ARCHIVED — Vol. 150, No. 7 — February 13, 2016

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GOVERNMENT NOTICES

DEPARTMENT OF HEALTH

CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999

Human Health Risk Assessment for Coarse Particulate Matter

The Minister of Health hereby gives notice of the availability of a science assessment document entitled Human Health Risk Assessment for Coarse Particulate Matter. This document consists of a detailed scientific assessment of the most relevant health- and exposure-related science for this air pollutant. Overall, this Health Canada assessment concludes that the data on the health effects of coarse particulate matter (PM10-2.5) are weaker than data on fine particles (PM2.5) but it cannot be dismissed that there are health effects resulting from short-term exposure to coarse PM, especially on the respiratory system. Some susceptible populations, such as children, people suffering from asthma, and the elderly, may also be at greater risk from coarse PM.

The full risk assessment report is available in both official languages upon request at the following Web site: http://www.healthycanadians.gc.ca/publications/healthy-living-vie-saine/particulate-particules/index-eng.php. Any person requiring further information may submit a request to the Air Health Effects Assessment Division, Health Canada, 269 Laurier Avenue West, Room 3-057, PL 4903c, Ottawa, Ontario K1A 0K9, AIR@hc-sc.gc.ca (email). All information requests must cite the Canada Gazette, Part I, as well as the date of publication of this notice.

January 27, 2016

JOHN COOPER
Acting Director General
Safe Environments Directorate

On behalf of the Minister of Health

APPENDIX

Human Health Risk Assessment for Coarse Particulate Matter — Summary

Health Canada has completed a detailed risk assessment entitled Human Health Risk Assessment for Coarse Particulate Matter, a stand-alone piece focusing on the potential health impacts of coarse particulate matter (PM10-2.5). The state of knowledge on the health effects of coarse PM has advanced and continues to advance, and approximately 150 new primary scientific publications were evaluated.

The assessment critically evaluated relevant information essential to establishing the weight of evidence for the various health effects associated with exposure to ambient coarse PM, and to establishing whether population health impacts can be expected from current ambient exposure. The health effects of coarse PM have been investigated through a number of different types of studies, with the strongest evidence coming from the epidemiological literature. These studies have primarily evaluated the impact of coarse PM on respiratory and cardiovascular outcomes. The results of work with human volunteers (controlled human exposure studies) and with animals (toxicological studies) in controlled laboratory settings support the epidemiological results and help to better understand the mechanisms of coarse PM impacts on heart and lung health.

The next few paragraphs provide a brief summary of the key health impacts of coarse particles and causality conclusions reached in the assessment.

Acute effects — Mortality

The health database supporting the relationship between coarse particles and mortality outcomes has grown over the past few years. There are fairly consistent positive associations between short-term exposure to ambient coarse PM and non-accidental, respiratory and cardiovascular mortality in the available epidemiological studies. However, the associations observed in these studies are sometimes not statistically significant, demonstrating only limited strength of association. Generally, the associations between coarse particles and mortality are similar in magnitude, but less precise, than those observed for fine particles, though this lack of precision is not unexpected given the larger exposure measurement error for the coarse fraction. There is also only limited support for coarse PM–related mortality in other lines of evidence. For example, respiratory morbidity is prominent in the toxicological and epidemiological studies, with little indication of effects that may be related to cardiovascular mortality, which comprises the bulk of non-accidental mortality. Uncertainty also remains about the potential for confounding by the fine PM fraction and/or gaseous pollutants. Overall, the epidemiology data are suggestive of a causal relationship between short-term exposure to the coarse PM fraction and mortality.

