600 mg/m3, respectively). Exposed volunteers employed for at least 5 years at an acetate fibre manufacturing plant. Controls were never exposed to acetone.

Reported average urinary acetone levels were 93 mg/L and 62 mg/L for high- and low-exposure groups, respectively.

No statistically significant differences in hematological and clinical parameters noted, after adjusting for confounding factors such as smoking, alcohol consumption, age and past medical histories (liver and kidney damage).

 Grampella et al. (1987)
157 (71 occupationally exposed workers, 86 matched controls) Exposure to TWA acetone concentrations of 988–2114 mg/m3 over an 8 h shift. Workers employed for an average length of 14 years.

Compared with controls, increased prevalence of neurotoxic syndrome (mood disorders, irritability, memory difficulties, sleep disturbances, headache, and numbness in hands and feet) and irritation syndrome (upper respiratory tract irritation), and significant differences in motor nerve conduction velocity in median, ulna and peroneal nerves

Questions have been raised about the study methods (Graham 2000)

 Mitran et al. 1997
800 workers Exposure to acetone concentrations ranging from 1425 to 5100 mg/m3. Length of exposure not reported.

Sensory irritation and systemic toxicity (hematology and urinalysis) evaluated

No systemic toxicity or adverse health effects noted

NOEC for human sensory irritation was 3560 mg/m3

 Oglesby et al. 1949
410 volunteers (150 occupationally exposed employees, 260 non-exposed controls) Exposure to an average 8 h TWA concentration of 900 ppm (2140 mg/m3). Length of exposure not reported.

ALT, AST, total bilirubin and hematocrit were not significantly different between exposed and control groups

No difference in response rates for symptoms such as loss of memory, headache or dizziness between the exposed and control groups

 Soden 1993
9 workers Exposure for the 1st and 2nd years of study to short-term (about 2–3 h) acetone concentrations of 2300 ppm (5500 mg/m3) and 300 ppm (710 mg/m3) in the breathing zone at two different work stations. Acetone concentration in the general air was 110 ppm (260 mg/m3).

Exposure caused transient and intermittent eye, throat and nasal irritation, headaches and lightheadedness in individuals only when concentration exceeded 1000 ppm (2400 mg/m3)

CNS effects attributable to acetone exposure not observed

 Raleigh and McGee 1972

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2024-05-16