Ontario Air Standards for Chlorine DioxideOntario Air Standards for Chlorine Dioxide ii remained relatively constant from 1995 through 2004. For the year 2004 Ontario reported releases

Ontario Air Standards

For

Chlorine Dioxide

June 2007

Standards Development Branch

Ontario Ministry of the Environment Ontario

Ontario Air Standards for Chlorine Dioxide

Executive Summary

The Ontario Ministry of the Environment (MOE) has identified the need to develop and/or update air quality standards for priority contaminants. The Ministry’s Standards Plan, which was released in October, 1996 and revised in November, 1999, identified candidate substances for which current air quality standards will be reviewed or new standards developed. Chlorine dioxide was identified as a priority for review based on both its pattern of use in Ontario and toxicological information that has been published subsequent to the development of the existing standard in 1974. Once a decision is made on the air standards, they will be incorporated into Ontario Regulation 419: Air Pollution – Local Air Quality (O. Reg. 419/05). The Ambient Air Quality Criterion (AAQC) will be incorporated into Schedule 3 of the regulation and the half hour standards will be incorporated into Schedule 2. An ‘Information Document’ containing a review of scientific and technical information relevant to setting an air quality standard for chlorine dioxide was previously posted on the Environmental Bill of Rights Registry for public comments. This was followed more recently by the posting of a document providing the rationale (‘Rationale Document’) for recommending an Ambient Air Quality Criterion (AAQC) and a half hour standard for chlorine dioxide. This document, referred to as the ‘Decision Document’, summarizes the comments received from stakeholders on the proposed standards and the Ministry responses to these comments. This document also provides the rationale for the decision on the air quality standards for chlorine dioxide.

Chlorine dioxide (CAS # 10049-04-4) is a yellow to reddish-yellow gas at room temperature that has a pungent, sharp odour similar to that of chlorine and nitric acid. An odour threshold of 26 mg/m3 has been reported for chlorine dioxide. Chlorine dioxide is believed to be released to the atmosphere entirely from anthropogenic processes and activities. The dominant stationary sources of chlorine dioxide emissions appear to be the pulp and paper processing industry and preserved fruit and vegetable products. Chlorine dioxide is primarily used as a bleaching agent for flour, textiles, oils, wood pulp, fat and beeswax. It is used in cleaning and detanning of leather, to control microorganisms in fruit and vegetables, in the manufacture of chlorite salts, as an oxidizing agent, and as a biocide in drinking water disinfection. Chlorine dioxide is also used to disinfect farm animals, milking equipment and food processing areas.

Data from the National Pollutant Release Inventory (NPRI) indicates that there has been a substantial decrease in the release of chlorine dioxide in Canada between 1995-2004. The majority of the emissions of chlorine dioxide in Canada can be attributed to pulp mills located in British Columbia, New Brunswick and Ontario. Ontario’s proportion of air releases of chlorine dioxide are modest on a national scale (20%) and have

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remained relatively constant from 1995 through 2004. For the year 2004 Ontario reported releases of 114 tonnes, which accounted for just over 21% of the total releases in Canada. Activities in the pulp industry were responsible for 98% of the releases of chlorine dioxide in Ontario.

No studies regarding the toxicokinetics of chlorine dioxide in humans or animals following the inhalation route of exposure were identified in the literature reviewed. There is only limited information available regarding the toxicokinetics of chlorine dioxide following oral exposure. After oral exposure in drinking water, approximately 90% of chlorine dioxide is absorbed in the gastrointestinal tract. Following absorption, chlorine dioxide is widely distributed throughout the body, and may be found in blood, kidney, stomach, intestines, liver, spleen, bone marrow, testes, and skin tissue. Chlorine dioxide is metabolized primarily to chloride, with smaller amounts of chlorite and chlorate formed as metabolites. The excretion of chlorine dioxide metabolites occurs primarily via the urine.

Symptoms of acute human exposure to chlorine dioxide generally involve irritation of the eyes, nose and respiratory tract, and may also include chest pain, coughing, bloody nose, and sputum. Short-term exposure to high levels of chlorine dioxide may result in pulmonary edema. Symptoms of chronic exposure to chlorine dioxide in humans are also of an irritant nature and may include cough, phlegm, bronchitis, and shortness of breath. Permanent lung damage may occur with repeated long-term exposures to chlorine dioxide. Little information is available on the reproductive and developmental toxicity of chlorine dioxide; with no inhalation studies identified in the available scientific literature. Limited data suggest that chlorine dioxide is not mutagenic. No studies regarding carcinogenic effects in humans or animals following inhalation exposure to chlorine dioxide were identified in the available scientific literature. The US EPA currently classifies chlorine dioxide as Group D, not classifiable as to human carcinogenicity, based on inadequate human and animal data. There are no IARC, Health Canada, or ACGIH cancer classifications for chlorine dioxide at this time.

Currently in Ontario, the Ambient Air Quality Criteria (24-hour value) and the half-hour Point of Impingement standard for chlorine dioxide are 30 and 85 μg/m3, respectively. The half-hour standard is based on the ACGIH TLV-STEL of 830 μg/m3, while the 24-hour standard is based on the ACGIH TLV-TWA of 280 μg/m3. A safety factor of 10 was applied to both values to provide an additional margin of safety for sensitive groups.

In revising the air quality standards for Ontario, the Ministry of the Environment is considering risk assessments and standards and guidelines used by environmental agencies worldwide. This report reviews the scientific basis for air quality guidelines and standards for chlorine dioxide developed by the Provinces of Alberta and Quebec,


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the U.S. EPA, and the States of California, Louisiana, Michigan, New Jersey, New York, Ohio and Texas.

In examining the basis of the air quality guidelines reviewed, there is some consensus on the use of the Paulet and Desbrousses studies (1970, 1972) or alternatively the ACGIH’s rationale based on the animal study of Dalhamn (1957) and the epidemiological study of Gloemme and Lundgren (1957).

The U.S. EPA’s RfC and the California EPA’s chronic REL value have formed the basis of many of the U.S. States’ air quality guidelines. Both the U.S. EPA and the California EPA have chosen the studies of Paulet and Desbrousses (1970, 1972), as the basis of their guideline value, however, the application of uncertainty factors has lead to differences in the final guideline value derived.

The occupational guideline values derived by the ACGIH were also a source of many of the guideline values derived by the jurisdictions reviewed. The ACGIH in developing their limits relied on an animal and an epidemiological study in defining an acceptable exposure for chlorine dioxide. The exposure limits derived by the ACGIH have not been updated since 1976 and are based on data from studies published in 1957. The ACGIH in their documentation in support of their occupational exposure limits values does not review the studies of Paulet and Desbrousses (1970, 1972) and only reviews one study post-1970. The lack of up-to-date toxicological information in deriving their exposure limit values places lower confidence in their scientific rationale. The single stakeholder providing comment on the information draft maintained that it was not appropriate to derive AAQCs by simply applying uncertainty factors to an occupational exposure limit. The Ministry agrees with this view and has decided on the following approach for chlorine dioxide:

• Start with the LOAEL of 2.8 mg/m3 (based on vascular congestion and peribronchiolar edema in rats) from the subchronic studies of Paulet and Desbrousses, (1972).

• Adjust for continuous exposure to get LOAELADJ :

LOAELADJ = 2,800 µg/m3 × 5 hours/24 hours × 5 days/7 days

= 416 µg/m3

• Convert to a human equivalent concentration by multiplying by the regional gas dose ratio (RGDR):

LOAELHEC = LOAELADJ × RGDRTH

= 410 µg/m3 × 1.57 = 650 µg/m3 (rounded)


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• Apply an uncertainty factor (UF) of 300 (10 for protection of sensitive human subpopulations, 3 for interspecies extrapolation, 3 for use of a LOAEL instead of a NOAEL, 3 for use of subchronic data (instead of chronic) and lack of reproductive or developmental data for inhalation exposure) to the LOAELHEC to yield a chronic exposure limit:

LOAELHEC / UF = 650 µg/m3 / 300 = 2.0 µg/m3.(rounded)

This value can be supported with information from a human occupational study.

Based on an evaluation of the scientific rationale of air guidelines from leading agencies, an examination of current toxicological research, and comments from stakeholders, the following air quality standards are set for Chlorine dioxide (10049-04-4):

• A 24-hour average AAQC of 2.0 μg/m3 (micrograms per cubic metre of air) for chlorine dioxide based on adverse effects to the respiratory system; and

• A half-hour standard of 6.0 μg/m3 (micrograms per cubic metre of air) for chlorine dioxide based on adverse effects to the respiratory system.

These effects-based standards (which include the AAQCs and the corresponding effects-based half hour standards) will be incorporated into Ontario Regulation 419/05: Air Pollution – Local Air Quality (O. Reg 419/05). The AAQCs will be incorporated into Schedule 3 of O. Reg. 419/05; the half-hour standard will be incorporated into Schedule 2.

MOE generally proposes a phase-in for new standards or standards that will be more stringent than the current standard or guideline. The phase-in for chlorine dioxide is set out in O. Reg. 419/05.

Among other things, O. Reg. 419/05 sets out the applicability of standards, appropriate averaging times, phase-in periods, types of air dispersion model and when various sectors are to use these models. There are 3 guidelines that support O. Reg. 419/05. These guidelines are:

• “Guideline for the Implementation of Air Standards in Ontario” (GIASO);

• “Air Dispersion Modelling Guideline for Ontario” (ADMGO); and

• “Procedure for Preparing an Emission Summary and Dispersion Modelling Report” (ESDM Procedure).


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GIASO outlines a risk-based decision making process to set site specific alternative air standards to deal with implementation barriers (time, technology and economics) associated with the introduction of new/updated air standards and new models. The alternative standard setting process is set out in section 32 of O. Reg. 419/05.

For further information on these guidelines and O. Reg. 419/05, please see the Ministry’s website http://www.ontario.ca/environment and follow the links to local air quality.

http://www.ontario.ca/environment


Table of Contents

Executive Summary ....................................................................................................... i Table of Contents......................................................................................................... vi 1.0 Introduction......................................................................................................... 1

2.0 General Information ........................................................................................... 3 2.1 Physical and Chemical Properties .................................................................... 3 2.2 Production and Uses of Chlorine Dioxide ......................................................... 4 2.3 Sources and Levels .......................................................................................... 4 2.4 Environmental Fate........................................................................................... 5

3.0 Toxicology of Chlorine Dioxide......................................................................... 6 3.1 Acute Toxicity.................................................................................................... 7 3.2 Subchronic and Chronic Toxicity....................................................................... 7 3.3 Developmental and Reproductive Toxicity ........................................................ 9 3.4 Genotoxicity .................................................................................................... 10 3.5 Carcinogenicity ............................................................................................... 11 3.6 Environmental Effects ..................................................................................... 11

4.0 Review of Existing Air Quality Criteria ........................................................... 12 4.1 Overview......................................................................................................... 12 4.2 Evaluation of Existing Criteria ......................................................................... 16

5.0 Responses of Stakeholders to the Information Draft.................................... 17

6.0 Responses of Stakeholders to the Rationale Document .............................. 18

7.0 Considerations in the Development of an Ambient Air Quality Criterion for Chlorine Dioxide.......................................................................................................... 20

8.0 Decision ............................................................................................................ 24

9.0 References ........................................................................................................ 26

10.0 Appendix: Agency-Specific Reviews of Air Quality Guidelines ................... 35 10.1 Agency-Specific Summary: Federal Government of Canada......................... 35 10.2 Agency-Specific Summary: Federal Government of the United States........... 37 10.3 Agency-Specific Summary: California............................................................. 42 10.4 Agency-Specific Summary: Massachusetts .................................................... 46 10.5 Agency-Specific Summary: Michigan.............................................................. 48 10.6 Agency-Specific Summary: North Carolina ..................................................... 50 10.7 Agency-Specific Summary: World Health Organization (WHO) ...................... 52

11.0 Acronyms, Abbreviations, and Definitions .................................................... 54

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1.0 Introduction

Ontario regulates air emissions in order to achieve and maintain air quality which is protective of human health and the environment. The Environmental Protection Act (Section 9) requires stationary sources that emit, or have the potential to emit, a contaminant to obtain a Certificate of Approval which outlines the conditions under which the facility can operate.

