Vol. 151, No. 29 — July 22, 2017

GOVERNMENT NOTICES

DEPARTMENT OF THE ENVIRONMENT
DEPARTMENT OF HEALTH

CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999

Publication after screening assessment of four thiols specified on the Domestic Substances List [paragraphs 68(b) and 68(c) or subsection 77(1) of the Canadian Environmental Protection Act, 1999]

Whereas three of the four thiol substances identified in the annex below are identified under subsection 73(1) of the Canadian Environmental Protection Act, 1999;

Whereas a summary of the draft screening assessment conducted on dimethyl sulfide pursuant to paragraphs 68(b) and (c) and pursuant to section 74 of the Act for the remaining three substances is annexed hereby;

And whereas it is proposed to conclude that these four substances do not meet any of the criteria set out in section 64 of the Act,

Notice therefore is hereby given that the Minister of the Environment and the Minister of Health (the ministers) propose to take no further action at this time under section 77 of the Act for the substances identified under subsection 73(1) of the Act.

Notice is further given that options are being considered for follow up activities to track changes in environmental exposure to tert-dodecyl mercaptan and grapefruit mercaptan.

Public comment period

Any person may, within 60 days after publication of this notice, file with the Minister of the Environment written comments on the measure the ministers propose to take and on the scientific considerations on the basis of which the measure is proposed. More information regarding the scientific considerations may be obtained from the Canada.ca (Chemical Substances) website (www.canada.ca/en/health-canada/services/chemical-substances.html). All comments must cite the Canada Gazette, Part I, and the date of publication of this notice and be sent to the Executive Director, Program Development and Engagement Division, Department of the Environment, Gatineau, Quebec K1A 0H3, by fax to 819-938-5212, or by email to eccc.substances.eccc@canada.ca.

In accordance with section 313 of the Canadian Environmental Protection Act, 1999, any person who provides information in response to this notice may submit with the information a request that it be treated as confidential.

Jacqueline Gonçalves
Director General
Science and Risk Assessment Directorate

On behalf of the Minister of the Environment

David Morin
Director General
Safe Environments Directorate

On behalf of the Minister of Health

ANNEX

Summary of the draft screening assessment of four thiol substances

Pursuant to section 68 of the Canadian Environmental Protection Act, 1999 (CEPA), the Minister of the Environment and the Minister of Health have conducted a draft screening assessment of four of six substances referred to collectively under the Chemicals Management Plan as the Thiols Group. These four substances were identified as priorities for assessment as they met categorization criteria under subsection 73(1) of CEPA or were considered a priority on the basis of other human health concerns. Two of the six substances were subsequently determined to be of low concern through other approaches, and decisions for these substances are provided in separate screening assessments (see footnote 1). Accordingly, this draft screening assessment addresses the four substances listed in the table below.


Substances in the Thiols Group

CAS RN (see footnote 2)

Domestic Substances List name

Common name

75-18-3 (see footnote a)

Thiobis-methane

Dimethyl sulfide

150-60-7

Bis(phenylmethyl) disulfide

Benzyl disulfide

25103-58-6 (see footnote b)

tert-Dodecanethiol

tert-Dodecyl mercaptan

71159-90-5

alpha, alpha, 4-Trimethyl-3-cyclohexene-1-methanethiol

Grapefruit mercaptan

According to information submitted under section 71 of CEPA, there were no reports of manufacture of tert-dodecyl mercaptan in 2008 or of dimethyl sulfide, benzyl disulfide, or grapefruit mercaptan in 2011 above the reporting threshold of 100 kg in Canada. Dimethyl sulfide and tert-dodecyl mercaptan were imported into Canada in 2011 and 2008 at ranges of 10 000 to 100 000 kg and 100 000 to 1 000 000 kg, respectively. There were no reports of imports of benzyl disulfide and grapefruit mercaptan above the reporting threshold of 100 kg into Canada in 2011.

Dimethyl sulfide, benzyl disulfide, and grapefruit mercaptan may be used as food flavouring agents. The substance tert-dodecyl mercaptan has been identified as a component in the manufacture of some food packaging materials and may also be present as an impurity in paints and coatings. Dimethyl sulfide is being imported as an odorant in natural gas, and tert-dodecyl mercaptan is used in vinyl coverings, paper products, plastic and rubber materials, and metal materials.

The ecological risks of the substances in the Thiols Group were characterized using the Ecological Risk Classification of Organic Substances, which is a risk-based approach that employs multiple metrics for both hazard and exposure based on weighted consideration of multiple lines of evidence for determining risk classification. Hazard profiles are established based principally on metrics regarding mode of toxic action, chemical reactivity, food web-derived internal toxicity thresholds, bioavailability, and chemical and biological activity. Metrics considered in the exposure profiles include potential emission rate, overall persistence, and long-range transport potential. A risk matrix is used to assign a low, moderate or high level of potential concern for substances based on their hazard and exposure profiles. The Ecological Risk Classification of Organic Substances identified the four substances in the Thiols Group as having low potential to cause ecological harm.

Considering all available lines of evidence presented in this draft screening assessment, there is a low risk of harm to organisms and the broader integrity of the environment from dimethyl sulfide, benzyl disulfide, tert-dodecyl mercaptan and grapefruit mercaptan. It is proposed to conclude that dimethyl sulfide, benzyl disulfide, tert-dodecyl mercaptan and grapefruit mercaptan do not meet the criteria under paragraph 64(a) or (b) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity or that constitute or may constitute a danger to the environment on which life depends.

The assessment of dimethyl sulfide by the Organization for Economic Cooperation and Development (OECD) did not identify effects of concern for human health. The Joint FAO/WHO (Food and Agriculture Organization/World Health Organization) Expert Committee on Food Additives (JECFA) determined that there are no safety concerns related to the use of benzyl disulfide and grapefruit mercaptan as food flavouring agents. The assessment of tert-dodecyl mercaptan by OECD noted effects on the liver in laboratory animals via the inhalation route, as well as the absence of developmental effects.

Dimethyl sulfide is imported as an odorant in natural gas and potential exposure to the general population from this use is expected to be limited. There is potential for dietary exposure to dimethyl sulfide and grapefruit mercaptan from possible uses of these substances as food flavouring agents and to tert-dodecyl mercaptan from its use in the manufacture of some food packaging materials such as coatings. The substance tert-dodecyl mercaptan may also be present as an impurity in some paints and coatings. There are no reports of benzyl disulfide and grapefruit mercaptan being identified in products available to consumers in Canada. Based on a consideration of the assessments by other organizations and their limited uses, the potential risk to human health is considered to be low for the substances in the Thiols Group. A concern for human health was not identified for tert-dodecyl mercaptan in a comparison of the levels Canadians may be exposed to from its presence as an impurity in some paints and coatings and of the levels associated with health effects in laboratory studies.

Based on the information presented in this draft screening assessment, it is proposed to conclude that dimethyl sulfide, benzyl disulfide, tert-dodecyl mercaptan and grapefruit mercaptan do not meet the criteria under paragraph 64(c) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

Proposed conclusion

It is proposed to conclude that the four thiol substances in this draft screening assessment do not meet any of the criteria set out in section 64 of CEPA.

Consideration for follow-up

While exposure of the environment to two of the four substances, tert-dodecyl mercaptan and grapefruit mercaptan, is not of concern at current levels, these substances are associated with environmental effects of concern. Therefore, there may be a concern for the environment if exposures were to increase. Follow-up activities to track changes in exposure and/or commercial use patterns are under consideration.

Stakeholders are encouraged to provide, during the 60-day public comment period on the draft screening assessment, any information pertaining to these substances that may help inform the choice of follow up activity. This could include information on new or planned import, manufacture or use of the substances, if the information has not previously been submitted to the ministers.