Acute effects — Morbidity
Respiratory effects

Fairly consistent coarse PM–related increases in hospital admissions and emergency room visits (ERVs) for respiratory conditions, most often for asthma in children, have been reported in epidemiological studies. These findings are mostly statistically significant, particularly for hospitalizations, and are supported by even more consistent significant increases in respiratory symptoms and asthma medication use in panel studies of asthmatic children. These findings have been robust across a number of study designs and model specifications, and also across different pollutant mixtures and health care systems. There is also fairly coherent evidence (across hospital admissions, ERVs, and panel, controlled human exposure and animal toxicology studies) that asthma exacerbation is a critical effect of coarse PM exposure and that children and the elderly are susceptible subgroups. Studies have provided experimental support for the epidemiological findings and emerging plausible mechanisms of action / toxic moieties (e.g. endotoxins). The main proposed mechanisms for PM–induced health effects are inflammation-induced injury and oxidative stress, with the specific component or components of particles responsible for the stimulation of various biological parameters being presently unknown (although biological matter, metal contaminants, and polycyclic aromatic hydrocarbons such as benzo(a)pyrene have all been implicated). Further, there is some indication of specificity of effect, with coarse PM being associated with effects in the upper respiratory tract and fine PM more with those in the lower respiratory tract, corresponding to their principal regions of deposition. However, important uncertainties remain concerning the possible role of co-pollutants in the observed associations. This is particularly important considering the relatively large measurement error and variation in composition of the coarse fraction. Overall, the epidemiology data and the limited results from controlled human exposure and toxicological studies are suggestive of a causal relationship between short-term exposure to the coarse PM fraction and respiratory effects.

Cardiovascular effects

There is little indication of coherence in the limited and sometimes inconsistent cardiovascular findings from available panel and controlled human exposure studies, and uncertainty remains with respect to the possible role of fine PM and gaseous pollutants in the associations observed in many epidemiology studies. However, the risk estimates for cardiovascular hospitalizations and mortality in relation to ambient coarse PM are generally positive, and there were significant and robust coarse PM–related increases in mortality from certain cardiovascular causes in two U.S. multi-centre studies. Overall, the findings in these population-based epidemiology studies are suggestive of a causal relationship between short-term exposure to the coarse PM fraction and cardiovascular effects, though investigations of cardiovascular endpoints in panel studies and in toxicological studies in animals and humans are too limited to shed much light on the weight of evidence.

Chronic effects — Mortality and morbidity

In contrast to the large number of studies of short-term variations in air pollutants associated with a range of mortality and morbidity endpoints, there have been relatively few studies that examined the respiratory and cardiovascular effects of long-term exposure to air pollutants. The associations of chronic exposure to ambient coarse particles with mortality and both respiratory and cardiovascular health effects have been examined more recently in prospective cohort studies, and the results do not provide significant insight into the role, if any, played by the coarse PM fraction. In addition, a limited number of studies have investigated the association between chronic exposure to coarse particles and adverse birth outcomes and infant mortality and results have been contradictory: a small negative effect on birth weight was observed in an American multi-city study, but this association varied widely with the geographical location, the study samples, and the covariates included in the model. There are important uncertainties with respect to the possible role of co-pollutants, the appropriate measure of exposure to PM, and critical periods of exposure during pregnancy. Overall, the epidemiology data are inadequate to infer a causal relationship between chronic exposure to the coarse PM fraction and mortality, respiratory and cardiovascular health effects, as well as with the incidence of developmental outcomes.

Overall conclusions

The body of evidence on the health effects of coarse PM has grown since the previous assessment but is still limited compared to that available on fine PM. The respiratory system appears to be the critical target for adverse effects following exposure to coarse particles. Overall, the data on the health effects of coarse particles are weaker than for fine particles and subject to larger measurement errors. These particles are also characterized by a more heterogeneous chemical composition. However, based on dosimetric, epidemiological, and toxicological studies performed in industrialized/urban areas, the existence of adverse health effects on the respiratory system resulting from short-term exposure to coarse particles cannot be dismissed.

An electronic copy of the document Human Health Risk Assessment for Coarse Particulate Matter may be obtained by contacting AIR@hc-sc.gc.ca.