The Ministry of the Environment uses a combination of regulated point of impingement (POI) standards and guidelines (MOE, 2005a) in reviewing Emission Summary and Dispersion Modelling Reports submitted to support a Certificate of Approval application or a Ministry request for a compliance assessment. Ambient Air Quality Criteria form the basis for an air standard or guideline and represent human health or environmental effects-based values, normally set at a level not expected to cause adverse effects based on continuous exposure. As such, factors such as technical feasibility and costs are not considered when establishing AAQCs or the equivalent half hour standards which are derived from the AAQCs using a mathematical scaling factor. The risk based process for alternative standards, as set out in section 32 of O. Reg. 419/05, is the mechanism created to deal with the time, technical and economic issues. The Guideline for the Implementation of Air Standards in Ontario (GIASO) is the supporting document for stakeholders who are interested in more information on alternative standards. For further information on O.Reg. 419/05 and GIASO, please see the Ministry’s website http://www.ene.gov.on.ca/envision/air/regulations/localquality.htm.

Air standards referenced in O. Reg. 419/05 are used for compliance and enforcement. Dispersion modelling, as referenced in the regulation, is used to relate emission rates from a source to resulting concentrations of a particular contaminant. Air standards specified under O. Reg. 419/05 apply to stationary sources only.

In addition to air standards established under O. Reg. 419/05, the Ministry also has a large number of guidelines (including AAQCs). Similar to standards, guidelines are used by the Ministry to assess general air quality and the potential for causing adverse effect (MOE, 2005). Like the air standards specified in O. Reg. 419/05, guidelines (and now AAQCs) are used in reviewing Emission Summary and Dispersion Modelling reports submitted in support of applications for Certificates of Approval, to approve new and modified emission sources or other requirements. Once incorporated into a legal instrument such as a Certificate of Approval, guidelines can become legally binding.

http://www.ene.gov.on.ca/envision/air/regulations/localquality.htm


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The Ontario Ministry of the Environment continues to develop and/or update air standards for priority toxic contaminants. The Ministry’s Standards Plan, which was released in October 1996 and revised in November 1999 (MOEE, 1996 & MOE, 1999), identified candidate substances for which current air standards will be reviewed. The MOE 1999 Standards Plan outlines a multi-step process for developing air quality standards (MOE, 1999). Each standard has undergone a two step consultation process involving postings on the Environmental Registry, under the Environmental Bill of Rights (EBR):

• Information Drafts (Risk assessment/science review only)

• Rationale Documents (Proposed numerical limits)

Chlorine dioxide was identified as a priority for review based on its pattern of use in Ontario, and recent toxicological information. The initial step, an Information Draft (MOE 2005b), provided risk assessment information relevant to establishing a standard for a particular substance. This provided stakeholders with the opportunity to critically review the information and provide any additional information they felt should be considered by the Ministry in setting an air quality standard for a particular compound. The Ministry considered comments received on the Information Draft and recommended proposed standards: Ambient Air Quality Criterion (AAQC) and a half hour point of impingement (POI) standard, in a Rationale Document (MOE 2006 ) and again solicited comments from stakeholders by posting on the Environmental Registry. After assessing comments on the Rationale Document the Ministry has finalized its work by making a decision on the air quality standards for chlorine dioxide. This decision, which also highlights key comments from stakeholders on the proposed standards and the responses provided by the MOE, is documented by posting a Decision Notice (and supporting ‘Decision Document’, which provides the rationale for the decision on the air quality standards) onto the Environmental Registry.

In the 1999 Standards Plan, MOE made a commitment to consider time, technical, and economic issues for air standards and develop a risk management framework to address implementation issues. The risk-based framework has been developed and is part of O. Reg. 419/05. The alternative standards setting process is a risk-based process that considers time, technical and economic issues on a site specific basis. For further information on Regulation 419/05 and the process for requesting an alternative site specific air standard, please see the Ministry’s website and follow the links to local air quality.

http://www.ene.gov.on.ca/envision/air/regulations/localquality.htm


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2.0 General Information

2.1 Physical and Chemical Properties

Chlorine dioxide is a yellow to reddish-yellow gas at room temperature. This compound is very reactive and has a strong oxidizing potential with a pungent, sharp odour similar to that of chlorine and nitric acid. Chlorine dioxide will react violently with organic chemicals and can be detonated by heat, sunlight or contact with carbon monoxide or mercury (Budavari et al., 1996). This compound is soluble in water, alkaline and sulfuric acid solutions (Budavari et al., 1996). An odour threshold of 26 mg/m3 has been reported for chlorine dioxide (Amoore and Hautala, 1983). The following list provides some specific information on chlorine dioxide and its properties (ACGIH, 2001; Budavari et al., 1996; HSDB, 2002; NIOSH, 1978; Sax, 1989):

Chemical Name chlorine dioxide

CAS # 10049-04-4

RTECS # FO3000000

Molecular Formula ClO2

Molecular Weight 67.46 g/mol

Melting Point -59EC

Boiling Point 11EC

Vapour Pressure 760 mmHg at 20EC

Water Solubility Soluble; 8g/L at 20 EC

Odour Threshold 26 mg/m3 (9.4 ppm)

Specific Gravity 1.642 at 0EC (liquid)

Vapour Density (air = 1) 2.3

Conversion Factors 1 ppm = 2.76 mg/m3

Common Synonyms chlorine oxide; alcide; anthium dioxide; chlorine peroxide; chloryl radical; chloroperoxyl; doxcide 50


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2.2 Production and Uses of Chlorine Dioxide

Wood pulp bleaching is the largest use of chlorine dioxide in both Canada and the U.S. In general, the trend in the pulp industry has been to eliminate chlorine and hypochlorite as bleaching agents and replace them with chlorine dioxide (ATSDR, 2004). Chlorine dioxide is also used as a bleaching agent for flour, textiles, oils, fat and beeswax. It is also used in cleaning and detanning of leather (HSDB, 1991; HSDB, 1994) and to control microorganisms in fruit and vegetables (NIOSH, 1978).

Chlorine dioxide is registered as a fungicide, algaecide and bactericide. It also has a major use in purifying and disinfecting potable water systems, commercial water cooling towers and metal cutting fluids. It is also used to control taste and odour issues associated with drinking water (NIOSH, 1978; ATSDR, 2004). In addition, chlorine dioxide is used to disinfect farm animals, milking equipment and food processing areas (ATSDR, 2004).

2.3 Sources and Levels

Chlorine dioxide is a highly reactive chemical that will exist only in the immediate vicinity of where it is produced or used. Some stakeholders have interpreted that property to suggest that chlorine dioxide plumes will be reduced to below measurable levels by the time the plume reaches the fenceline of the facility. However, in Ontario there have been two studies (MOE, 1985; MOE, 1986) in the vicinity of wood pulp bleaching operations in which ambient levels of chlorine dioxide have been measured beyond the fenceline. For one study, in daylight hours (mid-morning to late afternoon, September), the ½-hour average concentrations were in the range 0.2 to 4 μg/m3 with peak instantaneous values of 43 μg/m3. In the other study (mid-afternoon to late afternoon, September), the highest ½-hour average was 17 μg/m3, with several other periods in the 4 to 10 μg/m3 range. The majority of the periods showed less than 1.0 μg/m3 (peak values unreported).

In the U.S. it has been estimated that 337,026 kg of chlorine dioxide was released to the atmosphere in the year 2000 (ATSDR, 2004). The releases of chlorine dioxide to air in the year 2000 accounted for approximately 72.7% of the estimated total environmental releases in the U.S. (ATSDR, 2004).

According to the National Pollutant Release Inventory (NPRI) there has been a substantial decrease in the release of chlorine dioxide in Canada between 1995-2004 (NPRI, 1995, 1996, 1997, 1998, 1999, 2000, 2001, 2002, 2003, 2004). Release amounts for 1995, 1996, 1997, 1998, 1999, 2000, 2001, 2002, 2003 and 2004 were 990, 1100, 1136, 782, 890, 660, 611, 535, 486 and 532 tonnes, respectively. A significant decrease in the release of chlorine dioxide began in


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1998 and has continued into 2004. On-site releases in Ontario in past years have remained relatively constant with significant increases only being reported in 1998 and 1999. In the years 1995, 1996, 1997, 1998, 1999, 2000, 2001, 2002, 2003 and 2004, Ontario released 162, 147, 158, 211, 201, 158, 158, 166, 130 and 114 tonnes, respectively. Over this time period Ontario contributed on average 20% of the total chlorine dioxide released in Canada, with its highest proportions occurring between 1998-2000 and again in 2003. In Ontario in 2004, pulp mills were responsible for 98% of the reported chlorine dioxide releases.

2.4 Environmental Fate

Production and use of chlorine dioxide as a bleaching agent and for disinfection of water may result in its release to the atmospheric environment.

In the atmosphere, chlorine dioxide is an unstable gas that is highly reactive and rapidly decomposes to form chlorine and oxygen (ASTDR, 2002). The decomposition of chlorine dioxide in the atmosphere is promoted by mild heat (ASTDR, 2002) and also by sunlight (Vogt et al. 1986). In sunlight, the atmospheric lifetime (time for compound concentration to reduce to 1/e (i.e. 37%) of its original value) of chlorine dioxide has been determined to be approximately 15 seconds (NCASI, 1999). At concentrations in excess of 10% the decomposition reaction can be explosive (Windholz et al., 1983). In non-sunlight conditions, the atmospheric lifetime is more likely in the range of 40 to 80 hours (NCASI, 1999), mainly due to chemical reactions with hydroxyl radical (OH-), ozone or nitric oxide (NO).

Chlorine dioxide is readily soluble in water. However, given its rapid decomposition in air, its unassisted transfer to water and moist soil may be limited. Neither chlorine dioxide, nor its degradation products (oxyanions and chloride), will adsorb to suspended particles or to sediments or soil (ATSDR, 2004). On contact with sediments or moist soil, chlorine dioxide will react rapidly to form oxyanions and chloride (ATSDR, 2004). Any such anions formed in soil will be mobile, and will be readily leached to groundwater (ATSDR, 2004). However, due its reactivity, the oxyanions will not persist as such, and will be converted to chloride.

In water, chlorine dioxide is a strong oxidizer, and reacts rapidly with organic and inorganic compounds to form chlorite (ClO2

-) and chloride (Cl-) ions, as well as lower chlorinated organics (Aieta and Berg 1986; Chang, 1982; Stevens, 1982). In contrast to chlorine, chlorine dioxide does not produce trihalomethanes in water. In the absence of oxidizable substances and in the presence of hydroxide ions (basic solution) chlorine dioxide will decompose slowly to form chlorite and chlorate (ClO3

-) ions. At pH 12, with chlorine dioxide concentrations of 5 to 10 mg/L, the decomposition half-life was reported to range from 20 to 180 minutes


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(Aieta and Berg 1986; Stevens, 1982; WHO, 2000). In the presence of ultraviolet light, chlorine dioxide readily dissociates to form chlorate, hypochlorite (OCl-) and chloride (Zika et al., 1984). The oxy anions formed by degradation of chlorine dioxide react more slowly than chlorine dioxide; however, they are not expected to persist in water.

3.0 Toxicology of Chlorine Dioxide

The following toxicological review of chlorine dioxide is focussed primarily on the inhalation route of exposure, as this is the predominant route of human exposure to chlorine dioxide in air. Data on other exposure routes are included in this review where relevant or where inhalation exposure data are lacking.