The draft screening assessment for these substances is available on the Canada.ca (Chemical Substances) website (www.canada.ca/en/health-canada/services/chemical-substances.html).

[29-1-o]

DEPARTMENT OF THE ENVIRONMENT
DEPARTMENT OF HEALTH

CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999

Publication after screening assessment of two arenes — benzene, (1-methylethyl) (cumene), CAS RN (see footnote 3) 98-82-8, and benz[a]anthracene, 7,12-dimethyl- (DMBA), CAS RN 57-97-6 — specified on the Domestic Substances List (subsection 77(1) of the Canadian Environmental Protection Act, 1999)

Whereas cumene and DMBA are substances identified under subsection 73(1) of the Canadian Environmental Protection Act, 1999;

Whereas a summary of the draft screening assessment conducted on these two substances pursuant to section 74 of the Act is annexed hereby;

And whereas it is proposed to conclude that these two substances do not meet any of the criteria set out in section 64 of the Act,

Notice therefore is hereby given that the Minister of the Environment and the Minister of Health (the ministers) propose to take no further action on these two substances at this time under section 77 of the Act.

Notice is further given that options are being considered for follow-up activities to track changes in exposure to these two substances.

Public comment period

As specified under subsection 77(5) of the Canadian Environmental Protection Act, 1999, any person may, within 60 days after publication of this notice, file with the Minister of the Environment written comments on the measure the ministers propose to take and on the scientific considerations on the basis of which the measure is proposed. More information regarding the scientific considerations may be obtained from the Canada.ca (Chemical Substances) website (www.canada.ca/en/health-canada/services/chemical-substances.html). All comments must cite the Canada Gazette, Part I, and the date of publication of this notice and be sent to the Executive Director, Program Development and Engagement Division, Department of the Environment, Gatineau, Quebec K1A 0H3, by fax to 819-938-5212, or by email to eccc.substances.eccc@canada.ca.

In accordance with section 313 of the Canadian Environmental Protection Act, 1999, any person who provides information in response to this notice may submit with the information a request that it be treated as confidential.

Jacqueline Gonçalves
Director General
Science and Risk Assessment Directorate

On behalf of the Minister of the Environment

David Morin
Director General
Safe Environments Directorate

On behalf of the Minister of Health

ANNEX

Summary of the draft screening assessment of two arenes

Pursuant to section 74 of the Canadian Environmental Protection Act, 1999 (CEPA), the Minister of the Environment and the Minister of Health have conducted a screening assessment of two of nine substances referred to collectively under the Chemicals Management Plan as the Arenes Group. These two substances were identified as priorities for assessment as they met categorization criteria under subsection 73(1) of CEPA. Seven of the nine substances were subsequently determined to be of low concern through other approaches, and decisions for these substances are provided in separate reports. (see footnote 4), (see footnote 5) Accordingly, this screening assessment addresses the two substances listed in the table below.

Substances in the Arenes Group

CAS RN (see footnote 6)

Domestic Substances List name

Common name

98-82-8

Benzene, (1-methylethyl)-

Cumene; isopropylbenzene

57-97-6

Benz[a]anthracene, 7,12-dimethyl-

7,12-dimethylbenz[a]anthracene (DMBA)

In 2011, between 100 000 and 1 000 000 kg of cumene (CAS RN 98-82-8) were reported to be manufactured in Canada, and the same quantity was imported into Canada. There were no reports of manufacture or import for 7,12-dimethylbenz[a]anthracene (DMBA, CAS RN 57-97-6) above the reporting threshold of 100 kg for the same year. In Canada, cumene is primarily used as a chemical intermediate, but it is also used in products available to consumers, including adhesives, paints, automotive-related products, and lubricants. In Canada, DMBA is used as a research chemical in laboratories. It can also be produced unintentionally from industrial processes as a by-product.

The ecological risks of cumene and DMBA were characterized using the ecological risk classification (ERC). The ERC is a risk-based approach that employs multiple metrics for both hazard and exposure based on weighted consideration of multiple lines of evidence for determining risk classification. Hazard profiles are established principally on the basis of metrics regarding mode of toxic action, chemical reactivity, food web-derived internal toxicity thresholds, bioavailability, and chemical and biological activity. Metrics considered in the exposure profiles include potential emission rate, overall persistence, and long-range transport potential. A risk matrix is used to assign a low, moderate or high level of potential concern for substances based on their hazard and exposure profiles. The ERC identified cumene and DMBA as having low potential to cause ecological harm.

Considering all available lines of evidence presented in this draft screening assessment, there is a low risk of harm to organisms and the broader integrity of the environment from cumene and DMBA. It is proposed to conclude that cumene and DMBA do not meet the criteria under paragraph 64(a) or (b) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity or that constitute or may constitute a danger to the environment on which life depends.

The risks to human health for cumene and DMBA were characterized on the basis of available health effects and exposure information.

For cumene, laboratory studies have identified carcinogenicity as a critical health effect following long-term exposure by the inhalation route. As well, following oral administration for six months or inhalation for three months, non-cancer effects were observed in laboratory studies on the kidney (six-month oral study) and liver (three-month inhalation study). Systemic adverse effects were not observed in acute and short-term laboratory studies following inhalation or dermal administration. General population exposure to cumene from environmental media and from its possible presence in food was characterized using measured levels. The predominant source of exposure was indoor air. On the basis of a comparison of exposure estimates and critical effect levels identified in health effects studies, margins of exposure were considered to be adequate to address uncertainties in the human health effects and exposure databases. Estimates of exposure to cumene from the use of various consumer products were derived and were not identified as a concern for human health, as available laboratory studies do not identify acute and short-term exposures to be of concern.

DMBA is genotoxic and laboratory studies have identified carcinogenicity to multiple organs as a critical health effect following administration by the oral and dermal routes. It is considered that the substance could be carcinogenic via the inhalation route, and estimates of potency were derived on the basis of route-specific potencies of a well-studied polycyclic aromatic hydrocarbon. General population exposure to DMBA was characterized using measured levels in ambient air in Canada. On the basis of a comparison of exposure estimates and the derived critical effect level in health effects studies, the margin of exposure was considered adequate to address uncertainties in the human health effects and exposure databases.

Based on the information presented in this draft screening assessment, it is proposed to conclude that cumene and DMBA do not meet the criteria under paragraph 64(c) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

Proposed conclusion

It is proposed to conclude that cumene and DMBA do not meet any of the criteria set out in section 64 of CEPA.

Consideration for follow-up

While exposure of the general population and the environment to cumene and DMBA is not of concern at current levels, cumene is associated with human health effects of concern, and DMBA is associated with environmental and human health effects of concern. Therefore, there may be a concern for human health and the environment if exposure were to increase. Follow-up activities to track changes in exposure and/or commercial use patterns are under consideration.

Stakeholders are encouraged to provide, during the 60-day public comment period on the draft screening assessment, any information pertaining to the substance that may help inform the choice of follow-up activity. This could include information on new or planned import, manufacture or use of the substance, if the information has not previously been submitted to the ministers.

The draft screening assessment for this substance is available on the Canada.ca (Chemical Substances) website (www.canada.ca/en/health-canada/services/chemical-substances.html).

[29-1-o]

DEPARTMENT OF THE ENVIRONMENT
DEPARTMENT OF HEALTH

CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999

Publication after screening assessment of 57 substances specified on the Domestic Substances List (paragraphs 68(b) and 68(c) or subsection 77(1) of the Canadian Environmental Protection Act, 1999)

Whereas 55 of the 57 substances identified in the annex below are on the Domestic Substances List identified under subsection 73(1) of the Canadian Environmental Protection Act, 1999;

Whereas a summary of the draft screening assessment conducted on the 55 substances pursuant to section 74 of the Act and on the remaining 2 substances pursuant to paragraphs 68(b) and (c) is annexed hereby;

And whereas it is proposed to conclude that the 57 substances do not meet any of the criteria set out in section 64 of the Act,

Notice therefore is hereby given that the Minister of the Environment and the Minister of Health (the ministers) propose to take no further action at this time under section 77 of the Act for the 55 substances identified under subsection 73(1) of the Act.