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DEPARTMENT OF HEALTH

CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999

Human Health Risk Assessment for Sulphur Dioxide

The Minister of Health hereby gives notice of the availability of a science assessment document entitled Human Health Risk Assessment for Sulphur Dioxide. This document consists of a detailed scientific assessment of the most relevant health- and exposure-related science for this air pollutant. Overall, this Health Canada assessment identified potential health risks to the Canadian population from exposure to ambient concentrations of SO2, which are below the current National Ambient Air Quality Objectives (NAAQOs), and recommended that a new Canadian Ambient Air Quality Standard (CAAQS) be introduced.

The full risk assessment document is available in both official languages upon request at the following Web site: http://www.healthycanadians.gc.ca/publications/healthy-living-vie-saine/sulphur-soufre/index-eng.php. Any person requiring further information may submit a request to the Air Health Effects Assessment Division, Health Canada, 269 Laurier Avenue West, Room 3-057, PL 4903c, Ottawa, Ontario K1A 0K9, AIR@hc-sc.gc.ca (email). All information requests must cite the Canada Gazette, Part I, as well as the date of publication of this notice.

January 27, 2016

JOHN COOPER
Acting Director General
Safe Environments Directorate

On behalf of the Minister of Health

APPENDIX

Human Health Risk Assessment for Sulphur Dioxide — Executive Summary

The Air Quality Assessment Section of Health Canada undertook a health risk assessment of sulphur dioxide (SO2) in order to update the available information on adverse effects of SO2 to human health, determine recent Canadian SO2 exposure levels, and to inform the revision or development of Canadian ambient air quality objectives/standards.

Background

The existing National Ambient Air Quality Objectives (NAAQOs) for SO2 were published in the Canada Gazette, Part I, in 1989 (Table 1).

Table 1: Existing National Ambient Air Quality Objectives for SO2

Standard (see note *) Concentration SO2 (ppb) Concentration SO2 (µg/m3)
Maximum acceptable level: 1-h average 344 900
Maximum acceptable level: 24-h average 114 300
Maximum acceptable level: annual average 23 60
Maximum desirable level: 1-h average 172 450
Maximum desirable level: 24-h average 57 150
Maximum desirable level: annual average 11 30
Maximum tolerable level: 24-h average 305 800
  • Note 1
    (*) At 25ºC and 760 mmHg

Since that time, a large number of publications relevant to the potential human health effects of SO2 have become available. Additionally, exposures have changed with total SO2 levels decreasing by 96% in Canada since 1970 (Environment Canada, 2011), largely as a result of the use of alternative (low-sulphur) fuels and pollution reduction programs that limited SO2 emissions (Chen et al., 2007).

Fine particles, including sulphate particles, were evaluated by Health Canada as part of the Canadian Smog Science Assessment document (Government of Canada, 2012), so for the purposes of this current assessment, only gaseous SO2 will be considered.

Environmental concentrations of SO2 in Canada

National Air Pollution Surveillance (NAPS) data from the most recent year available (2011) were used to model Canadian exposure to SO2. NAPS data from each monitor were analyzed on an all-monitor basis, as well as stratified by urban and rural designations. Annual averages for SO2 ranged from below the detection limit to 8.6 ppb. The 24-h averages from urban residential sites ranged from below the detection limit to 56 ppb and the 1-h averages ranged from below the detection limit to 314 ppb. The majority of NAPS monitors did not detect SO2 on a regular basis. Additional ambient monitoring during the 2009–2011 period by Airpointer monitors also indicated that SO2 levels are typically close to the limit of detection, but there are short-lived spikes in concentrations. Shorter-term averaging times were available from the Airpointer data (e.g. 30-min and 10-min) and reflect these spikes with a maximum 10-min value of 322 ppb for a site with a nearby industrial source.