No studies regarding the toxicokinetics of chlorine dioxide in humans or animals following the inhalation route of exposure were identified in the literature reviewed. There is only limited information available regarding the toxicokinetics of chlorine dioxide following oral exposure. According to the recent ATSDR (2004) review of the available data on the toxicokinetics of chlorine dioxide following oral exposure, approximately 30-35% of chlorine dioxide is absorbed from the gastrointestinal tract. However, it is believed that chlorine dioxide is chemically altered prior to absorption, due to its strong oxidant properties. Following absorption, chlorine dioxide is widely distributed throughout the body, and after 72 hours, may be found in blood, kidney, stomach, intestines, liver, spleen, bone marrow, testes, and skin tissue. Chlorine dioxide is metabolized primarily to chloride (27%), with smaller amounts of chlorite (3.5%) and chlorate (0.7%) formed as metabolites. The excretion of chlorine dioxide metabolites is monophasic with approximately 31% of a radiolabeled dose recovered in the urine and 10% in the feces after 72 hours.

No studies regarding the mechanism of toxic action of chlorine dioxide following exposure by any route were identified in the literature reviewed. Studies with chlorates and chlorites (the principal by-products of chlorine dioxide decomposition in water) indicate that the hematopoietic system is the target site in mammals, and that damage to this system occurs as a result of the strong oxidant effects of these by-products. Chlorate and chlorite have been found to oxidize red blood cell glutathione, oxidize hemoglobin to methemoglobin, and induce an increase in hydrogen peroxide formation, which results in an accumulation of this compound in red blood cells, leading to oxidative stress (Bercz et al., 1982; Couri and Abdel-Rahman, 1980).


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3.1 Acute Toxicity

Studies regarding the acute toxicity of humans following inhalation exposure to chlorine dioxide are limited. Symptoms of acute human exposure to chlorine dioxide generally involve irritation of the eyes, nose and respiratory tract, and may also include conjunctivitis, headache, breathing difficulties, chest pain, coughing, bloody nose, sputum, cardio-respiratory symptoms, reduced lung function and vomiting (Berg, 1955; Elkins, 1959; Exner-Freisfeld et al., 1986; NJ DHSS, 1998; Petry, 1954). Such effects have been reported following exposure to concentrations as low as 1.7 mg/m3; in this case, effects were reversible after one to two weeks (Dalhamn, 1957). High short-term exposure levels may result in pulmonary edema and fatality (Elkins, 1959; NJ DHSS, 1998).

Acute and subacute animal studies support the findings cited in human studies. Short term exposure of rats has been associated with respiratory distress, copious nasal and ocular discharge, and depressed body weight gain during exposure; many of these lesions were reversible if a recovery period was allowed (Dalhamn, 1957; Paulet and Desbrousses, 1974). Histological changes were observed in lungs (including edema and circulatory engorgement) and kidneys (Dalhamn, 1957). Rats exposed to 5 ppm (14 mg/m3) for 15-minute periods, 2 or 4 times/day for 1 month did not exhibit any exposure-related changes in clinical signs, body weight gain, hematological parameters, or gross pathology of the lungs (Paulet and Desbrousses, 1974) and hence this was identified as a NOAEL. The same study identified a LOAEL of 10 ppm for lung damage. The ratio of LOAEL to NOAEL in this case is 2 (= 10/5) instead of the often used uncertainty factor values of 10 or 3.

3.2 Subchronic and Chronic Toxicity

Symptoms of chronic exposure to chlorine dioxide in humans are also of an irritant nature and may include cough, phlegm, bronchitis, and shortness of breath; permanent lung damage may occur with repeated long-term exposures (ATSDR, 2004; NJ DHSS, 1998). There are few epidemiological or occupational studies available which investigate human inhalation exposure to chlorine dioxide on a long-term basis. In a comparison of pulp mill workers (exposed to chlorine and chlorine dioxide at concentrations of trace amounts to 0.69 mg/m3) and paper mill workers (controls, exposed to sulfur dioxide), no differences were found among the workers with regard to pulmonary function tests, although there were significant differences in the incidence of subjective respiratory complaints (Ferris et al., 1967).

Dalhamn (1957) identified a NOAEL of 0.28 mg/m3 (5 hours/day for 10 weeks), based on a lack of effects on rat behaviour and histopathology of the liver, kidney, or lung.


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A clinical investigation of 12 workers in a sulfite-cellulose plant exposed to chlorine dioxide (as well as chlorine and sulfur dioxide) for 5 years, at concentrations that generally did not exceed 0.28 mg/m3, found that 7 of 12 workers showed signs and symptoms of ocular and respiratory irritation leading to slight bronchitis (Gloemme and Lundgren, 1957). Although the levels of chlorine dioxide were not quantified, these effects were attributed to short-term exposure to levels well above 0.28 mg/m3 due to leaks from faulty vacuum equipment. The findings of this study, in conjunction with those of Dalhamn (1957), were used by ACGIH to set a TLV-TWA of 0.28 mg/m3; this value is expected to prevent irritation and possible bronchitis (ACGIH, 2002).

In a more recent and extensive epidemiological study, 321 pulp mill workers exposed to chlorine and chlorine dioxide reported significant increases in the incidence of wheezing, wheezing accompanied by breathlessness, and work-related wheezing (Kennedy et al., 1991). Personal time-weighed average (TWA) exposure concentration for chlorine at the pulp mill ranged from 13.8 to 38.6 mg/m3, whereas the TWA for chlorine dioxide was below 0.3 mg/m3. However, 60% of the pulp mill workers reported one or more chlorine or chloride dioxide “gassing” incidents. No significant effects were observed in tests of pulmonary function.

Paulet and Desbrousses (1972) exposed eight Wistar rats to 2.76 mg/m3 for 5 hours/day, 5 days/week for 2 months. Despite normal appearance, weight gain, and hematology, microscopic evaluation of the lungs revealed vascular congestion, hemorrhagic alveoli, peribronchiolar edema and congested lung capillaries in all test animals. The LOAEL of 2.76 mg/m3 was converted to a human equivalent concentration (HEC) of 0.64 mg/m3 by the US EPA (2000a) and used as the basis for deriving an RfC of 0.2 μg/m3, with the application of a 3000-fold uncertainty factor.

Paulet and Desbrousses (1972; 1970) also exposed rabbits and rats to chlorine dioxide under four different regimens with exposures occurring for 2 to 7 hours per day over 30 to 45 days; duration-adjusted exposure concentrations were reported to be 1.6 mg/m3, 0.82 mg/m3, 1.4 mg/m3, and 0.82 mg/m3. Clinical signs included respiratory irritation and bronchiolar and alveolar lesions, inflammatory infiltrations, pulmonary congestion, hemorrhagic alveoli and altered red and white blood cell counts. In addition, weight gain in rats was reported to be "slightly slowed". Recovery from the pulmonary lesions was observed in both rats and rabbits during a 10 day recovery period. From this study, a LOAEL for thoracic respiratory effects and hematological effects in rats and rabbits of 0.82 mg/m3 (adjusted for continual exposure) was identified. Conversion to a LOAEL (HEC) and the application of a 3000-fold uncertainty factor also resulted in an RfC very close to 0.2 μg/m3 (see U.S. EPA approach in Section 10.2).


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The toxicity of chlorine dioxide in experimental animals following oral administration via drinking water has been extensively studied in light of the use of chlorine dioxide as a disinfectant in some public drinking water supplies. Adverse effects on the hematopoietic system, including mild hemolytic anemia, as well as decreased body weight, organ weights, food and water consumption, and inflammatory nasal lesions have been observed following oral administration of chlorine dioxide and its two principal metabolites, chlorite (ClO2-) and chlorate (ClO3-) (Abdel-Rahman et al., 1980;1985; Daniel et al., 1990; Moore and Calabrese, 1980; 1982; Couri et al., 1982). These effects appear to be mediated by chlorite, and are most likely due to the strong oxidizing activity of both chlorite and chlorate. Chlorine dioxide has also been shown to induce a hypothyroid effect in monkeys and developing rats, thought to be due to its effects on gastrointestinal bioavailability of dietary iodine (Bercz et al., 1982; Harrington et al., 1986; Orme et al., 1985; Taylor and Pfohl, 1985).

3.3 Developmental and Reproductive Toxicity

No studies regarding developmental or reproductive toxicity in humans or animals following inhalation exposure to chlorine dioxide were identified in the available scientific literature. The New Jersey Department of Health and Senior Services (NJ DHSS, 1998) states that there is limited evidence which suggests that chlorine dioxide may harm the developing fetus.

Limited data are available regarding the reproductive or developmental impacts of oral exposure in humans. A retrospective epidemiologic study based on records from a population in Massachusetts that used chlorine dioxide as a primary drinking water disinfectant in the 1940s suggested a positive association between exposure and premature births (based on diagnosis of attending physician) (Tuthill et al., 1982).

Animal data are similarly limited, with only a few studies of reproductive or developmental impacts of oral exposure. Effects reported in rats include decreased number of implants and live fetuses per dam and increased fetal weight, without maternal toxicity, at 100 mg/L (2.5 months prior to, and throughout gestation) (Suh et al., 1983), although other studies with rats, mice and rabbits exposed to Alcide liquid and gel (Alcide consists of sodium chlorite and lactic acid that form chlorine dioxide when mixed) in the drinking water failed to show fetal effects (Abdel-Rahman et al., 1987; Gerges et al., 1985; Skowronski et al., 1985). However, fetal weights and lengths in rabbits dermally exposed to Alcide gel were significantly reduced, relative to controls. Oral administration by gavage of 5 daily doses comprising as much as 0.4 mg chlorine dioxide to B6C3F1 mice failed to induce any sperm-head abnormalities (Meier et al., 1985). A potential developmental effect of chlorine dioxide exposure is the suppression of thyroid activity and resulting effects on growth and maturation, as


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indicated by depressed T4 levels, delayed exploratory or locomotive activity and a reduction in cell number in the cerebella in rat pups exposed via gavage to 100 mg/L on postnatal days 5-20 (Orme et al., 1985; Taylor and Pfohl, 1985). Carlton et al., (1991) observed no changes in thyroid hormone parameters or in reproductive and developmental indices in Long Evans rats that were dosed with 0, 2.5, 5, or 10 ml/kg body weight chlorine dioxide in deionized water for up to 73 days prior to mating through to lactation.

Toth et al. (1990) administered chlorine dioxide to male and female rat pups at a daily gavage dose of 14 mg/kg on postnatal days 1-20. Examinations were performed on selected pups at ages 11, 21, and 35 days and results were compared to control pups. Significantly lower (5-7% lower) body weights and decreased ratio of forebrain content to cerebellum weight were noted at all three examination times. Significantly lower forebrain weights were observed on days 21 and 35, along with accompanying reductions in protein content (days 21 and 35) and reduced DNA content (day 35). This study identified a LOAEL of 14 mg/kg/day for decreased brain weight and protein content.

3.4 Genotoxicity

No studies regarding the genotoxicity or mutagenicity of chlorine dioxide in humans or animals following inhalation exposure were identified in the available scientific literature.

There are relatively few studies which have evaluated the mutagenic potential of chlorine dioxide. Both positive and negative results have been reported in in vitro (bacterial) assays. Water samples disinfected with chlorine dioxide did not induce reverse mutations in Salmonella typhimurium with or without activation (Miller et al., 1986). It has been reported that the reaction products of chlorine dioxide and certain amino acids and peptides are mutagenic in the Ames assay and have resulted in increased sister chromatid exchanges in Chinese hamster ovary cells (Owusu-Yaw et al., 1990; 1991; Tan et al., 1987). Chlorine dioxide was also not found to increase chromosome aberrations in Chinese hamster fibroblast cells, but did increase reverse mutation in Salmonella typhimurium (with activation) (Ishidate et al., 1984).

The available data indicate that chlorine dioxide is not mutagenic in in vivo mammalian studies: the mouse micronucleus assay, the bone marrow chromosomal aberration assay, and the mouse sperm-head abnormality assay (Meier et al., 1985).


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3.5 Carcinogenicity

No studies regarding carcinogenic effects in humans or animals following inhalation exposure to chlorine dioxide were identified in the available scientific literature. The US EPA (2000a) currently classifies chlorine dioxide as Group D, not classifiable as to human carcinogenicity, based on inadequate human and animal data. There are no IARC, Health Canada, or ACGIH cancer classifications for chlorine dioxide at this time.