Notice is further given that the ministers propose to take no further action on the remaining two substances at this time.

Public comment period

Any person may, within 60 days after publication of this notice, file with the Minister of the Environment written comments on the measure the ministers propose to take and on the scientific considerations on the basis of which the measure is proposed. More information regarding the scientific considerations may be obtained from the Canada.ca (Chemical Substances) website (www.canada.ca/en/health-canada/services/chemical-substances.html). All comments must cite the Canada Gazette, Part I, and the date of publication of this notice and be sent to the Executive Director, Program Development and Engagement Division, Department of the Environment, Gatineau, Quebec K1A 0H3, by fax to 819-938-5212, or by email to eccc.substances.eccc@canada.ca.

In accordance with section 313 of the Canadian Environmental Protection Act, 1999, any person who provides information in response to this notice may submit with the information a request that it be treated as confidential.

Jacqueline Gonçalves
Director General
Science and Risk Assessment Directorate

On behalf of the Minister of the Environment

David Morin
Director General
Safe Environments Directorate

On behalf of the Minister of Health

ANNEX

Summary of the draft screening assessment of the Sector-specific Inorganic UVCBs Group

Pursuant to sections 68 and 74 of the Canadian Environmental Protection Act, 1999 (CEPA), the Minister of the Environment and the Minister of Health have conducted a screening assessment of 57 Unknown or Variable Composition, Complex Reaction Products and Biological Materials (UVCB) substances, referred to collectively as the Sector-specific Inorganic UVCBs Group. The substances in this group were identified as priorities for assessment, as they met categorization criteria under subsection 73(1) of CEPA or were considered a priority on the basis of other human health concerns. The Chemical Abstracts Service Registry Numbers (CAS RN (see footnote 7)), the Domestic Substances List (DSL) names and the common names of the substances are listed in the table below.

The 57 substances included in the Sector-specific Inorganic UVCBs Group

CAS RN

DSL name

Common name

65996-69-2

Slags, ferrous metal, blast furnace

Blast furnace slag

65996-71-6

Slags, steelmaking

Steelmaking slag

66071-92-9

Sulfite liquors and Cooking liquors, spent

Black liquor or red liquor (see footnote c)

67711-90-4

Flue dust, copper-refining

Copper smelting dusts

67711-91-5

Matte, copper

Copper matte

67711-95-9

Slimes and Sludges, copper electrolytic

Electrowinning cell sludge

67712-00-9

Slimes and Sludges, copper refining

Precipitates and slurries, copper refining

68131-30-6 (see footnote d)

Sulfite liquors and Cooking liquors, green

Green pulping liquor

68131-31-7 (see footnote e)

Sulfite liquors and Cooking liquors, spent, alkali-treated

Alkaline treated spent sulfite liquor

68475-76-3

Flue dust, portland cement

Kiln dust

69011-50-3

Zinc, dross

Zinc dross

69011-54-7

Silver, bullion

Dore

69011-59-2

Lead alloy, base, dross

Arsenic-nickel dross

69011-69-4

Cadmium, dross

Cadmium dross

69011-70-7

Cadmium, sponge

Cadmium sponge

69011-71-8

Aluminum dross

Aluminum dross

69011-72-9 (see footnote f)

Aluminum, manufg. cathodes, carbon

Carbon cathode

69011-86-5

Zinc ores, concs., preleached

Zinc, preleached concentrates

69012-17-5

Waste solids,
copper-casting

Copper casting scales and solids

69012-24-4

Wastewater, zinc sulfate electrolytic, acid

N/A

69012-43-7

Slimes and Sludges, zinc sulfate electrolytic

Electrolytic zinc residue

69012-48-2

Residues, zinc-refining wastewater, zinc hydroxide

Zinc hydroxide precipitate

69012-50-6

Matte, nickel

Nickel matte

69012-65-3

Fumes, zinc

Zinc fumes

69012-67-5

Leach residues, copper cake

Copper residue

69012-69-7

Leach residues,
zinc-fume

Zinc fume leach residue

69012-70-0

Leach residues, zinc ore-calcine

Zinc calcine leach residue

69012-73-3

Leach residues, zinc ore-calcine, zinc sulfur

Zinc sulfur residue

69012-79-9

Calcines, zinc ore-conc.

Calcined zinc ore concentrates

69029-50-1

Lead, antimonial

Antimonial lead

69029-52-3

Lead, dross

Lead dross

69029-67-0

Flue dust, lead-refining


Lead smelter flue dust

69029-80-7

Residues, precious metal recovery lead refining

N/A

69029-82-9

Residues, zinc dross

N/A

69029-84-1

Slags, lead smelting

Lead smelter slag

69029-85-2

Slags, precious metal recovery lead refining

N/A

69029-93-2

Slimes and Sludges, lead refining

N/A

69227-11-8

Lead, dross, copper-rich

Copper dross

84583-61-9

Slimes and Sludges, zinc electrolytic

N/A

84776-00-1

Slimes and Sludges, tin electrolytic

N/A

85116-70-7

Ashes (residues), galvanization

Zinc ash

94552-05-3

Waste solids, lead silver anode

N/A

96690-57-2

Waste solids, aluminum oxide electrolysis, cathodic

Hydrated recovered carbon

98072-44-7

Flue dust, precious metal refining

Precious metal melting dusts

98072-60-7

Slags, precious metal refining

Precious metals smelting slag

98072-61-8

Slimes and Sludges, precious metal refining

Precious metals refining slimes, sludges and residues

121053-32-5

Flue dust, nickel-refining

Nickel smelting dusts

121053-33-6

Slags, nickel-refining

Nickel melting furnace slag

124222-16-8

Residues,
copper-refining

Residue, copper electrolytic

124222-19-1

Slimes and Sludges, nickel electrolytic

Precipitates and slurries, nickel electrolytic

124222-20-4

Slimes and Sludges, precious metal electrolytic

Precipitates and slurries, precious metal electrolytic

124316-01-4

Slags, copper-refining

Copper smelter or refinery slag

125408-74-4

Slags, ferrous metal, blast furnace, desulfurizing

N/A

128704-79-0

Leach solutions, zinc refining

N/A

129618-34-4

Electrolytes, nickel-manufg.

N/A

129618-37-7

Solutions, precious metal hydrometallurgical

Precious metals refining solutions

175448-53-0

Slags, lead smelting, zinc-reduced

N/A

Abbreviation: N/A = Not available

These 57 UVCBs were grouped for assessment, as their commercial activity is restricted to a small number of industrial sectors, and exposure is either not expected or is considered to be negligible. The approach used in this assessment focuses on the exposure characterization of the substances and includes consideration of information on commercial activity (i.e. manufacturing or import into Canada), uses, as well as existing measures to prevent or limit exposure to the environment and consequently to the general population of Canada.

The main sectors of activity for the substances are the base metals processing, iron and steel manufacturing, aluminum manufacturing, pulp and paper, and cement manufacturing sectors. The potential for exposure to the environment was assessed by grouping the substances among five “types” to clarify the release potential of the substances: “no longer manufactured or imported,” “intermediate,” “waste,” “by-product” or “substances with other commercial uses in other sectors.” For substances that were no longer manufactured or imported, and intermediates, exposure was not expected, as the substances were either no longer in commerce or were found to be consumed on-site (or at other facilities) as feedstock or for energy recovery. For substances determined to be wastes or by-products, exposure to the environment was considered negligible because the substances were either disposed of on-site at the facility (e.g. some wastes from the base metals processing sector) or sent to a specialized hazardous waste facility, or they met regulation standards to confirm lack of hazardous characteristics.