Human health assessment

Based upon the U.S. EPA Integrated Science Assessment (ISA) for Sulfur Oxides — Health Criteria (U.S. EPA, 2008) and an evaluation of the toxicology, controlled human exposure, epidemiology and mode of action/mechanistic literature since 2007, as well as the guidance on causal determinations, it has been concluded that the evidence supports a causal relationship between short-term exposure to ambient levels of SO2 and respiratory morbidity in adults, particularly in the asthmatic subpopulation. Similarly, the literature is suggestive of a causal relationship between short-term exposure to ambient levels of SO2 and respiratory morbidity in children. The epidemiology papers on respiratory morbidity support the conclusion that there are effects on lung function after short-term exposures to concentrations below the short-term maximum concentration identified in the NAPS data, suggesting a potential risk to the Canadian population. The effects of co-pollutants and confounding factors cannot be fully ruled out in epidemiology studies; therefore, the lowest observed adverse effect concentration (LOAEC) for lung function decrements, from controlled human exposure studies of asthmatics exposed to SO2 for 5–10 min at increased ventilation, was used to derive a reference concentration (RfC). Individuals in the controlled human exposure studies were found to react at a level that was below the maximum measured ambient concentration for the 10-min averaging time, which suggests that there is a potential risk to the Canadian population at current exposure levels.

The available information is suggestive of a causal relationship between short-term SO2 exposure and all-cause and cardiopulmonary mortality at current ambient exposure concentrations, particularly in people over 40 years of age (most strongly associated with the over-65 age group). However, some inconsistency in this database and confounding of the signal in these studies is possibly indicative of SO2 acting as a surrogate for certain sources (e.g. coal fired power plants) or reflecting effects after conversion to a particulate form.

The literature is weakly suggestive of a causal relationship with preterm birth and congenital heart malformation in babies exposed to SO2 in utero. The epidemiology data on reproductive and developmental endpoints identified risks of congenital malformations and preterm delivery after SO2 exposure during gestation at concentrations below the ambient annual maximum concentration identified in the NAPS data, suggesting a potential risk to the Canadian population at current exposure levels. However, even more so than as indicated above, SO2 may be acting in these studies as a surrogate for source or other pollutants with which it is correlated.

The databases were found to be inadequate to infer a causal relationship for other endpoints, including mortality and respiratory morbidity with long-term exposure, cardiovascular morbidity with short- or long-term exposure, carcinogenicity and low birth weights.

It should be noted that there are a number of issues related to interpretation of the epidemiology literature. Most importantly, it remains difficult to determine the role of confounding co- pollutants such as fine particulate matter (PM2.5) and coarse particulate matter (PM10) on the effects being reported. Therefore, it is important to consider the controlled human exposure study data in conjunction with the epidemiology literature, when it is available, as it is for respiratory morbidity. Additional lines of evidence are also considered to support the epidemiology findings, including evidence for potential mechanisms or modes of action and personal exposure analyses for systemic effects.

A 10-min RfC of 67 ppb was derived from the controlled human exposure studies for respiratory morbidity and uncertainties, including intraspecies variability.

Public health impacts

Although the magnitude of the risks of health effects associated with epidemiology, with respect to SO2 exposure, is relatively small, the risks represent important impacts on public health due to the number of people potentially affected. The subpopulations that appear to have increased susceptibility to adverse effects from SO2 exposure represent a considerable proportion of the population, with asthmatics and the elderly alone accounting for 8.9% and 14.8% of Canadians, respectively (Statistics Canada, 2011; Asthma Society of Canada, 2012).

Similarly, with respect to the amount of SO2-related mortality, Judek et al. (2004) estimated that 8% of total non-accidental mortality in Canadian urban census divisions between 1998 and 2000 was due to air pollution (described by a multi-pollutant model of particulate matter [PM], ozone, nitrogen dioxide, SO2 and carbon monoxide), and that most of this 8% was due to long-term exposure to ambient fine PM, which has a strong signal correlation to SO2.

While there is currently insufficient information to relate SO2 to specific reproductive effects, the lifelong implications of pre-term birth and various congenital issues indicate that this is an area in need of more attention.