Very few animal studies have investigated the potential carcinogenicity of chlorine dioxide. In a series of experiments in which concentrates prepared from chlorine dioxide-treated drinking water were orally and topically administered to rats and mice, no significant increase in the frequency of tumors or preneoplastic lesions was observed (Miller et al., 1986). An early study by Haag (1949) in which a small number of albino rats (7 per sex per dose) were administered 0, 0.5, 1, 5, 10 or 100 mg/L chlorine dioxide in drinking water for 2 years, found that mean life span was reduced approximately 20% in the high-dose (12.5 mg/kg/day for males and 13.4 mg/kg/day for females) animals compared to controls. Survival was not significantly affected in the 10 mg/L group (1.3 mg/kg/day). Histopathological examinations performed on representative animals from each dose group found no tumors or lesions.

3.6 Environmental Effects

There was no available data for measured toxicological effects of chlorine dioxide on terrestrial plants and very little data for aquatic plants. Giant kelp germination was reduced at aqueous concentrations of 25 to 250 mg/L (Hose et al., 1989).

Available data for chlorine dioxide toxicity to aquatic animals indicates a species-dependent sensitivity. The 96-hour LC50 for brown trout was reported as10,000 mg/L (Woodiwiss and Fretwell, 1974) whereas the 96-hour LC50 for zebra mussels was 0.35 mg/L (Matisoff et al., 1996). Adult and juvenile 96-hour LC50 values for fathead minnows were found to be 0.17 and 0.02 mg/L, respectively (Wilde et al., 1983).

Toxicity data for hypochlorous acid are relevant to the hypochlorite ion which is the dissociated form of the acid. Some of the reported response levels presented below are considered questionable since they are below an accepted reliable minimum detection limit of 0.010 mg/L. Reported 96-hour LC50’s were 0.004 mg/L for coho salmon (Rosenberger, 1971), 0.075, 0.082 and 0.094 mg/L for juvenile cutthroat trout (Larson et al., 1978), 0.059 mg/L for rainbow trout and 0.304 mg/L for golden shiners (Fisher et al., 1999). Acute toxicity tests with invertebrates indicated 24-hour LC50’s of 0.005 and 0.006 mg/L for Ceriodaphnia dubia neonates (Taylor, 1993), a 48-hour LC50 of 0.023 mg/L for the amphipod


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Gammarus minus, and 48-hour LC50’s 0.027, 0.0093 and 0.020 mg/L for the mayflies Ephemerella lata and Isonychia sp. and the stonefly Peltaperla maria, respectively (Gregg, 1974). Fisher et al., (1999) reported a 48-hour LC50 for Daphnia magna of 0.032 mg/L and a 96-hour LC50 for Hyalella azteca of 0.078 mg/L. The aquatic plant Myriophyllum spicatum showed significantly reduced growth after a 96-hour exposure to 0.050 mg/L (Watkins and Hammerschlag, 1984) and the algae Chlorella pyreniodosa showed 50% reduced growth after a 24-hour exposure to 0.180 mg/L (Kott et al., 1966). Chronic tests with brook trout indicated reduced activity at 0.005 mg/L and 100% lethality at 0.040 mg/L (Dandy, 1972). Chronic tests with invertebrates indicated reduced zooplankton density and protozoan species numbers after exposure to 0.024 and 0.025 mg/L for 28 days, respectively (Pratt et al., 1998) and reduced protozoan species numbers after exposure to 0.0027 mg/L for 7 days (Cairns et al., 1990). Others tests included a 360-day LC50 of 0.031 mg/L to the crayfish Pacifastacus trowbridgii (Larson et al., 1978), and a 12-day LT50 and a 37-day LC100 of 0.050 mg/L for the Asiatic clam Corbicula fluminea (Belanger et al., 1978). Chronic tests with algae indicated significantly depressed chlorophyll a levels in green algae exposed for 28-days to 0.0021 mg/L (Pratt et al., 1988).

Since chlorine dioxide is a gas, potential for bioconcentration in aquatic organisms is low.

While chlorine dioxide and some of its degradation products can be quite toxic in water, an atmospheric release will be subject to rapid decomposition in air and is unlikely to partition substantially to either water or soil. It is therefore unlikely that chlorine dioxide will have a significant impact on ecological receptors at a level that is protective of human health.

4.0 Review of Existing Air Quality Criteria

4.1 Overview

Currently in Ontario, the 24-hour AAQC value and the half-hour Point of Impingement standard for chlorine dioxide are 30 and 85 μg/m3, respectively. The half-hour standard is based on the ACGIH TLV-STEL of 830 μg/m3, while the 24-hour standard is based on the ACGIH TLV-TWA of 280 μg/m3 (MOE, 2005).

In revising the air quality standards for Ontario, the Ministry of the Environment is considering risk assessments and standards and guidelines used by environmental agencies world-wide. This report reviews the scientific basis for air quality guidelines and standards developed by the Provinces of Alberta and Quebec as well as the US EPA, the States of California, Louisiana, Michigan,


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New Jersey, New York, Ohio and Texas. No environmental standards were found for chlorine dioxide for the Canadian Federal Government, the State of North Carolina, the Commonwealth of Massachusetts, the World Health Organization, the Netherlands, Sweden and the United Kingdom. Agency specific summaries of guideline information for chlorine dioxide are presented in Section 11.0, the Appendix of this report. A brief summary is presented in Table 1.

Table 1: Summary of Existing Air Quality Guidelines1 for Chlorine Dioxide

Agency Guideline Value Basis of Guideline Date2 Comments

Canada (CEPA)

No guideline listed. Not listed as a priority substance by CEPA

85 µg/m3

(half-hour average, POI)

Derived from the ACGIH TLV-STEL value of 830 µg/m3

1974 Half-hour Point of Impingement limit (standard)

Ontario (MOE)

30 µg/m3

(24-hour AAQC)

Derived from the ACGIH TLV-TWA value of 280 µg/m3

1974 Ambient Air Quality Criteria

Alberta 2.8 µg/m3

(1-hour average)

Derived from the Texas

1-hour ESL

2000 Guideline value based on a

1-hour average

Quebec

(MinistPre de L’Environnement)

0.2 μg/m3 (annual criterion)

Derived from the US EPA RfC

2000 Annual average.

US EPA

(IRIS)

0.2 µg/m3

(RfC)

Vascular congestion and peribronchiolar edema in rats (Paulet and Desbrousses, 1972)

2000 Reference Concentration for inhalation exposure.

California

(OEHHA)

0.6 µg/m3

(Chronic REL)

Vascular congestion and peribronchiolar edema in rats (Paulet and Desbrousses, 1970; 1972)

2000 Chronic Reference Exposure Level is equivalent to RfC.

Louisiana

(DEQ)

6.67 μg/m3 (8-hour AAS)

Derived from the ACGIH TLV-TWA value of 280 µg/m3

1995 To obtain the AAS, ACGIH TLV-TWA was adjusted for continuous exposure (40 hrs/168 hrs) and an uncertainty factor (1/10) was applied to account for sensitive populations.

Massachusetts

(DEP)

No guideline listed.


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Agency Guideline Value Basis of Guideline Date2 Comments

Michigan

(DEQ)

0.2 µg/m3

(24-hr ITSL)


1998 Initial Threshold Screening Level.

New Jersey

(DEP)

0.2 µg/m3

(RfC)


1997 To be compared with maximum annual average ambient air concentration.

83 µg/m3

(1-hour SGC)

Derived from the ACGIH TLV-STEL value of

830 µg/m3

2000 Short-term Guideline Concentration

New York

(DEC)

0.2 µg/m3

(AGC)


1995 Annual Guideline Concentration.

Ohio

(EPA)

7 μg/m3 (1-hour MAGLC)

Derived from the ACGIH TLV-TWA value of

280 Fg/m3

1999 1-hr MAGLC is based on the following formula using the most current ACGIH TLV-TWA:

TLV-TWA/42

2.8 μg/m3 (1-hour ESL)


280 µg/m3

1997 Based on occupational human studies, but other reviews by agencies are also considered. A Safety factor of 100 was applied to the TLV-TWA

Texas

(NRCC)

0.3 μg/m3 (Annual ESL)


280 µg/m3

1997 Based on occupational human studies, but other reviews by agencies are also considered A Safety factor of 1000 was applied to the TLV-TWA

The Netherlands No guideline listed.

Sweden No guideline listed.

WHO (Europe & PHE)

No guideline listed.

1. Guidelines in this table can refer to: guidelines, risk-specific concentrations based on cancer potencies, and non-cancer-based

reference concentrations. 2. Date here refers to when the health-based guideline background report or original legislative initiative was issued. The sources

were the respective agency documents. For the US EPA, date refers to when the latest review of the RfC was conducted, if applicable, or the date the IRIS database was accessed, in the case where no RfC has been developed.

In reviewing the air quality guidelines and exposure limits presented in Table 1, it should be noted that the Ministry of the Environment typically uses a factor of 15 to convert from guidelines based on annual average concentrations to half-hour point-of-impingement limits and a factor of 3 to convert from guidelines based on 24-hour average concentrations. These factors are derived from empirical


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measurements and are selected to ensure that if the short-term limit is met, air quality guidelines based on longer-term exposures will not be exceeded. However, depending on the health end-point being considered, other conversion factors may also be employed.

The current U.S. EPA (IRIS) inhalation RfC is 0.2 μg/m3, which is based on vascular congestion and periobronchiolar edema in rats, and congested capillaries and hemorrhagic alveoli in lungs of rabbits (Paulet and Desbrousses, 1970; 1972). A number of U.S. States, as well as the Province of Quebec utilize standards that are based on the U.S. EPA RfC. Quebec currently uses an annual criterion of 0.2 μg/m3, while Michigan’s 24-hour initial threshold screening level (ITSL), New Jersey’s RfC, and New York’s Annual Guideline Concentration (AGC) are all 0.2 μg/m3.

The state of California derived a chronic Reference Exposure Level (REL) for chlorine dioxide based on the studies of Paulet and Desbrousses (1970, 1972). However, the California EPA’s interpretation of the studies resulted in a chronic REL value of 0.6 μg/m3, differing slightly from that of the U.S. EPA’s RfC value.

The American Conference of Governmental Industrial Hygienists (ACGIH, 2002) occupational exposure limit for chlorine dioxide is a Threshold Level Value, Time-Weighted Average (TLV-TWA) of 280 μg/m3 and a Short-term Exposure Limit (TLV-STEL) of 830 μg/m3 both based on the animal study of Dalhamn (1957) and the epidemiological study of Gloemme and Lundgren (1957). The TLV-TWA value is considered the average exposure concentration for a conventional 8-hour work day or a 40-hour work week, while the TLV-STEL is a 15-minute time-weighted average exposure that should not be exceeded at any time during the workday.

A number of States have based their air standards, guidelines or criteria on the ACGIH TLV-TWA of 280 μg/m3, as Louisiana uses an 8-hour AAS of 6.7 μg/m3 and Ohio uses a 1-hour MAGLC of 7 μg/m3. Both Texas and the Province of Alberta have also derived their respective air quality criteria based on the ACGIH TLV-TWA, as Alberta chose to adopt the Texas 1-hour Effects Screening Level (ESL). The State of New York was the only jurisdiction reviewed which has derived a short-term air quality guideline based on the ACGIH TLV-STEL value. New York has derived a 1-hour short-term guideline of 83 Fg/m3. All of these States used different uncertainty factors to account for some or all of the following factors: continuous versus occupational exposures; adult versus child sensitivities; sensitive groups versus health workers; and inadequacy of toxicological data.