This approach used information submitted by companies in response to either a voluntary survey or to Phase 2 of the DSL Inventory Update (IU), as well as other technical information, including technical reports generated for Environment Canada. Based on the information received, 38 substances were determined to be no longer manufactured or imported or intermediates; 10 were determined to be intermediates or wastes; 3 were determined to be by-products or wastes; and 5 were determined to be wastes. Based on the information available, the potential for exposure of these substances to the environment is either negligible or not expected. One additional substance, a sulfite liquor (CAS RN 68131-31-7), was determined to be an intermediate within the pulp and paper sector for which exposure to the environment is not expected, and the exposure characterization of the substance for a number of applications within other sectors determined that its potential for exposure to the environment is negligible.

Considering all available lines of evidence presented in this draft screening assessment, there is a low risk of harm to organisms and the broader integrity of the environment from all 57 substances in the Sector-specific Inorganic UVCBs Group. It is proposed to conclude that these 57 substances do not meet the criteria under paragraph 64(a) or (b) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity or that constitute or may constitute a danger to the environment on which life depends.

Given that ecological exposure was either negligible or not expected, general population exposure to substances through environmental media was consequently considered to be either negligible or not expected. In addition, uses identified (beyond the pulp and paper sector) were not considered to result in exposure to the general population. Accordingly, risk to human health is considered to be low for all 57 substances.

Based on the information presented in this draft screening assessment, it is proposed to conclude that the 57 substances in the Sector-specific Inorganic UVCBs Group do not meet the criteria under paragraph 64(c) of CEPA, as they are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

Proposed conclusion

It is proposed to conclude that the 57 substances in the Sector-specific Inorganic UVCBs Group do not meet any of the criteria set out in section 64 of CEPA.

The draft screening assessment for these substances is available on the Canada.ca (Chemical Substances) website (www.canada.ca/en/health-canada/services/chemical-substances.html).

[29-1-o]

DEPARTMENT OF HEALTH

CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999

Residential indoor air quality guideline for acetaldehyde

Pursuant to subsection 55(3) of the Canadian Environmental Protection Act, 1999, the Minister of Health hereby gives notice of the issuance of a residential indoor air quality guideline for acetaldehyde.

The following exposure limits are recommended:

Exposure period

Concentration

Micrograms per Cubic Metre
(µg/m3)

Parts per Billion (ppb)

Short-term (1 hour)

1 420

795

Long-term (24 hours)

280

157

Acetaldehyde is a volatile organic compound commonly found in indoor air. These recommended exposure limits are protective against the potential health effects of exposure to acetaldehyde via inhalation. The Government of Canada had previously conducted an evaluation of the human health effects associated with exposure to acetaldehyde (Environment Canada and Health Canada, 2000). This current assessment provides an update on the health effects of acetaldehyde based on scientific information published since the previous report.

July 22, 2017

David Morin
Director General
Safe Environments Directorate

On behalf of the Minister of Health

ANNEX

Residential indoor air quality guideline for acetaldehyde

Background

Acetaldehyde is a colourless, flammable liquid with a pungent and irritating odour, is volatile at ambient temperature and pressure, and is found in both indoor and outdoor air. In Environment Canada and Health Canada’s 2000 Priority Substances List Assessment Report: Acetaldehyde, it was concluded that acetaldehyde is toxic under the Canadian Environmental Protection Act, 1999 (CEPA) because it may be a genotoxic carcinogen; however, there was considerable uncertainty as to the actual cancer risk. Since the publication of the report, a number of key studies have been published, including those related to the mode of action for acetaldehyde carcinogenesis. Therefore, in order to address the uncertainty in regard to the mode of action of acetaldehyde carcinogenesis, and to more accurately determine the risk to health from levels commonly found in Canadian homes, taking into account recently published scientific data, this substance was given high priority for a full health risk assessment and development of a residential indoor air quality guideline (RIAQG).

The present document reviews the epidemiological, toxicological, and exposure research on acetaldehyde, as well as the conclusions from a number of comprehensive reviews from internationally recognized health and environmental organizations. The document places an emphasis on research published since the most recent comprehensive review, and proposes new short- and long-term indoor air exposure limits. This RIAQG for acetaldehyde is intended to provide recommended exposure limits that would minimize risks to human health and support the development of actions to limit acetaldehyde emissions. This document also shows that, when compared to the newly proposed guidelines, levels in Canadian houses do not present a health risk.

Sources and exposure

Acetaldehyde is found ubiquitously throughout the ambient environment. Natural outdoor sources include higher plant respiration processes and emissions from forest fires. Combustion represents a major anthropogenic source of acetaldehyde, through incomplete combustion of organic material and fuels in motor vehicles. Emissions from industrial production, storage, transport, or disposal of products with residual acetaldehyde can also contribute to ambient concentrations. Secondary formation of acetaldehyde can occur through the oxidation of natural and anthropogenic volatile organic compounds (VOCs) present in the atmosphere.

There are numerous sources of acetaldehyde emissions in the indoor environment, often resulting in higher levels compared to outdoors. Incomplete combustion in fireplaces, wood-burning stoves and environmental tobacco smoke, along with certain cooking processes (notably those that use cooking oil), can emit significant quantities of acetaldehyde indoors. Emissions from products for interior finishes (e.g. vinyl flooring and carpets) and wood-based building materials (e.g. fibreboard and particleboard), as well as paints, stains, adhesives, caulking and foam sealants, may also contribute to indoor levels of acetaldehyde. An additional source of acetaldehyde indoors is from the infiltration of vehicle exhaust fumes into the home from an attached garage.

Some consumer products may directly contribute to indoor acetaldehyde levels, such as fragranced consumer products (e.g. air fresheners, liquid fabric softeners, dryer sheets, which may contain acetaldehyde), as well as indirectly via secondary formation of acetaldehyde from indoor reactions of ozone with other organic aerosols. Elevated indoor acetaldehyde levels have been shown to be associated with higher occupant density, likely due to “occupant activities” including, but not limited to, respiration releasing endogenously produced acetaldehyde.

Median acetaldehyde levels from Health Canada exposure studies measured in four cities (Edmonton, Halifax, Regina and Windsor) during winter and summer from 2005 to 2010 ranged from 10.5 to 48.7 µg/m3 (indoors) and from 2.4 to 7.2 µg/m3 (outdoors) [Health Canada 2010a, 2010b, 2012, 2013]. In one study (Windsor), personal exposure measurements were also collected, with a median range of 18.6 to 39.3 µg/m3. In these studies, the ratio of indoor to outdoor acetaldehyde concentrations was in general consistently above 2.5, which is indicative of a predominance of indoor sources of acetaldehyde.

Health effects

The health effects of exposure to acetaldehyde have been examined in toxicological and controlled human exposure studies, with very little epidemiological evidence related to indoor acetaldehyde exposure. In this assessment, the short-term exposure limit is derived from the results of a controlled human exposure study, whereas the long-term exposure limit is based on toxicological data from a study in a rodent model. Supporting evidence is provided by the results of other toxicological and controlled human exposure studies.

Based on the evidence from human and toxicological studies, the effects of short-term and long-term acetaldehyde inhalation are observed at the site of entry. Key health effects include tissue damage and cancer development, mainly in the upper respiratory tract.