Conclusions and recommendations

In conclusion, the human health assessment has identified potential health risks to the Canadian population from exposure to ambient concentrations of SO2 that is below the current National Ambient Air Quality Objectives. It is therefore recommended that the current National Ambient Air Quality Objectives be revised or new Ambient Air Quality Objectives or Standards be introduced with consideration of the following:

  • The strongest evidence of causality was between short term SO2 exposure and respiratory morbidity, based largely on the 5–10 minute controlled human exposure studies. A 10-min human health RfC of 67 ppb has been identified in the assessment.
  • The more recent literature also adds to the weight of evidence for a “suggestive of causal” relationship between non-accidental and cardiopulmonary mortality risks and short-term exposure to SO2.
  • Additional endpoints (reproductive/developmental) have been identified based on the more recent literature. Although these endpoints have also been designated as having a weakly “suggestive of causal” relationship with SO2 exposure, the database is limited.
  • Intermittent spikes in exposure are linked to respiratory morbidity and are suspected for most other endpoints, including reproductive/developmental endpoints. Current Canadian monitoring data support that Canadian exposure is likely to see intermittent spikes in concentrations. Mechanistic and personal exposure modelling also support intermittent spikes in exposure as being relevant to the health effects observed.
  • There is inadequate evidence to infer a causal relationship between long-term exposure of SO2 and health effects.
References

Asthma Society of Canada. 2012. About Asthma. http://www.asthma.ca/adults/about/.

Chen T. M., Shofer S., Gokhale J., and Kuschner W. G. 2007. Outdoor air pollution: overview and historical perspective. Am J Med Sci 333:230–34.

Environment Canada. 2011. National Air Pollution Surveillance Program (NAPS) http://www.ec.gc.ca/rnspa-naps/.

Government of Canada. 2012. Canadian smog science assessment highlights and key messages. (http://www.ec.gc.ca/Publications/AD024B6B-A18B-408D-ACA2-59B1B4E04863%5CCanadianSmogScienceAssessmentHighlightsAndKeyMessages.pdf).

Judek S., Jessiman B., and Stieb D. 2004. Estimated number of excess deaths in Canada due to air pollution. Unpublished document dated August 30, 2004, from Air Health Effects Assessment Division, Health Canada.

Statistics Canada. 2011. Canadian Census Data. 2011. http://www12.statcan.gc.ca/census-recensement/index-eng.cfm.

U.S. EPA. 2008. Integrated Science Assessment for Sulphur Oxides – Health Criteria. http://www.epa.gov/ncea/isa/.

An electronic copy of the document Human Health Risk Assessment for Sulphur Dioxide may be obtained by contacting AIR@hc-sc.gc.ca.

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DEPARTMENT OF HEALTH

CONTROLLED DRUGS AND SUBSTANCES ACT

Notice to interested parties — Proposal regarding the scheduling of W-18 under the Controlled Drugs and Substances Act and its regulations

This notice provides interested stakeholders with the opportunity to provide comments on Health Canada’s proposal to add W-18 (4-chloro-N-[1-[2-(4-nitrophenyl)ethyl]-2piperidinylidene]benzenesulfonamide), its salts, derivatives, isomers and analogues and salts of derivatives, isomers and analogues to Schedule I to the Controlled Drugs and Substances Act (CDSA) and to Part I of the Schedule to Part J of the Food and Drug Regulations (FDR).

W-18 is a synthetic opioid that was initially developed for its analgesic potential and patented in Canada and the United States in 1984. W-18 has never been marketed commercially and there is no known evidence demonstrating that W-18 has any actual or potential uses apart from scientific research. The use of W-18 as a “legal” substitute for other controlled substances was first detected in Europe in 2013, in the context of recreational use. In 2014, W-18 was added to the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) list of New Psychoactive Substances. This list highlights substances that the EMCDDA monitors as they may pose a public health threat comparable to that posed by substances already controlled internationally under United Nations drug conventions. W-18 first appeared in Canada in 2015, found in samples seized by law enforcement authorities. Samples included counterfeit tablets that had W-18 as the only active ingredient, but were made to appear like prescription oxycodone tablets.