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4.2 Evaluation of Existing Criteria


Both the U.S. EPA and the California EPA have developed guidelines for chlorine dioxide based on the studies of Paulet and Desbrousses (1970, 1972). The studies did not observe a NOAEL, however a LOAEL of 2.8 mg/m3 (1 ppm) was identified based on vascular congestion and peribronchiolar edema in rats (Paulet and Desbrousses, 1972). The U.S. EPA in developing their RfC value used a composite uncertainty factor (UF) of 3000. The UF comprised a factor of 10 to account for extrapolation of a chronic RfC from a subchronic study, 3 for interspecies extrapolation, 10 for intraspecies variability and 10 to account for extrapolation from a LOAEL to a NOAEL and for the lack of a sufficient toxicological database for chlorine dioxide (U.S. EPA, 2000a,b). The U.S. EPA has a policy to limit the size of a composite UF to 3000 in recognition of the lack of independence of these factors (U.S. EPA, 2000a,b). Therefore, the LOAEL to NOAEL and database uncertainties were combined into one UF of 10. The California EPA in 1997, originally proposed a chronic REL based on the U.S. EPA’s RfC, however in finalizing the value in 2000, the California EPA decided upon the use of an uncertainty of only 3 (compared to 10 by the U.S. EPA) to account for the extrapolation from subchronic to chronic effects (OEHHA, 2000). The California EPA also differed from the U.S. EPA as they did not feel that an UF of 3 was required for a lack of a sufficient toxicological database for chlorine dioxide. However, the California EPA imposed an UF of 10 to account for the extrapolation from a LOAEL to a NOAEL.

Both the U.S. EPA and the California EPA agreed that their respective guideline values have many uncertainties, but that the studies of Paulet and Desbrousses (1970, 1972) provide the best available data describing the inhalation toxicity of chlorine dioxide (OEHHA, 2000; U.S. EPA, 2000a,b). Uncertainties identified from the studies of Paulet and Desbrousses (1970, 1972) included a lack of multiple exposure concentration, the relatively short duration of exposure and the small number of animals examined. Both the U.S. EPA and the California EPA also point out the lack of toxicity data concerning effects not related to the lungs (OEHHA, 2000; U.S. EPA, 2000a,b).

A number of the U.S. States and the Province of Alberta have developed air quality guidelines based on the occupational exposure limits of the ACGIH. The rationale used by the ACGIH in deriving their TLV-TWA and TLV-STEL is not transparent. The guideline values were based on the animal study of Dalhamn (1957) and the epidemiological study of Gloemme and Lundgren (1957) (ACGIH,


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2001). There have been many studies conducted since these two studies were done in 1957. However, in the documentation in support of the TLV-TWA and TLV-STEL values, the studies of Paulet and Desbrousses (1970, 1972) were not discussed and only one study post-1970 was examined in the ACGIH’s rationale. Therefore, confidence in the guideline values derived by the ACGIH is low.

The ACGIH derived the TLV-TWA and the TLV-STEL values to minimize the potential for irritation and possible bronchitis as were documented in the above studies (Dalhamn, 1957; Gloemme and Lundgren, 1957). While the TLV-TWA and the TLV-STEL derived by the ACGIH are below the experimental NOAELs, no rationale has been provided concerning UFs used to provide adequate protection. A number of uncertainties must be addressed if an occupational exposure guideline is used as an ambient air quality guideline, such as exposure to children, and continuous versus discontinuous exposure.

5.0 Responses of Stakeholders to the Information Draft

In August 2005, the Ministry posted Information Draft documents for 12 chemicals, including chlorine dioxide, for air standards development under the Standards Plan (MOEE, 1996; MOE, 1999) to the Environmental Registry. The Ministry requested input regarding: the completeness of relevant toxicological information examined by the Ministry; the uncertainty factors used by the agencies (U.S. EPA, California EPA) that the Ministry has considered appropriate for the development of reference values for chlorine dioxide in ambient air; and an appropriate minimum mix of uncertainty factors that could be applied to occupational guidelines to develop AAQCs.

During the consultation period the Ministry received a submission from one stakeholder regarding the draft document for chlorine dioxide. Representatives of the forest industry association submitted comments. The only comment of a technical nature was directed to the question concerning uncertainty factors that could be applied to occupational guidelines to develop AAQCs. The stakeholder maintained that it was not appropriate to derive AAQCs in this manner, although it was appropriate to consider the derivation process for the occupational exposure limit and the underlying studies that were used. The stakeholder’s position was that ambient air quality standards ought to be derived independently.


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6.0 Responses of Stakeholders to the Rationale Document

In June, 2006, the Ministry posted to the Environmental Registry a document titled “Rationale for the Development of Ontario Air Standards for Chlorine Dioxide” and requested public comments over a period of 91 days. The Ministry received comments from six stakeholders: five general comments and one comment specific to chlorine dioxide standard. Highlights from these comments are summarized below.

Comments Specific to Chlorine Dioxide:

Comment: The Paulet and Desbrousses studies of 1970, 1972 seem to be heavily relied upon in spite of a number of acknowledged inadequacies (and the studies seem dated) just because they are the best available.

Response: The U.S. EPA and California EPA both rely on these same studies (as being the best available) to develop their ambient air reference levels. The limitations of the available data are compensated for by these jurisdictions by the use of a reasonable number of uncertainty factors, the MOE has used a similar approach. In terms of supporting information, the rationale document notes that several different approaches have yielded similar results: a human occupational study could support a chronic exposure limit of 1 to 3 μg/m3, a subchronic animal study has been used to develop chronic exposure limits by the U.S. EPA (0.2 μg/m3) and California (0.6 μg/m3), and the same animal study results were used to develop a chronic limit of 2.0 μg/m3 (MOE) and an intermediate screening level (MRL by ATSDR) of 3 μg/m3.

Comment: The Rationale Document reports that chlorine dioxide is an unstable gas that is highly reactive and rapidly decomposes in air. In spite of this, the MOE O.Reg. 419/05 and its related guidelines do not provide for this reactivity and the degradation that would take place between a point of release and a property boundary or point of impingement (POI). Instead, the regulatory process is to simply use the O.Reg 419/05 or the AERMOD (prime) dispersion model to predict POIs. This approach is overly conservative and in the case where an exceedance of the POI would be predicted, “refinement” could be used that would then consider this reactivity and degradation. In the case of chlorine dioxide this approach is burdensome to the industry and the facilities and, instead, the MOE should build this consideration into its standard-setting approach.

Given the highly reactive nature of chlorine dioxide, then, typically, generator scrubbers are oversized to control most upsets. As a result, chlorine dioxide


19

releases are not significant in terms of an ambient standard, given that any releases from pulp mills (which would be small) break down prior to the fence-line.

The stakeholder recommends that the Ministry of Environment build consideration of the high reactivity rate into its standard-setting approach for chlorine dioxide, rather than setting a stage where every user of chlorine dioxide would be expected to go through a “refinement” process for predicting its POIs.

Response: The highest rates of reactivity and decomposition of chlorine dioxide in air occur during daylight hours when sunlight is present. The time required for the chlorine dioxide concentration to decrease to 1/e (i.e. 37%) of its original value is the lifetime, which has been determined to be approximately 15 seconds (NCASI,1999) for decomposition by sunlight (photolysis). Lifetime estimates for decomposition by other means, such as reaction with hydroxyl radical (OH -), ozone or nitric oxide (NO), range from 40 to 80 hours. During hours of daylight with wind speeds of 10 feet per second (7 miles per hour), a release of chlorine dioxide will reduce to approximately 37% of its original concentration by the time it has travelled 150 feet, or approximately 14% of its release concentration by the time it has travelled twice that far (300 feet). The distance from the release point to the fence-line, the wind speed, and the intensity of the sunlight are all important variable factors in determining how much chlorine dioxide will survive as far as the fence-line. Releases during hours of darkness are likely to be reduced only by normal plume dispersion and not significantly affected by degradation for the first few hours. As confirmation that ClO2 plumes can be detected at significant levels beyond the fence-line, the Ministry has reliable evidence from two ambient air monitoring studies that were carried out near a pulp and paper mill in Ontario (MOE, 1985; MOE, 1986).

Since the potential effects experienced at the point of impingement depend only on the concentration of the chlorine dioxide at that point and not on the particular paths taken by the chlorine dioxide plume to arrive there, the determination of an effects-based standard and the issue of the plume reactivity/degradation must be dealt with separately. The Ministry believes that the most appropriate approach is exactly the type of “refinement” (to the AERMOD usage) noted in the comment above since every release of chlorine dioxide from every facility will be different. It is likely that the “refinement” process will be relatively simple and mainly influenced by the wind speed and wind direction (to determine plume transit time to the fence-line), and whether or not there is sunlight present.


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General Comments:

In addition to technical comments on this specific substance, MOE received ‘general’ comments related to the standard setting process, implementation of standards and odour issues. Some of these comments formed part of the response to the Rationale Documents, which were posted from June 26, 2006 to September 25, 2006. Other comments were in response to the "Proposal to amend Ontario Regulation 419/05: Air Pollution-Local Air Quality" posted from June 15 to September 25, 2006, with a subsequent posting April 7, 2007 to May 7, 2007 of the proposed draft amendments to O. Reg. 419/05. With the June to September, 2006 posting the MOE also introduced a “Proposed Approach for the Implementation of Odour-Based Standards and Guidelines” to which it also received comments.

A detailed summary of these general comments and MOE’s responses to them can be found in the following two related postings:

1) EBR #: 010-0000 – Proposal to Amend Ontario Regulation 419/05: Air Pollution-Local Air Quality under the Environmental Protection Act; and

2) EBR #: RA06E0006 – Proposed Approach for the Implementation of Odour-Based Standards and Guidelines.

7.0 Considerations in the Development of an Ambient Air Quality Criterion for Chlorine Dioxide

Currently in Ontario, the 24-hour AAQC value and the half-hour Point of Impingement standard for chlorine dioxide are 30 and 85 μg/m3, respectively. The half-hour standard is based on the ACGIH TLV-STEL of 830 μg/m3, while the 24-hour standard is based on the ACGIH TLV-TWA of 280 μg/m3 (MOE, 2005).


The occupational guideline values derived by the ACGIH were also a source of many of the guideline values derived by the jurisdictions reviewed. The ACGIH

http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=MTAwMDAw&statusId=MTQ5Mzgx&language=en

http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=MTAwMDAw&statusId=MTQ5Mzgx&language=en

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http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=Mjc4ODc=&statusId=Mjc4ODc=&language=en


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in developing their limits relied on an animal and an epidemiological study in defining an acceptable exposure for chlorine dioxide. The exposure limits derived by the ACGIH have not been updated since 1976 and are based on data from studies published in 1957. The ACGIH in their documentation in support of their occupational exposure limits values does not review the studies of Paulet and Desbrousses and only reviews one study post-1970. The lack of up-to-date toxicological information in deriving their exposure limit values places lower confidence in their scientific rationale.

The single stakeholder providing comment on the information draft maintained that it was not appropriate to derive AAQCs by simply applying uncertainty factors to an occupational exposure limit. The Ministry generally agrees with the stakeholder, and one current MOE practice is to find key studies in which NOAELs (or LOAELs) are determined and to apply appropriate uncertainty factors to derive a suitable ambient air quality limit (e.g. AAQC). One such study is the same study (Gloemme and Lundgren,1957) on which the ACGIH occupational limit is based. As noted in section 3.2, this was a human, clinical investigation of 5-year exposures that generally did not exceed 0.1 ppm chlorine dioxide, but occasionally included co-exposure to chlorine and sulphur dioxide. It was reported that the adverse health effects (symptoms of ocular and respiratory irritation leading to slight bronchitis) were due mainly to higher chlorine dioxide levels during periods of equipment leaks. It is also likely that adverse effects during co-exposure were worse than during exposure to chlorine dioxide alone, so selecting a LOAEL for chlorine dioxide alone during periods of co-exposure would likely be conservatively low. However, a strong limiting condition on this study is the fact that chlorine dioxide levels were not actually measured. Thus, the decision about selecting a particular level as the LOAEL is not well supported by the evidence. It may be that the selected LOAEL (0.1 ppm) is actually a NOAEL (ACGIH, 2001). If 0.1 ppm (280 μg/m3) is selected as a human LOAEL, then the application of a few uncertainty factors may yield an acceptable reference level (AAQC) for chlorine dioxide. Appropriate uncertainty factors could include: 10 for human variability, 3 for use of a LOAEL instead of a NOAEL, 3 for subchronic duration instead of chronic, and 3 for database uncertainty (including a small number of people in the study, and occasional co-exposure to other chemicals). The uncertainty factors are commonly multiplied together to yield the total uncertainty factor, but with the usual convention that two factors of 3 will combine to yield 10. In this manner 10, 3, 3, 3 will yield a total UF = 300. The resulting reference value (280/300) of 1 μg/m3 (approximately) could be considered a conservatively low estimate of a chronic exposure limit (24-hour AAQC). The uncertainty about the LOAEL or NOAEL suggests that an appropriate characterization of the available information is as follows: limited occupational data can support a chronic exposure limit (24-hour AAQC) in the range of 1 to 3 μg/m3.