Human studies

From the studies with human participants, acute exposure induced eye irritation and potentiated the bronchoconstriction response to methacholine challenge at acetaldehyde concentrations as low as 22 mg/m3, with nose and throat irritation reported at 50–200 ppm (89–357 mg/m3) [Myou et al. 1994b; Silverman, Schulte and First 1946]. At higher concentrations (350–1 000 mg/m3), aerosolized acetaldehyde was shown to directly cause bronchoconstriction in people with asthma (Myou et al. 1993, 1994b, 1994c, 1995; Fujimura et al. 1997; Prieto et al. 2000; 2002a; 2002b), and a bronchoconstrictive effect was induced in people with allergic rhinitis (2 240 mg/m3) [Prieto et al. 2002b]. Epidemiological data on the long-term effects in humans are limited to a single cross-sectional study of school children (Flamant-Hulin et al. 2010), demonstrating a significant association between acetaldehyde exposure (measured in classrooms) and increased pulmonary inflammation for non-asthmatic children, but not for asthmatic children.

Toxicological studies

In laboratory animals, acute acetaldehyde exposure induced irritation and bronchoconstriction responses. For sensory irritation, the lowest concentration that elicited a 50% decrease in respiratory rate was 2 845 ppm (5 080 mg/m3) for a 10-minute exposure in mice (Steinhagen and Barrow 1984), while exposure at ≥ 25 ppm (45 mg/m3) to acetaldehyde in rats increased vasodilation in the upper respiratory tract (Stanek et al. 2001).

In animal studies, long-term inhalation exposure to acetaldehyde caused a number of non-neoplastic effects primarily in the upper respiratory tract, specifically inflammation and tissue injury (degeneration, hyperplasia, and metaplasia). In rat studies, long-term acetaldehyde exposure caused adverse effects in the olfactory and respiratory epithelia of the nasal cavity, with lesions noted at exposure concentrations as low as 268 mg/m3, and tissue injury sometimes reported in the larynx, pharynx, and trachea, typically at higher exposure levels (Woutersen et al. 1984, 1986; Saldiva et al. 1985; Appelman et al. 1986; Woutersen and Feron 1987; Cassee et al. 1996; Cassee, Groten and Feron 1996; Oyama et al. 2007; Dorman et al. 2008; Feron, Kruysse and Woutersen 1982). In hamster studies, tracheal and laryngeal tissues were more sensitive than the nasal cavity was, although effects were observed at higher concentrations than in the rat studies (Kruysse, Feron and Til 1975; Feron 1979; Feron, Kruysse and Woutersen 1982), indicating a species-related difference. In a small number of animal studies, other adverse effects, namely reduced pulmonary bactericidal activity (Aranyi et al. 1986), increased airway hyperresponsiveness (Kawano et al. 2012), neurological effects (Ortiz, Griffiths and Littleton 1974; Shiohara et al. 1985), and altered gonad weight (Kruysse, Feron and Til 1975) were noted. Growth retardation and mortality were observed at the highest exposure levels (4 464–8 929 mg/m3) [Kruysse, Feron and Til 1975; Feron 1979; Feron, Kruysse and Woutersen 1982].

The International Agency for Research on Cancer (IARC) categorized acetaldehyde as a class 2B carcinogen (possibly carcinogenic to humans) [IARC 1999]. Acetaldehyde has been shown to be genotoxic and mutagenic, inducing DNA damage in the form of DNA adducts, DNA–DNA crosslinks, DNA–protein crosslinks as well as more complex adducts (reviewed in Albertini 2013), and mutagenicity in in vitro test systems (Environment Canada and Health Canada 2000) as well as in an in vivo inhalation study in aldehyde dehydrogenase 2 (ALDH2) knockout mice (Kunugita et al. 2008). Chronic inhalational exposure has caused carcinogenic effects in rats and hamsters at concentrations that induce tissue changes in the upper respiratory tract, with specific-related differences in concentrations consistent with the non-neoplastic effects. In rats, chronic exposure resulted in a concentration-dependent increase in adenocarcinoma of the olfactory epithelium and squamous cell carcinoma of the respiratory epithelium occurring at the lowest exposure level (1 339 mg/m3) [Woutersen et al. 1986]. In hamsters, chronic exposure at ≥ 2 946 mg/m3 acetaldehyde resulted in a significant increase in tumour incidence of the larynx (Feron 1979; Feron, Kruysse and Woutersen 1982).

Susceptible sub-populations

Studies of short-term exposure in human volunteers provide evidence for asthmatics being a sensitive subgroup to inhaled acetaldehyde (Myou et al. 1993; Prieto et al. 2000, 2002b). An ALDH2 polymorphism (ALDH2-2, the non-functional variant, prevalent in 40% to 50% of the Asian population, which greatly alters the rate of acetaldehyde metabolism following alcohol consumption) may confer additional susceptibility to acetaldehyde exposure. Although an increased severity of acetaldehyde-induced effects has been demonstrated in studies using ALDH2 knockout mice (as compared to wild-type mice) [Isse et al. 2005; Oyama et al. 2007, 2010], in human studies, no significant difference in hyperresponsiveness was observed following inhaled aerosolized acetaldehyde (Teeguarden et al. 2008).

Mode of action for carcinogenesis

The weight of evidence points to a non-linear (or threshold) mode of action (MOA) for acetaldehyde carcinogenesis. The pattern of genotoxicity and mutagenicity is consistent with a cytotoxic (secondary to a proliferative response), rather than mutagenic (critical early event), MOA for carcinogenicity. Tumour development is proposed to be related to the occurrence of tissue damage and is dependent on saturation of capacity for acetaldehyde metabolism, enhanced cellular proliferation, and mutation in the nasal cavity.

There is evidence that the toxic effects of acetaldehyde may be due, in part, to an overwhelming of the acetaldehyde detoxification capacity at the site of exposure. Evidence indicates that acetaldehyde toxicity is associated with decreased ALDH activity, and is most predominant in ALDH knockout mouse models. In addition, decreased upper respiratory tract uptake of acetaldehyde at elevated concentrations appears to be related to ALDH activity. Following saturation of the metabolic capacity for acetaldehyde, the carcinogenicity of acetaldehyde is proposed to be dependent on the induction of cytotoxicity, leading to increased cell turnover from recurrent tissue damage and repair. While no studies examining the association between acetaldehyde inhalation and cell proliferation in the upper respiratory tract were identified, enhanced cell proliferation of the tongue, epiglottis and forestomach (i.e. tissues related to route of entry) was observed in a rat study following administration in drinking water (Homann et al. 1997). In addition, acetaldehyde has been shown to induce DNA damage in the form of DNA adducts, DNA–DNA crosslinks, DNA–protein crosslinks and more complex adducts. These types of damage, under certain conditions, including at high exposure concentrations and in association with tissue damage, lead to mutation.

The pattern of key events leading to tumour development resembles that observed for formaldehyde, which is also proposed in the literature to act via a non-linear MOA for carcinogenesis. There is a high degree of similarity in formaldehyde and acetaldehyde carcinogenesis, including similarities in the structure and toxicity of the two compounds, the critical key events including DNA–protein crosslink formation, the development of nasal carcinomas in animals at highly irritating and damaging concentrations, and limited evidence of genotoxicity in vivo.

Residential indoor air quality guideline for acetaldehyde

The determination of a RIAQG is carried out in two stages. First, a reference concentration (RfC) is derived by applying uncertainty factors to the concentrations at which the most sensitive adverse health endpoint was observed. The RfC approach is used for the determination of a guideline to reduce potential health impacts such as those observed in key toxicological, controlled human exposure, and indoor epidemiological studies.

For the short-term exposure RfC, the exposure period is specified; in the present case, one hour. For the long-term exposure RfC, the exposure is considered to occur over months or years, up to a lifetime.

In the second stage, the short- and long-term exposure RfCs are compared with measured exposures in residential indoor air, and evaluated with respect to their technical feasibility. If the RfC is considered attainable where reasonable control measures are followed, the RIAQG is set equal to the RfC. If the RfC is considered unattainable with currently available risk management technology and practices, the RIAQG may be set at a higher concentration. Setting the RIAQG at a higher concentration than the RfC results in a smaller margin of exposure between the RIAQG and the concentration at which effects have been observed in health studies. Nonetheless, a RIAQG derived in this manner does provide a measure of health protection, while remaining an achievable target for improving indoor air quality when evaluating risk management measures.