Although there are no published studies regarding the toxicity of W-18, the high analgesic potency of W-18, according to the patent, suggests a potential severe risk for overdose. In addition to the risk of overdose, risks associated with W-18 can be elevated because of lack of data about toxicity, bioavailability, tolerance, half-life and onset of effects, which can lead users to experiment blindly with this substance.

In order to capture substances that are structurally related to W-18 and have psychoactive effects, it is also proposed that the salts, derivatives, isomers and analogues of W-18 and the salts of these substances be scheduled along with the parent substance.

These proposed amendments would prohibit, among other activities, the possession, trafficking, possession for the purpose of trafficking, importation, exportation, possession for the purpose of exportation, and production of the above-mentioned substances, except as authorized under Part J of the FDR or through an exemption under section 56 of the CDSA.

The publication of this notice in the Canada Gazette, Part I, initiates a 30-day comment period. Interest in this process or comments on this notice should be expressed to Legislative and Regulatory Affairs, Controlled Substances Directorate, Healthy Environments and Consumer Safety Branch, Health Canada, by mail at Address Locator: 0302A, 150 Tunney’s Pasture Driveway, Ottawa, Ontario K1A 0K9, or by email at ocs_regulatorypolicy-bsc_politiquereglementaire@hc-sc.gc.ca.

February 13, 2016

JACQUELINE GONÇALVES
Director General
Controlled Substances Directorate
Healthy Environments and Consumer Safety Branch

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DEPARTMENT OF INDUSTRY

OFFICE OF THE REGISTRAR GENERAL

Appointments

Name and position Order in Council
Charette, Janice 2016-22
  • Senior Advisor to the Privy Council Office
 
Hoy, The Hon. Alexandra H. 2016-43
  • Government of Ontario
 
  • Administrator
 
  • February 3 to February 17, 2016
 
Wernick, Michael 2016-23
  • Clerk of the Privy Council and Secretary to the Cabinet
 

February 4, 2016

DIANE BÉLANGER
Official Documents Registrar

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DEPARTMENT OF INDUSTRY

OFFICE OF THE REGISTRAR GENERAL

Appointments

Name and position

Instrument of Advice dated November 4, 2015

(see footnote **) Duncan, Kirsty

  • Minister of State to assist the Minister of Industry to be styled Minister of Science

February 4, 2016

DIANE BÉLANGER
Official Documents Registrar

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DEPARTMENT OF TRANSPORT

CANADA MARINE ACT

Trois-Rivières Port Authority — Supplementary letters patent

BY THE MINISTER OF TRANSPORT

WHEREAS letters patent were issued by the Minister of Transport (“Minister”) for the Trois-Rivières Port Authority (“Authority”), under the authority of the Canada Marine Act (“Act”), effective May 1, 1999;

WHEREAS Schedule C of the letters patent sets out the immovables, other than federal immovables, held or occupied by the Authority;

WHEREAS pursuant to subsection 46(2.1) of the Act, the Authority wishes to acquire the immovables known and designated as being lots 3 066 757, 4 039 689 and 5 058 161 of the cadastre of Quebec;

WHEREAS the board of directors of the Authority has requested that the Minister issue supplementary letters patent to set out the said immovables in Schedule C of the letters patent;

AND WHEREAS the Minister is satisfied that the amendment to the letters patent is consistent with the Act;

NOW THEREFORE, pursuant to subsection 9(1) of the Act, the letters patent are amended as follows:

1. Schedule C of the letters patent is amended by adding the following at the end of that Schedule:

Lot Description
3 066 757 An immovable known and designated as being lot 3 066 757 of the cadastre of Quebec, registration division of Trois-Rivières, city of Trois-Rivières, as described in the certificate of location prepared October 6, 2003, and shown on the accompanying plan, under number 1106 of the minutes of Michel Plante, land surveyor, containing an area of 5 152.5 m2.
4 039 689 An immovable known and designated as being lot 4 039 689 of the cadastre of Quebec, registration division of Trois-Rivières, city of Trois-Rivières, as described in the certificate of location prepared November 23, 2015, and shown on the accompanying plan, under number 7546 of the minutes of Pierre Roy, land surveyor, containing an area of 12 785.3 m2.
5 058 161 An immovable known and designated as being lot 5 058 161 of the cadastre of Quebec, registration division of Trois-Rivières, city of Trois-Rivières, as described in the certificate of location prepared July 14, 2015, and shown on the accompanying plan, under number 20 171 of the minutes of Jean Pinard, land surveyor, containing an area of 1 853.2 m2.

2. These supplementary letters patent take effect for each lot mentioned above on the date of registration in the Land Register of Quebec of the deed of sale evidencing the transfer of the immovable to the Authority.

ISSUED this 25th day of January, 2016.

____________________________________
The Honourable Marc Garneau, P.C., M.P.
Minister of Transport

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DEPARTMENT OF TRANSPORT

CANADA MARINE ACT

Windsor Port Authority — Supplementary letters patent

BY THE MINISTER OF TRANSPORT

WHEREAS letters patent were issued by the Minister of Transport (“Minister”) for the Windsor Port Authority (“Authority”) under the authority of the Canada Marine Act (“Act”), effective July 1, 1999;

WHEREAS Schedule C of the letters patent sets out the real property, other than federal real property, held or occupied by the Authority;

WHEREAS, pursuant to subsection 46(2.1) of the Act, the Authority wishes to acquire real property bearing property identification number (PIN) 01591-0112LT;

WHEREAS it is necessary to correct an error in the description of real property currently described in Schedule C of the letters patent as “Part 1 on plan of reference filed in the Land Registry Office in Windsor as 12R-6944”;

WHEREAS the board of directors of the Authority has requested that the Minister issue supplementary letters patent to set out the said real property in Schedule C of the letters patent;

AND WHEREAS the Minister is satisfied that the amendments to the letters patent are consistent with the Act,

NOW THEREFORE, pursuant to subsection 9(1) of the Act, the letters patent are amended as follows:

1. Schedule C of the letters patent of the Windsor Port Authority is amended by deleting the following:

ALL AND SINGULAR that certain parcel or tract of land and premises situate, lying and being in the City of Windsor, in the County of Essex and Province of Ontario, and being composed of that part of Lot Number Four (4) on the west side of Sandwich Street in the said City of Windsor according to Registered Plan Number Forty (40), and being designated as Part 1, on a plan of reference filed in the Land Registry Office in Windsor as 12R-6944.

2. Schedule C is amended by adding the following:

Item Property Identifier Description
1 Part 4 on reference plan 12R-6944 Those lands and premises situate in the City of Windsor, in the County of Essex and Province of Ontario, and being composed of that part of Lot Number Four (4) on the west side of Sandwich Street in the said City of Windsor according to Registered Plan Number Forty (40), and being designated as Part 4, on a plan of reference filed in the Land Registry Office in Windsor as 12R-6944.

3. Schedule C is amended by adding the following:

Item Property Identifier Description
2 01591-0112LT Those lands and premises situate in the City of Windsor, in the County of Essex and Province of Ontario, and being composed of that part of Lot Number Four (4) on the west side of Sandwich Street in the said City of Windsor according to Registered Plan Number Forty (40), and being designated as Parts l, 2, 3 and 5, on a plan of reference filed in the Land Registry Office in Windsor as 12R-6944, and being identified as P.I.N. 01591-0112LT.

4. Sections 1 and 2 of these supplementary letters patent take effect on the date of issuance mentioned below.

5. Section 3 of these supplementary letters patent takes effect on the date of registration in Ontario’s land registration system of the document evidencing the transfer of the real property to the Authority.

ISSUED this 29th day of January, 2016.

____________________________________
The Honourable Marc Garneau, P.C., M.P.
Minister of Transport

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