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Acute inhalation exposures to chlorine dioxide have been reported to cause varying severity of irritation to the respiratory system depending on the concentration. Acute animal studies support the findings cited in human studies. In addition to the irritative effects, histological changes have been observed in the lungs and the kidneys of rats. Symptoms of chronic exposure to chlorine dioxide in humans are also of an irritant nature; however, with repeated long-term exposure permanent lung damage may result. Results from occupational and epidemiological studies have described irritation to both the respiratory tract and the eyes with the development of bronchitis following chronic exposures as low as 0.28 mg/m3. Subchronic and chronic studies of inhalation exposure to chlorine dioxide in animals are few in number, but in one subchronic study (Paulet and Desbrousses (1972), rats exposed to 2.8 mg/m3 were found to exhibit vascular congestion in the lungs in addition to peribronchiolar edema.

In examining the potential for developmental or reproductive effects with exposure no information was available concerning inhalation exposures. However, several studies have examined oral exposure and one suggested that there is the potential for effects on fetal brain development.

Currently there are no studies regarding carcinogenic effects in humans or animals following inhalation exposure. The U.S. EPA currently classifies chlorine dioxide as Group D (not classifiable as to human carcinogenicity) based on inadequate human and animal data. There are no IARC, Health Canada, or ACGIH cancer classifications for chlorine dioxide at this time.

The U.S. EPA’s RfC (0.2 μg/m3) and the California EPA’s chronic REL value (0.6 μg/m3) have formed the basis of many of the U.S. States’ air quality guidelines. Both the U.S. EPA and the California EPA have chosen the studies of Paulet and Desbrousses (1970, 1972), as the basis of their guideline value; however, the application of uncertainty factors has lead to differences in the final guideline value derived.

If the Ministry also selects the studies of Paulet and Desbrousses (1970, 1972), as the basis of an air quality criterion value and then applies appropriate adjustments and uncertainty factors to derive a final limit, then the preferred approach is as follows:

• Although the studies did not observe a NOAEL, a LOAEL of 2.8 mg/m3 (1 ppm) was identified based on vascular congestion and peribronchiolar edema in rats (Paulet and Desbrousses, 1972).

• Adjust for continuous exposure to get LOAELADJ :



23

= 416 µg/m3

• Convert to a human equivalent concentration by multiplying by the regional gas dose ratio (RGDR):


= 416 µg/m3 × 1.57

= 650 µg/m3 (rounded)

• A total uncertainty factor (UF) of 300 (10 for protection of sensitive human subpopulations, 3 for interspecies extrapolation, 3 for use of a LOAEL instead of a NOAEL, 3 for use of subchronic data (instead of chronic) and lack of reproductive or developmental data for inhalation exposure) is applied to the LOAELHEC to yield a chronic exposure limit:

LOAELHEC / UF = 650 µg/m3 / 300 = 2.0 µg/m3 (rounded) = AAQC

A similar (magnitude) result is obtained if the data for exposure to rabbits (Paulet and Desbrousses, 1970) is used, which lends support to the final result. The calculation of RGDR is explained in the Appendix section 10.2.

Recently, the Agency for Toxic Substances and Disease Registry (ATSDR, 2004), affiliated with the U.S. EPA, has also developed a reference value, known as a Minimal Risk Level (MRL), which is based on noncancer health effects only and is intended to act as a screening level during health assessments. ATSDR used the results from Paulet and Desbrousses (1972), calculated a slightly different RGDR value (1.907, based on the pulmonary area of the respiratory tract instead of thoracic), and used the same uncertainty factors as used for the RfC with one exception. Since the MRL is not intended to screen against adverse effects for a lifetime but, in this case, only for an intermediate duration, a factor 10 for adjusting from subchronic to chronic exposure was not included. The combined uncertainty factor of 300 was applied to the LOAELHEC to give an MRL of 1 ppb (3 µg/m3, rounded).

In summary, a human occupational study could support a chronic exposure limit of 1 to 3 µg/m3, a subchronic animal study has been used to develop chronic exposure limits by the U.S. EPA (0.2 µg/m3) and California (0.6µg/m3), and the same animal study results were used as described above, to develop (Ministry approach) a chronic limit of 2.0 µg/m3 and an intermediate screening level (MRL by ATSDR) of 3 µg/m3.


24

8.0 Decision

The Ministry of the Environment has reviewed and considered air quality guidelines and standards used by leading agencies worldwide. After reviewing additional toxicological information, the Ministry considers the results from the studies of Paulet and Desbrousses (1970, 1972), based on the respiratory system effects of this compound, with supporting information from a human occupational study, to be the most appropriate basis for the derivation of health-based air standards for chlorine dioxide.

The Ministry of the Environment uses a factor of 3 to convert from criteria based on 24-hour average concentrations to half-hour average concentration. This factor is derived from empirical measurements and is selected to ensure that if the short-term limit is met, air quality standards based on longer-term exposures will not be exceeded (MOE, 1987; MOEE, 1994).

After an evaluation of the scientific rationale of air guidelines from leading agencies and an examination of current toxicological research for chlorine dioxide (10049-04-4), the standards for chlorine dioxide are as follows:

• A 24-hour average AAQC of 2.0 μg/m3 (micrograms per cubic metre of air) based on adverse health effects (respiratory system); and

• A half-hour standard of 6.0 μg/m3 (micrograms per cubic metre of air) based on adverse health effects (respiratory system).

These effects-based AAQCs and the corresponding effects-based half hour standards will be incorporated as standards into Ontario Regulation 419/05: Air Pollution – Local Air Quality (O. Reg. 419/05). The AAQCs will be incorporated into Schedule 3 of O. Reg. 419/05; the half-hour standard will be incorporated into Schedule 2.

MOE generally proposes a phase-in period for new standards or standards that will be more stringent than the current standard or guideline. The phase-in for this compound is as set out in O. Reg. 419/05.

Among other things, O. Reg. 419/05 sets out the applicability of standards and appropriate averaging times, phase-in periods, types of air dispersion models and when various sectors are to use these models. There are 3 guidelines that support O. Reg. 419/05. These guidelines are:

• “Guideline for the Implementation of Air Standards in Ontario” (GIASO);


25

• “Air Dispersion Modelling Guideline for Ontario” (ADMGO); and

• “Procedure for Preparing an Emission Summary and Dispersion Modelling Report” (ESDM Procedure).

GIASO outlines a risk-based decision making process to set site specific alternative air standards to deal with implementation barriers (time, technology and economics) associated with the introduction of new/updated air standards and new models. The alternative standard setting process is set out in section 32 of O. Reg. 419/05.

For further information on these guidelines and O. Reg. 419/05, please see the Ministry’s website http://www.ontario.ca/environment and follow the links to local air quality.

http://www.ontario.ca/environment


26

9.0 References

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27

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Chang, S.L. 1982. The safety of water disinfection. Annu Rev Public Health 3: 393-418.

Couri, D. and Abdel-Rahman, M.S. 1980. Effect of chlorine dioxide and metabolites on glutathione dependent systems in rat, mouse and chicken blood. J Environ Pathol Toxicol 3:451-460.

Couri, D., Abdel-Rahman, M.S. and Bull, R.J. 1982. Toxicological effects of chlorine dioxide, chlorite, and chlorate. Environ Health Perspect 46:13-17.

Dalhamn, T. 1957. Chlorine dioxide: Toxicity in experimental animals and industrial risks. AMA Arch Ind Hyg 15:101-107.

Dandy, J.W.T. 1972. Activity response to chlorine in the brook trout (Salvelinus fontinalis) (Mitchill). Can J Zool 50: 405–410.


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Daniel, F.B., Condie, L.W., Robinson, M., Stober, J.A.,York, R.G., Olson, G.R. and Wang, S. 1990. Comparative subchronic toxicity of three disinfectants. J AWWA 82:61-69.

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DeMore, W.B., Sander, S.P., Golden, D.M., Hampson, R.F., Kurylo, M., Howard, C.J. Ravishankara, A.R., Kolb, C.E. and Molina, M.J. 1994. Chemical Kinetics and Photochemical Data for use in Stratospheric Modeling, Evaluation No. 11, NASA Panel for Data Evaluation, Jet Propulsion Laboratory Publication 94-26. Pasadena, California. Cited In: OEHHA, 2000.

Elkins, H.B. 1959. The Chemistry of Industrial Toxicology, 2nd ed. Wiley and Sons, Inc., New York. p. 89-90. Cited In: US EPA, 2000a.

Environment Canada. 1996. National pollutant Release Inventory (NPRI). Canadian Environmental Protection Act.

Exner-Freisfeld, H., Kronenberger, H., Meier-Sydow, J. and Nerger, K.H. 1986. Intoxication from bleaching with sodium chlorite. The toxicology and clinical course. Dtsh Med Wochenschr 111:1927-1930. (Eng. Abstract). Cited In: US EPA, 2000a.

Ferris, B.G. Jr., Burgess. W.A. and Worcester, J. 1967. Prevalence of chronic respiratory disease in a pulp mill and a paper mill in the United States. Br J Ind Med 24:26-37. Cited In: US EPA, 2000a.

Fisher, D.J., Burton, D.T., Yonkos, L.T., Turley, S.D. and Ziegler, G.P. 1999. The relative acute toxicity of continuous and intermittent exposures of chlorine and bromine to aquatic organisms in the presence and absence of ammonia. Water Res 33: 760–768.

Gerges, S.E., Abdel-Rahman, M.S., Skowronski, G.A. and Von Hagen, S. 1985. Effects of Alcide gel on fetal development in rats and mice. II. J Appl Toxicol 5:104-109. Cited In: US EPA, 2000a.

Gloemme, J., and Lundgren. K.D. 1957. Health hazards from chlorine dioxide. Arch Ind Health 16:169-176.

Gregg, B.C. 1974. The effects of chlorine and heat on selected stream invertebrates. Ph.D. thesis. Virginia Polytechnic Institute and State University, Blacksburg, VA.


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Haag, H.B. 1949. The effect on rats of chronic administration of sodium chlorite and chlorine dioxide in the drinking water. Report to the Mathieson Alkali Works from H.B. Haag of the Medical College of Virginia. February. Cited In: US EPA, 2000a.

Harrington, R.M., Shertzer. H.G. and Bercz, J.P. 1986. Effects of chlorine dioxide on thyroid function in the African green monkey and the rat. J Toxicol Environ Health 19:235-242. Cited In: US EPA, 2000a.

Hose, J.E., Fiore Di, D., Parker, H.S. and Sciarrotta, T. 1989. Toxicity of chlorine dioxide to early life stages of marine organisms. Bull Environ Contam Toxicol 42 (3): 315-319.

HSDB. 2002. Hazardous Substances Databank. The National Library of Medicine, Bethesda, MD, USA.

Ishidate, M., Sofuni, T., Yoshikawa, K., Hayashi, M., Nohmi, T., Sawada, M. and Matsuoka, A. 1984. Primary mutagenicity screening of food additives currently used in Japan. Food Chme Toxicol 22:623-636.

Kennedy, S.M., Enarson, D.A., Janssen, R.G. and Chan-Yeung, M. 1991. Lung health consequences of reported accidental chlorine gas exposures among pulpmill workers. Am Rev Respir Dis 143:74-79.

Kott, Y., Hershkovitz, G., Shemtob, A., and Sless, J.B. 1966. Algicidal effect of bromine and chlorine on Chlorella pyrenoidosa. Appl Microbiol 14(1): 8–11.