Short-term residential indoor air quality guideline

For short-term exposure to acetaldehyde, in a study investigating bronchoconstriction response in human volunteers, a provocative concentration required to produce a 20% fall in forced expiratory volume in one-second (FEV1) geometric mean for asthmatic subjects of 527 mg/m3 (95% CI: 142–1 149 mg/m3) acetaldehyde following a two-minute exposure was identified (Prieto et al. 2000). The lower 95% confidence level of 142 mg/m3 was chosen as the point of departure, and uncertainty factors (UFs) of 10 to account for a use of a lowest observed adverse effects level (LOAEL) and 10 to account for additional sensitivity in the human population (e.g. more severe asthmatics, children, ALDH polymorphisms) were applied. Thus, the short-term RfC is 1 420 µg/m3. The Health Canada residential indoor air exposure studies provide a 24-hour integrated sample of acetaldehyde measurements, which does not represent acute or peak exposure. It is evident from these 24-hour measurements that the short-term reference exposure level is significantly higher than the median range of indoor air concentrations. Therefore, as this exposure limit is achievable in Canadian homes, the proposed short-term RIAQG for acetaldehyde is 1 420 µg/m3.

It is recommended that the short-term exposure limit be compared to a one-hour air sample.

Long-term residential indoor air quality guideline

For chronic exposure, the most sensitive neoplastic endpoint was adenocarcinoma in the nasal cavity of male rats, with the most sensitive non-neoplastic endpoint being degeneration of the olfactory epithelium in rats. As discussed above, a strong body of evidence has also emerged to support the notion that acetaldehyde exerts its carcinogenic effect through a non-linear MOA, with non-neoplastic effects being precursors to a carcinogenic response. Therefore, derivation of an RfC for the neoplastic effects of acetaldehyde is based on the observation of the non-neoplastic effects. A no observed adverse effect level (NOAEL) of 89 mg/m3 is selected, based on degeneration of the olfactory epithelium in rats (Dorman et al. 2008). Using an upper respiratory tract physiologically based pharmacokinetic model for acetaldehyde inhalation, the human equivalent concentration (HEC) calculated is 120 mg/m3. This value is adjusted for continuous exposure, resulting in an adjusted HEC of 21 mg/m3. Uncertainty factors of 2.5 to account for toxicodynamic differences between animals and humans, 10 for additional sensitivity in the human population, and 3 for uncertainty in the shape of the lower region of the concentration–response curve were applied, resulting in a total UF of 75. Thus, the long-term RfC is 280 µg/m3. The range of median indoor air acetaldehyde concentrations measured in Canadian homes from the Health Canada residential indoor air exposure studies for a 24-hour averaging period was 10.5 to 48.7 µg/m3, with the 95th percentile ranging from 35.6 to 149.5 µg/m3. This indicates that Canadian homes would not exceed the RfC of 280 µg/m3. Therefore, the proposed long-term RIAQG for acetaldehyde is 280 µg/m3.

When comparing a measured acetaldehyde concentration with the long-term exposure limit, the sampling time should be at least 24 hours.

Residential maximum exposure limits for acetaldehyde

Exposure period

Concentration

Critical effects

µg/m3

ppb

Short-term
(1 hour)

1 420

795

Increased airway responsiveness in asthmatics

Long-term
(24 hours)

280

157

Olfactory epithelial degeneration in the nasal cavity of rats

Levels of acetaldehyde in a typical Canadian home are likely well below both the short-term and long-term exposure limits, and accordingly are unlikely to pose a health risk.

Strategies for reducing exposure to acetaldehyde include controlling indoor emissions from combustion appliances and smoking. Control measures include the following:

Use of these strategies will help reduce exposure to acetaldehyde and other indoor air contaminants, particularly those in combustion gases and consumer products, including other VOCs.

References

Albertini, R. J. (2013) Vinyl acetate monomer (VAM) genotoxicity profile: Relevance for carcinogenicity. Critical reviews in toxicology, 43(8), 671–706.

Appelman, L. M., Woutersen, R. A., Feron, V. J., Hooftman, R. N. and Notten, W. R. (1986) Effect of variable versus fixed exposure levels on the toxicity of acetaldehyde in rats. Journal of Applied Toxicology, 6(5), 331–336.

Aranyi, C., O’Shea, W. J., Graham, J. and Miller, F. J. (1986) The effects of inhalation of organic chemical air contaminants on murine lung host defenses. Fundamental and Applied Toxicology, 6(4), 713–720.

Cassee, F. R., Arts, J. H. E., Groten, J. P. and Feron, V. J. (1996) Sensory irritation to mixtures of formaldehyde, acrolein, and acetaldehyde in rats. Archives of Toxicology, 70(6), 329–337.

Cassee, F. R., Groten, J. P. and Feron, V. J. (1996) Changes in the nasal epithelium of rats exposed by inhalation to mixtures of formaldehyde, acetaldehyde, and acrolein. Fundamental and Applied Toxicology, 29(2), 208–218.

Dorman, D. C., Struve, M. F., Wong, B. A., Gross, E. A., Parkinson, C., Willson, G. A., Tan, Y.-M., Campbell, J. L., Teeguarden, J. G., Clewell III, H. J. and Andersen, M. E. (2008) Derivation of an inhalation reference concentration based upon olfactory neuronal loss in male rats following subchronic acetaldehyde inhalation. Inhalation toxicology, 20(3), 245–256.

Environment Canada and Health Canada. (2000) Canadian Environmental Protection Act, 1999. Priority Substance List Assessment Report: Acetaldehyde; Minister of Public Works and Government Services, Ottawa, Canada.

Feron, V. J. (1979) Effects of exposure to acetaldehyde in syrian hamsters simultaneously treated with benzo(a)pyrene or diethylnitrosamine. Progress in experimental tumor research, 24(1), 162–176.

Feron, V. J., Kruysse, A. and Woutersen, R. A. (1982) Respiratory tract tumours in hamsters exposed to acetaldehyde vapour alone or simultaneously to benzo(a)pyrene or diethylnitrosamine. European Journal of Cancer and Clinical Oncology, 18(1), 13–31.

Flamant-Hulin, M., Caillaud, D., Sacco, P., Penard-Morand, C. and Annesi-Maesano, I. (2010) Air pollution and increased levels of fractional exhaled nitric oxide in children with no history of airway damage. Journal of Toxicology and Environmental Health - Part A: Current Issues, 73(4), 272–283.

Fujimura, M., Myou, S., Kamio, Y. and Matsuda, T. (1997) Inhibitory effect of indomethacin on tachyphylaxis in response to acetaldehyde-induced bronchoconstriction in patients with asthma. Journal of Allergy and Clinical Immunology, 99(5), 620–623.

Health Canada. (2013) Edmonton Indoor Air Quality Study (2010): Volatile Organic Compounds (VOC) Data Summary. Health Canada, Ottawa, Ontario. Cat.: H144-15/2013E-PDF.

Health Canada. (2012) Halifax Indoor Air Quality Study (2009): Volatile Organic Compounds (VOC) Data Summary. Health Canada, Ottawa, Ontario, Cat.: H129-19/2012E-PDF.

Health Canada. (2010a) Regina Indoor Air Quality Study (2007): VOC Sampling Data Summary. Health Canada, Ottawa, Ontario, Cat.: H128-1/10-617E-PDF.

Health Canada. (2010b) Windsor Exposure Assessment Study (2005–2006): Data Summary for Volatile Organic Compound Sampling. Health Canada, Ottawa, Ontario, Cat.: H128-1/10-618E-PDF.