Larson, G.L., Warren, C.W., Hutchins, F.E., Lamperti, L.P., Schlesinger, D.A. and Siem, W.K. 1978. Toxicity of residual chlorine compounds to aquatic organisms. EPA-600/3-78-023. U.S. Environmental Protection Agency, Corvallis, OR.

Matisoff, G., Brooks, G., and Bourland, B.I. 1996. Toxicity of chlorine dioxide to adult zebra mussels. J Am Water Works Assoc 88: 93-10.

Meier, J.R., Bull, R.J., Stober, J.A. and Cimino, M.C. 1985. Evaluation of chemicals used for drinking water disinfection for production of chromosomal damage and sperm-head abnormalities in mice. Environ Mutagen 7: 201-211.

Miller, R.G., Kopfler, F.C., Condie, L.W., Pereira, M.A., Meier, J.R., Ringhand, H.P., Robinson, M. and Casto, B.C. 1986. Results of toxicological testing of Jefferson Parish pilot samples. Environ Health Persp 69:129-139. Cited In: US EPA, 2000a.

MOEE. 1996. Three-year Plan for Standards-setting. Standards Development Branch, Ministry of the Environment and Energy, Ontario.


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MOE. 1985. Technical Memorandum. ARB-067-85-AQM

MOE. 1986. Technical Memorandum. ARB-216-86-AQM

MOE. 1999. Setting Environmental Quality Standards in Ontario: The Ministry of the Environment’s Standards Plan. Standards Development Branch, Ministry of the Environment, Ontario.

MOE. 2005a. Summary of O.REG.419/05 Standards and Point of Impingement Guidelines & Ambient Air Quality Criteria (AAQCs). Standards Development Branch, Ontario Ministry of the Environment, Toronto, Ont. December 2005.

MOE. 2005b. Information Draft Information Draft on the Development of Ontario Air Standards For Chlorine Dioxide. June 2005.

MOE. 2006. Rationale for the Development of Ontario Air Standards for Chlorine Dioxide. June 2006

Moore, G.S. and Calabrese. E.J. 1980. The effects of chlorine dioxide and sodium chlorite on erythrocytes of A/J and C57L/J mice. J Environ Pathol Toxicol 4:513-524. Cited In: US EPA, 2000a.

Moore, G.S. and Calabrese. E.J. 1982. Toxicological effects of chlorite in the mouse. Environ Health Perspect 46:31-37.

NCASI. 1999. National Council For Air And Stream Improvement. Atmospheric Fate of Chlorine, Dioxide, Chlorine, Formaldehyde, Methanol, Chloroform, And Acetaldehyde. Technical Bulletin No. 791, September, 1999.

NJDHSS. (New Jersey Department of Health and Senior Services). 1998. Hazardous Substance Fact Sheet - Chlorine Dioxide.

NIOSH. 1978. National Institute for Occupational Safety and Health. Occupational Health Guideline for Chlorine Dioxide. US Department of Health and Human Services.

NPRI. 1995. National Pollutant Release Inventory. Report and online database of 1995.

http://www.pwc.bc.doe.ca/ep/npri/index.htmlhttp://www.npri-inrp.com/queryform.cfm


http://www.pwc.bc.doe.ca/ep/npri/index.html

http://www.npri-inrp.com/queryform.cfm



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OEHHA. 2000. Air toxics hot spots program risk assessment guidelines. Part III. Technical support document for the determination of noncancer chronic reference exposure levels. Draft for public review. October 2000. Office of Environmental Health Hazard Assessment (OEHHA), California Environmental Protection Agency (CalEPA), CA.

Orme, J., Taylor, D.H., Laurie, R.D. and Bull, R.J. 1985. Effects of chlorine dioxide on thyroid function in neonatal rats. J Toxicol Environ Health 15:315-322. Cited In: US EPA, 2000a.

Owusu-Yaw, J., Toth, J.P., Wheeler, W.B. and Wei, C.I. 1990. Mutagenicity and identification of the reaction products of aqueous chlorine or chlorine dioxide with L-tryptophan. J Food Sci 55:1714-1724.

Owusu-Yaw, J., Wheeler, W.B. and Wei, C.I. 1991. Genotoxicity studies of the reaction of chlorine or chlorine dioxide with L-tryptophan. Toxicol Letters 56:213-227.

















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Paulet, G. and Desbrousses, S. 1970. [Effect of a weak concentration of chlorine dioxide on laboratory animals.] Arch Mal Prof Med Trav Secur Soc 31:97-106. Cited In: US EPA, 2000a.

Paulet, G. and Desbrousses, S. 1972. On the toxicology of chlorine dioxide. Arch Mal Prof Med Trav Secur Soc 33:59-61. Cited In: US EPA, 2000a.

Paulet, G. and Desbrousses, S. 1974. Action of a discontinuous exposure to chlorine dioxide on the rat. Arch Mal Prof Med Trav Secur Soc 35:797-803. Cited In: US EPA, 2000a.

Petry, H. 1954. Chlordioxyd-ein gefahrliches Reizgas, Arch. Gewerbepath. u. Gewerbehyg 13: 363. Cited In: Gloemme and Lundgren, 1957.

Pratt, J.R., Bowers, N.J., Niederlehner, B.R. and Cairns, J. Jr. 1988. Effects of chlorine on microbia communities in naturally derived microcosms. Environ Toxicol Chem 7: 679–687.

Rosenberger, D.R. 1971. The calculation of acute toxicity of free chlorine and chloramines to coho salmon by multiple regression analysis. M.Sc. thesis. Michigan State University, East Lansing, MI.

Sax, N.I., Lewis, R.J., Sr. 1989. Dangerous Properties of Industrial Materials. Volumes 1-3. 7th edition. Van Nostrand Reinhold. New York, New York. Cited In: ARB, 1997.

Skowronski, G.A., Abdel-Rahman, M.S., Gerges, S.E. and Klein, K.M. 1985. Teratologic evaluation of Alcide liquid in rats and mice. I. J Appl Toxicol 5:97-103. Cited In: US EPA, 2000a.

Stevens, A.A. 1982. Reaction products of chlorine dioxide. Environ Health Perspect 46:101-110.

Suh, D.H., Abdel-Rahman, M.S. and Bull, R.J. 1983. Effect of chlorine dioxide and its metabolites in drinking water on fetal development in rats. J Appl Toxicol 3:75-79. Cited In: US EPA, 2000a.

Tan, H., Wheeler, W.B. and Wei, C. 1987. Reaction of chlorine dioxide with amino acids and peptides: kinetics and mutagenicity studies. Mutation Research 188:259-266.

Taylor, D.H., and Pfohl. R.J. 1985. Effects of chlorine dioxide on neurobehavioral development of rats. In: Water Chlorination, Vol 5. Chemistry, Environmental Impact and Health Effects, R.L. Jolley et al., Ed. Fifth Conference


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on Water Chlorination: Environmental Impact and Health Effects, Williamsburg, VA., USA. ISBN 0-87371-005-3; 0(0). p. 355-364. Cited In: US EPA, 2000a.

Taylor, P. 1993. An evaluation of the toxicity of various forms of chlorine to Ceriodaphnia dubia. Environ Toxicol Chem 12: 925–930.

Toth, G.P., Long, R.E., Mills, T.S. and Smith, M.K. 1990. Effects of chlorine dioxide on the developing rat brain. J Toxicol Environ Health 31:29-44.

Tuthill, R.W., Giusti, R.A., Moore. G.S., and Calabrese, E.J. 1982. Health effects among newborns after prenatal exposure to ClO2-disinfected drinking water. Environ Health Perspect 46:39-45.

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US EPA. 2000a. Toxicological review of chlorine dioxide and chlorite. In support of summary information on the Integrated Risk Information System (IRIS). US Environmental Protection Agency.

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Vogt, H., Balej, J., Bennett, J.E., et al. 1986. Chlorine oxides and chlorine oxygen acids. In: Gerhartz, W., Yamamoto, Y.S., Campbell, F.T., et al., eds. Ullman’s encyclopedia of industrial chemistry. Vol. A6. New York, NY: VCH, 483-500.

Watkins, C.H. and Hammerschlag, R.S. 1984. The toxicity of chlorine to a common vascular aquatic plant. Water Res 18: 1037–1043.

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Zika, R.G., Moore, C.A., Gidel, L.T., et al. 1984. Sunlight-induced photodecomposition of chlorine dioxide. In: R.L. Jolley, R.J. Bull, W.P. Davis, et al., eds. Water chlorination-Chemistry, environmental impact and health effects. Vol. 5. Williamsburg, VA: Lewis Publishers, Inc.


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10.0 Appendix: Agency-Specific Reviews of Air Quality Guidelines

10.1 Agency-Specific Summary: Federal Government of Canada

1. Name of Chemical: Chlorine dioxide (CAS no. 10049-04-4)

2. Agency: Canadian Environmental Protection Act (CEPA) under the auspices of Health Canada and Environment Canada

3. Guideline Value(s):

No guideline is listed.

4. Application:

Under the Canadian Environmental Protection Act (CEPA), the Ministers of the Environment and Health are advised to investigate various substances with the potential to cause adverse effects on the environment and human health. In 1994, 44 chemicals were on the first Priority Substances List (PSL 1). Further to this, in 1995, the second PSL list was established and it identified other substances which were scheduled to be evaluated over the upcoming years.

Some of the substances listed in Health Canada (1996) have Tolerable Concentrations (TC) in mg/m3 for non-carcinogenic effects. These values are airborne concentrations which can be exposed to a person, continuously over a lifetime without adverse health effects.

Canadian Council of Ministers of the Environment (CCME) is in the process of developing new Canada-Wide Standards (CWSs) which include qualitative or quantitative standards, guidelines, objectives, and criteria for protecting the environment and reducing the risk to human health. The focus of the Standards Sub-Agreement is on ambient standards which will include air as a media. The CWSs will not be legally enforceable and governments will be responsible for implementing them.

5. Documentation Available:

No information.


36

Key Reference(s):

Not applicable.

6. Peer Review Process and Public Consultation:

No information.

7. Status of Guideline:

Not applicable.

8. Key Risk Assessment Considerations:

Not applicable.

9. Key Risk Management Considerations:

No information.

10. Multimedia Considerations of Guidelines:

No information.

11. Other Relevant Factors:

No information.


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10.2 Agency-Specific Summary: Federal Government of the United States


2. Agency: United States Environmental Protection Agency (US EPA)


No ambient air exposure limits are currently promulgated. The US EPA has National Ambient Air Quality Standards (NAAQS) for some “criteria pollutants” (i.e. carbon dioxide) but not for hazardous air pollutants. However, under the auspices of the US EPA is the Integrated Risk Information System (IRIS) database (on-line) in which inhalation and oral exposure limits are derived which can be used towards the derivation of ambient air guidelines or standards. Currently, in IRIS, the inhalation reference concentration (RfC) for chlorine dioxide is 0.2 µg/m3.

4. Application:

The IRIS database is designed to provide consistent information on chemical substances used in risk assessments, decision-making and regulatory activities. The main intention of IRIS is to provide information which can be used towards the protection of public health through risk assessment and risk management. The values presented in IRIS do not represent guidelines on their own. IRIS also contains a summary of current American government regulatory actions under various mandates.


US EPA. 2000a. Toxicological review of chlorine dioxide and chlorite. In support of summary information on the Integrated Risk Information System (IRIS). September, 2000. US Environmental Protection Agency, Washington, DC.

US EPA. 2000b. Chlorine dioxide. Integrated Risk Information System (IRIS) on-line database. United States Environmental Protection Agency (US EPA), Cincinnati, OH. URL: http://www.epa.gov/iris/subst/index.html

Key Reference(s):

Paulet, G., and Desbrousses, S. 1970. [Effect of a weak concentration of chlorine dioxide on laboratory animals.] Arch Mal Prof Med Trav Secur Soc 31(3):97-106.

http://www.epa.gov/iris/subst/index.html


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Paulet, G., and Desbrousses, S. 1972. Toxicology of chlorine dioxide. Arch Mal Prof Med Trav Secur Soc 33(1-2):59-61. .