Homann, N., Kärkkäinen, P., Koivisto, T., Nosova, T., Jokelainen, K. and Salaspuro, M. (1997) Effects of acetaldehyde on cell regeneration and differentiation of the upper gastrointestinal tract mucosa. Journal of the National Cancer Institute, 89(22), 1692–1697.

IARC. (1999) Re-Evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide. Summary of Data Reported and Evaluation. International Agency for Research on Cancer, Vol 71, World Health Organization, Lyon, France.

Isse, T., Oyama, T., Matsuno, K., Ogawa, M., Narai-Suzuki, R., Yamaguchi, T., Murakami, T., Kinaga, T., Uchiyama, I. and Kawamoto, T. (2005) Paired acute inhalation test reveals that acetaldehyde toxicity is higher in aldehyde dehydrogenase 2 knockout mice than in wild-type mice. Journal of Toxicological Sciences, 30(4), 329–337.

Kawano, T., Matsuse, H., Fukahori, S., Tsuchida, T., Nishino, T., Fukushima, C. and Kohno, S. (2012) Acetaldehyde at a low concentration synergistically exacerbates allergic airway inflammation as an endocrine-disrupting chemical and as a volatile organic compound. Respiration, 84(2), 135–141.

Kruysse, A., Feron, V. J. and Til, H. P. (1975) Repeated exposure to acetaldehyde vapor. Studies in Syrian golden hamsters. Archives of Environmental Health, 30(9), 449–452.

Kunugita, N., Isse, T., Oyama, T., Kitagawa, K., Ogawa, M., Yamaguchi, T., Kinaga, T. and Kawamoto, T. (2008) Increased frequencies of micronucleated reticulocytes and T-cell receptor mutation in Aldh2 knockout mice exposed to acetaldehyde. Journal of Toxicological Sciences, 33(1), 31–36.

Myou, S., Fujimura, M., Kamio, Y., Bando, T., Nakatsumi, Y. and Matsuda, T. (1995) Repeated inhalation challenge with exogenous and endogenous histamine released by acetaldehyde inhalation in asthmatic patients. American Journal of Respiratory and Critical Care Medicine, 152(2), 456–460.

Myou, S., Fujimura, M., Nishi, K., Matsuda, M., Ohka, T. and Matsuda, T. (1994b) Potentiating effect of inhaled acetaldehyde on bronchial responsiveness to methacholine in asthmatic subjects. Thorax, 49(7), 644–648.

Myou, S., Fujimura, M., Nishi, K., Ohka, T. and Matsuda, T. (1994c) Inhibitory effect of a selective thromboxane synthetase inhibitor, OKY-046, on acetaldehyde-induced bronchoconstriction in asthmatic patients. Chest, 106(5), 1414–1418.

Myou, S., Fujimura, M., Nishi, K., Ohka, T. and Matsuda, T. (1993) Aerosolized acetaldehyde induces histamine-mediated bronchoconstriction in asthmatics. American Review of Respiratory Disease, 148(4), 940–943.

Ortiz, A., Griffiths, P. J. and Littleton, J. M. (1974) A comparison of the effects of chronic administration of ethanol and acetaldehyde to mice: evidence for a role of acetaldehyde in ethanol dependence. Journal of Pharmacy and Pharmacology, 26(4), 249–260.

Oyama, T., Isse, T., Ogawa, M., Muto, M., Uchiyama, I. and Kawamoto, T. (2007) Susceptibility to inhalation toxicity of acetaldehyde in Aldh2 knockout mice. Frontiers in Bioscience, 12(5), 1927–1934.

Oyama, T., Nagayoshi, H., Matsuda, T., Oka, M., Isse, T., Yu, H. S., Pham, T. T. P., Tanaka, M., Kagawa, N., Kaneko, K. and Kawamoto, T. (2010) Effects of acetaldehyde inhalation in mitochondrial aldehyde dehydrogenase deficient mice (Aldh2-/-). Frontiers in Bioscience - Elite, 2 E(4), 1344–1354.

Prieto, L., Gutiérrez, V., Cervera, A. and Liñana, J. (2002a) Airway obstruction induced by inhaled acetaldehyde in asthma: Repeatability and relationship to adenosine 5′-monophosphate responsiveness. Journal of Investigational Allergology and Clinical Immunology, 12(2), 91–98.

Prieto, L., Sánchez-Toril, F., Gutiérrez, V. and Marín, M. J. (2002b) Airway responsiveness to inhaled acetaldehyde in subjects with allergic rhinitis: Relationship to methacholine responsiveness. Respiration, 69(2), 129–135.

Prieto, L., Sánchez-Toril, F., Brotons, B., Soriano, S., Casan, R. and Belenguer, J. L. (2000) Airway responsiveness to acetaldehyde in patients with asthma: Relationship to methacholine responsiveness and peak expiratory flow variation. Clinical and Experimental Allergy, 30(1), 71–78.

Saldiva, P. H., do Rio Caldeira, M. P., Massad, E., Calheiros, D. F., Cardoso, L. M., Böhm, G. M. and Saldiva, C. D. (1985) Effects of formaldehyde and acetaldehyde inhalation on rat pulmonary mechanics. Journal of Applied Toxicology, 5(5), 288–292.

Shiohara, E., Tsukada, M., Chiba, S., Yamazaki, H., Nishiguchi, K., Miyamoto, R. and Nakanishi, S. (1985) Effect of chronic administration of acetaldehyde by inhalation on (Na+ + K+)-activated adenosine triphosphatase activity of rat brain membranes. Toxicology, 34(4), 277–284.

Silverman, L., Schulte, H. F. and First, M. W. (1946) Further studies on sensory response to certain industrial solvent vapors. Journal of Industrial Hygiene and Toxicology, 28(6), 262–266.

Steinhagen, W. H. and Barrow, C. S. (1984) Sensory irritation structure-activity study of inhaled aldehydes in B6C3F1 and Swiss-Webster mice. Toxicology and applied pharmacology, 72(3), 495–503.

Teeguarden, J. G., Bogdanffy, M. S., Covington, T. R., Tan, C. and Jarabek, A. M. (2008) A PBPK model for evaluating the impact of aldehyde dehydrogenase polymorphisms on comparative rat and human nasal tissue acetaldehyde dosimetry. Inhalation toxicology, 20(4), 375–390.

Woutersen, R. A., Appelman, L. M., Feron, V. J. and Van Der Heijden, C. A. (1984) Inhalation toxicity of acetaldehyde in rats. II. Carcinogenicity study: Interim results after 15 months. Toxicology, 31(2), 123–133.

Woutersen, R. A., Appelman, L. M., Van Garderen-Hoetmer, A. and Feron, V. J. (1986) Inhalation toxicity of acetaldehyde in rats. III. Carcinogenicity study. Toxicology, 41(2), 213–231.

Woutersen, R. A. and Feron, V. J. (1987) Inhalation toxicity of acetaldehyde in rats. IV. Progression and regression of nasal lesions after discontinuation of exposure. Toxicology, 47(3), 295–305.

[29-1-o]

IMMIGRATION, REFUGEES AND CITIZENSHIP CANADA

AN ACT TO AMEND THE CITIZENSHIP ACT AND TO MAKE CONSEQUENTIAL AMENDMENTS TO ANOTHER ACT

Notice requesting comments on a proposal to amend the Citizenship Regulations, No. 2, and to implement provisions of An Act to amend the Citizenship Act and to make consequential amendments to another Act

Notice is hereby given that Immigration, Refugees and Citizenship Canada (IRCC) is seeking written comments from all interested parties on a proposal to amend the Citizenship Regulations, No. 2 (the Regulations) to align the Regulations with amendments to the Citizenship Act (the Act) made pursuant to Bill C-6, An Act to amend the Citizenship Act and to make consequential amendments to another Act (AACA).

Background

On June 19, 2017, the AACA received royal assent. The AACA is in line with the priorities set out in the mandate letter to the Minister of IRCC, which include repealing provisions of the Citizenship Act that provide for citizenship to be revoked on grounds that only apply to dual nationals, and that citizenship applicants must intend to continue to reside in Canada. The AACA also provides for greater flexibility for applicants to meet citizenship requirements by reducing physical presence requirements as well as allowing some time spent in Canada prior to becoming a permanent resident to count towards the physical presence requirement for citizenship. The AACA also includes additional measures to further enhance program integrity.

Description

The purpose of this notice of intent is to signal the Government’s intention to amend the Regulations in order to support the changes made to the Citizenship Act pursuant to the AACA. The Minister of Immigration, Refugees and Citizenship has the authority, through the Citizenship Act, to amend regulations in the areas described below.

Revocation notices: The AACA repeals subsections 10(2) and 10.1(2) of the Act that pertain to the revocation of citizenship of dual or multiple nationals based on certain acts against the national interest. It is proposed that the reference to subsection 10.1(2) in section 17 of the Regulations be removed from the Regulations, as the repeal of this subsection in the Act renders that segment of the Regulations unnecessary.

Physical presence requirements: The AACA repeals subparagraph 5(1)(c)(ii) of the Citizenship Act, which established the requirement that adult citizenship grant applicants be physically present in Canada for a minimum of 183 days in four calendar years out of the six years immediately before applying for citizenship. As paragraph 2(1)(c) of the Regulations includes a reference to subparagraph 5(1)(c)(ii) of the Act, it is proposed that this reference be removed from the Regulations, as the repeal of subparagraph 5(1)(c)(ii) renders that segment of the Regulations unnecessary.

Age range for language requirement: The AACA reduced the age range of citizenship applicants who must meet the language requirement from 14 to 64 years to 18 to 54 years. The proposed changes to the Regulations will align the age range under the Regulations with the new age range in the Citizenship Act by repealing the regulatory provision that minor citizenship grant applicants provide language evidence when submitting their application and amending the Regulations so that only adult citizenship grant applicants under 55 years of age at time of application are required to provide language evidence with their application.

Reference to tax filing period: The AACA includes an amendment to subparagraph 5(1)(c)(iii) of the Citizenship Act to change the tax filing requirement for applicants from four taxation years in a period of six years preceding the application, to three taxation years in a period of five years.

Paragraph 2(1)(f) of the Citizenship Regulations, No. 2 concerns applicants who do not have a tax filing number and were not required to file taxes in the applicable period, by requiring a declaration to be made to that effect. The declaration includes stating that they were not required to file a tax return within the six-year period preceding their application. Accordingly, paragraph 2(1)(f) will be amended to replace the reference to six years with five years to align the Regulations with the change in the AACA.

Age requirement for citizenship grant applications under subsection 5(1): The AACA includes amendments to the Citizenship Act that remove the age requirement for a grant of citizenship under subsection 5(1), which permits minors to apply for citizenship without a Canadian parent. The amendment includes a provision concerning who is permitted to make the application on behalf of the minor. Subsequently, amendments to paragraph 4(a) of the Citizenship Regulations, No. 2 are required to better align the terminology used in the Regulations with respect to who can make an application on behalf of a minor applicant under subsection 5(2) of the Act with the terminology in the Citizenship Act, as amended by the AACA. In addition, amendments are needed to paragraphs 2(1)(g), 2(2)(g) and 2(3)(c) of the Regulations to reflect that only applicants under subsection 5(1) who are 18 years of age or older are required to provide language and knowledge evidence to reflect the amendment introduced under the AACA.

Comments

The public is invited to provide comments and input into the proposed regulatory amendments described above before the Regulations are published in the Canada Gazette, Part II.

Anyone may, within 15 days of the publication of this notice, provide their comments on this notice of intent, in writing, to the person named below at the address provided.

Questions and requests for additional information may be directed to Teny Dikranian, Director, Legislation and Program Policy, Immigration, Refugees and Citizenship Canada, 180 Kent Street, 6th Floor, Ottawa, Ontario K1A 1L1, 613-991-2485 (fax), Citizenship-Citoyennete@cic.gc.ca (email).

Teny Dikranian
Director
Legislation and Program Policy

[29-1-o]

PRIVY COUNCIL OFFICE

Appointment opportunities

We know that our country is stronger — and our government more effective — when decision-makers reflect Canada’s diversity. Moving forward, the Government of Canada will use an appointment process that is transparent and merit-based, strives for gender parity, and ensures that Indigenous Canadians and minority groups are properly represented in positions of leadership. We will continue to search for Canadians who reflect the values that we all embrace: inclusion, honesty, fiscal prudence, and generosity of spirit. Together, we will build a government as diverse as Canada.

The Government of Canada is currently seeking applications from diverse and talented Canadians from across the country who are interested in the following positions.

Current opportunities

The following opportunities for appointments to Governor in Council positions are currently open for applications. Every opportunity is open for a minimum of two weeks from the date of posting on the Governor in Council Appointments website (http://www.appointments-nominations.gc.ca/slctnPrcs.asp?menu=1&lang=eng).

Position

Organization

Closing date

Directors

Canada Deposit Insurance
Corporation

August 8, 2017

Chairperson

Canada Foundation for Innovation

July 24, 2017

Directors

Canada Foundation for Innovation

August 8, 2017

Directors

Canada Lands Company Limited

August 4, 2017

Chairperson

Canada Mortgage
and Housing Corporation

August 14, 2017

Directors

Canada Mortgage
and Housing Corporation

August 14, 2017

Member

Canada–Newfoundland and Labrador Offshore Petroleum Board

August 16, 2017

Chairperson

Canadian Broadcasting Corporation

August 15, 2017

Directors

Canadian Broadcasting Corporation

August 15, 2017

President

Canadian Broadcasting Corporation

August 15, 2017

President

Canadian Centre for Occupational Health and Safety

August 16, 2017

Chairperson

Canadian Commercial Corporation

July 24, 2017

Directors

Canadian Commercial Corporation

August 10, 2017

Lay Members

Competition
Tribunal

July 24, 2017

Chairperson

Export
Development
Canada

July 24, 2017

Directors

Export
Development
Canada

August 10, 2017

Members

Great Lakes
Pilotage
Authority

August 1, 2017

Assistant Deputy Chairperson

Immigration
and Refugee
Board

August 2, 2017

President

International Development Research Centre

August 25, 2017

Members

Laurentian
Pilotage
Authority

August 1, 2017

Commissioner of Lobbying

Office of the Commissioner of Lobbying

 

Conflict of Interest
and Ethics Commissioner

Office of the Conflict of Interest and Ethics Commissioner

 

Information Commissioner

Office of the
Information Commissioner

 

Senate Ethics Officer

Office of the Senate Ethics Officer

August 25, 2017

Commissioner

Royal Canadian Mounted Police

September 15, 2017

Chairperson

Royal Canadian Mounted Police External Review Committee

August 16, 2017

Members

Standards Council
of Canada

August 8, 2017

Directors

Windsor-Detroit Bridge Authority

August 3, 2017

Ongoing opportunities

Opportunities posted on an ongoing basis.

Position

Organization

Closing date

Members

Veterans Review
and Appeal
Board

July 31, 2017

Upcoming opportunities

New opportunities that will be posted in the coming weeks.

Position

Organization

President (Chief Executive Officer)

Atomic Energy of Canada Limited

Director

Canada Post Corporation

Chairperson

Civilian Review and Complaints Commission for the Royal Canadian Mounted Police

Sergeant-at-Arms

House of Commons

Commissioner

International Joint
Commission

Chief Executive Officer

Invest in Canada Agency

Chief Electoral Officer

Office of the Chief Electoral Officer

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