The US EPA makes use of peer-reviewed scientific research data, analyses, and evaluations from various sources, including a variety of public and government agencies from around the world and the published scientific literature. Both the general assessment methodologies and the chemical-specific information found in IRIS undergo extensive scientific and policy reviews, both within the US EPA and within other science-based US regulatory agencies. Information is put on IRIS after results of the public review and comments on draft documents/information have been addressed.


The RfC is current and was last revised in December 2000.


The inhalation RfC for chlorine dioxide was derived from the information in the studies by Paulet and Desbrousses (1970, 1972). The studies were selected as co-critical to provide additional support since they were both shorter (30 to 60 days in duration) than the typical subchronic duration, and they both identified a LOAEL for respiratory effects.

In the study by Paulet and Desbrousses (1972), eight Wistar rats were exposed to one exposure concentration of 1 ppm (2,760 Fg/m3) for 5 hours per day, 5 days per week for 2 months. Measurements included body weight and blood counts, and histopathological examination of the lungs and liver at the end of the experiment. The exposed rats showed vascular congestion and peribronchiolar edema in the lungs without alteration of the epithelium or parenchyma. No effects on weight gain, red blood cell, and white blood cell counts were observed. The single exposure concentration of 2,760 Fg/m3 was identified as the LOAEL and was adjusted (ADJ) from intermittent exposure to continuous exposure:


= 410 µg/m3

The LOAELADJ was then converted to a human equivalent concentration (HEC) by multiplying the regional gas dose ratio (RGDR) for an observed effect of a gas in the thoracic region (TH) of the respiratory tract. The value for RGDRTH is calculated as follows:


39

RGDRTH = (MVa / Sa) / (MVh / Sh)

= ((0.17 m3/day) / 3,461 cm2) / ((20 m3/day) / 640,581 cm2)

= 1.57

where, MVa = minute ventilatory volume for experimental animal species,

MVh = minute ventilatory volume for humans,

Sa = surface area of the thoracic region for experimental animal species, and

Sh = surface area of the respiratory tract in humans.

The LOAELHEC would be calculated as follows:


= 410 µg/m3 × 1.57

= 640 µg/m3

In the study by Paulet and Desbrousses (1970), four different exposure regimens were used: rats, 10 ppm (28 mg/m3) at 2 hrs/day for 30 days; rats and rabbits, 5 ppm at 2 hrs/day for 30 days; rats 2.5 ppm at 7 hrs/day for 30 days; rabbits, 2.5 ppm at 4 hrs/day for 45 days. The duration-adjusted exposure concentrations were 1.6 mg/m3, 0.82 mg/m3, 1.4 mg/m3 and 0.82 mg/m3, respectively. IRIS assumed that the animals were exposed 5 days per week even though this was not explicitly stated in Paulet and Desbrousses (1970). An equal number of animals were exposed to room air to serve as controls. Measurements included body weight, blood cell counts, and histopathological examination of the liver and lungs and other tissues. Clinical signs of respiratory irritation, with focal bronchopneumonia and localized broncho-alveolar lesions were observed in the 5 ppm (13,800 µg/m3) group. Hemorrhagic alveoli and congested capillaries were observed in the lungs of the 2.5 ppm (6,900 µg/m3) group. No changes in weight gain or blood cell counts were found. A LOAEL of 2.5 ppm (6,900 µg/m3) was identified for thoracic respiratory effects and blood effects. The LOAEL was adjusted to continuous exposure:


= 820 µg/m3


40



= (1.1 m3 / 59,100 cm2) / (20 m3 / 640,581 cm2)

= 0.596

The LOAELHEC is calculated as follows:


= 820 µg/m3 × 0.596

= 490 µg/m3

An uncertainty factor (UF) of 3,000 (10 for the protection of sensitive human subpopulations, 3 for interspecies extrapolation, 10 for use of a subchronic study, and 10 for the use of a LOAEL for a mild effect and to account for the lack of developmental and reproductive studies) can be applied to the LOAELHEC from either study to obtain approximately the same RfC of 0.2 µg/m3:

RfC = LOAELHEC / UF or = LOAELHEC / UF

= 640 µg/m3 / 3,000 = 490 µg/m3 / 3,000

= 0.21 µg/m3 = 0.16 µg/m3


The RfC is an estimate of a daily inhalation exposure to the human population (including sensitive subgroups) that will not result in adverse effects during a lifetime.


The RfC considers inhalation exposure only.


The confidence in the study, database and RfC is low because the studies by Paulet and Desbrousses (1970, 1972) identified only a LOAEL of less-than-


41

subchronic duration and they lacked experimental detail; there were no adequate subchronic or chronic inhalation studies that examined lung effects and no acceptable developmental or reproductive studies on inhaled chlorine dioxide.

Chlorine dioxide is not classifiable as to its human carcinogenicity (Group D).


42

10.3 Agency-Specific Summary: California


2. Agency: California Environmental Protection Agency (CalEPA)


A chronic toxicity reference exposure level (REL) of 0.6 Fg/m3 has been derived by the Office of Environmental Health Hazard Assessment (OEHHA).

4. Application:

“The intent of the Committee in developing the guideline was to provide risk assessment procedures for use in the Air Toxics ‘Hot Spots’ program.” (CAPCOA, 1993). This program is based on a California State Law, the Air Toxics ‘Hot Spots’ Information and Assessment Act of 1987 (Health and Safety Code Section 44360 et Seq.). The act specifies how local Air Pollution Control Districts determine which facilities in the area will prepare a health risk assessment, how such health risk assessments should be prepared, and how the results are to be prioritized. These Guidelines were prepared to provide consistent risk assessment methods and report presentation to: 1) compare one facility against another, 2) expedite the review of risk assessments by reviewing agencies, and 3) minimize revisions and re-submission of risk assessments. The various health-based exposure levels developed for and employed in this program should not be used outside the framework of the program. That is to say, the State of California does not consider them to be general, independent, legally enforceable air quality guidelines or limit values at this time.


CalEPA. 1997. Toxic air contaminant identification list compound summaries. Final Report. State of California, California Environmental Protection Agency (CalEPA), Air Resources Board, Stationary Sources Division.

CAPCOA. 1993. Air toxics “hot spots” program: revised 1992 risk assessment guidelines. Prepared by CAPCOA (California Air Pollution Control Officers Association), the Office of Environmental Health Hazard Assessment and the California Air Resources Board.

OEHHA. 2000. Air toxics hot spots program risk assessment guidelines. Part III. Technical support document for the determination of noncancer


43

chronic reference exposure levels. Draft for public review. October 2000. Office of Environmental Health Hazard Assessment (OEHHA), California Environmental Protection Agency (CalEPA), CA.

Key Reference(s):

Paulet, G., and Desbrousses, S. 1970. [Effect of a weak concentration of chlorine dioxide on laboratory animals.] Arch Mal Prof Med Trav Secur Soc 31:97-106.

Paulet, G., and Desbrousses, S. 1972. Toxicology of chlorine dioxide. Arch Mal Prof Med Trav Secur Soc 33:59-61.


Cancer potency slope factors and acute and chronic reference levels were prepared by the California Office of Environmental Health Hazard Assessment (OEHHA) using peer-reviewed scientific data. Both the exposure and health assessments have undergone public review and comment prior to finalization. Under the CAPCOA risk assessment process, each assessment is site-specific and public notice to all exposed individuals is required when the assessment concludes that a significant health risk is associated with emissions from a facility. Public input is obtained in identifying and ranking areas and facilities for risk assessment screening. Further additional input is expected as the process moves forward.


Current.


The California EPA derived their chronic REL based on the study results of Paulet and Desbrousses (1970, 1972). In the 1972 study, eight rats (sex unspecified) were exposed for 5 hours/day, 5 days/week, for 2 months to 0 or 1 ppm (2.8 mg/m3) chlorine dioxide (Paulet and Desbrousses, 1972). The number of control animals was not specified. Microscopic evaluation of the lungs revealed vascular congestion and peribronchiolar edema in all animals exposed to chlorine dioxide. The subchronic LOAEL for respiratory effects was concluded by the authors to be 1 ppm (2.8 mg/m3).

Support for the conclusion of a 1 ppm LOAEL came from their 1970 study of the effects of exposure to 2.5, 5, or 10 ppm (7, 14, or 28 mg/m3) chlorine dioxide for several hours/day for 30 days in rats and rabbits (n = 4-10 animals per group). Body weights, blood cell counts, and histopathological


44

examination of the liver, lungs, and other tissues were measured in each group. At 10 ppm, nasal discharge, localized bronchopneumonia, and desquamated alveolar epithelium were observed. White and red blood cell counts were also increased with this exposure. Rats and rabbits exposed to 2.5 ppm for 7 hours/day for 30 days or for 4 hours/day for 45 days, respectively, showed significant respiratory effects, including hemorrhagic alveoli and inflammatory infiltration of the alveolar spaces.

The single exposure concentration of 2,760 µg/m3 was identified as the LOAEL from the 1972 study of Paulet and Desbrousses and was adjusted (ADJ) from intermittent exposure to continuous exposure:


= 410 µg/m3



= ((0.17 m3/day) / 3,460 cm2) / ((20 m3/day) / 640,581 cm2)

= 1.57

where, MVa = minute ventilatory volume for experimental animal species,

MVh = minute ventilatory volume for humans,

Sa = surface area of the thoracic region for experimental animal species, and

Sh = surface area of the respiratory tract in humans.

The LOAELHEC would be calculated as follows:


= 410 µg/m3 × 1.57

= 640 µg/m3

An uncertainty factor (UF) of 1,000 (10 for the protection of sensitive human subpopulations, 3 for interspecies extrapolation, 3 for use of a subchronic


45

study, and 10 for the uncertainty in the use of a LOAEL) can be applied to the LOAELHEC from the study to obtain the chronic REL of 0.6 µg/m3:

REL = LOAELHEC / UF

= 640 µg/m3 / 1,000

= 0.6 µg/m3


The exposure guidelines were prepared for non-cancer-based endpoints. The non-cancer guidelines are based on the most sensitive adverse health effect report in the scientific literature and are designed to protect the most sensitive individuals in the population.

The State of California allows local options to address the possible economic impacts of emission control. It appears that the options are under local control and are based on local risk, socioeconomic analyses, and feedback from public workshops and hearings. The enforcement mechanism is via operating permits. Thus, the process is primarily directed towards site-specific evaluations and development of further regulatory tools rather than towards enforceable levels in themselves.


In the exposure modelling process, non-inhalation pathways should be considered for a number of substances (specified in Table III-5 in CAPCOA, 1993). Chlorine dioxide is not one of the substances requiring non-inhalation modelling.


No information.


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10.4 Agency-Specific Summary: Massachusetts


2. Agency: Massachusetts Department of Environmental Protection



4. Application:

“...The Division of Air Quality Control, which is responsible for implementing the Department’s air programs, plans to employ the AALs in the permitting, compliance, and enforcement components of the commonwealth’s air program in general, and the air toxics program in particular.” (MADEP, 1990, Volume 1, p. ix). The Massachusetts Department of Environmental Protection (MADEP) is responsible for developing, among other environmental programs, the air toxics program, the primary objective of which is to protect human health. The limits generated by the program are “health-based only and were developed without regard to production volume, exposure level, or regulatory implication. Similarly, economic and control technology issues are neither discussed nor considered here.” (MADEP, 1990, Volume 1, p. 4). Thus, the ambient air levels developed in this process are not to be considered as legally enforceable air standards; rather, they should be employed as guidelines in the development of subsequent regulatory action which does not contain a broad consideration of all relevant concerns. Thus, the ambient air levels developed in this process are not to be considered as legally-enforceable air standards; rather, they should be employed as guidelines in the development of subsequent regulatory action.


No information.

Key Reference(s):

Not applicable.


No information.



47

Not applicable.


Not applicable.


Not applicable.


Not applicable.


No information.


48

10.5 Agency-Specific Summary: Michigan


2. Agency: Michigan Department of Environmental Quality (MDEQ)


MDEQ has adopted 0.2 µg/m3 for its 24-hour initial threshold screening level (ITSL).

4. Application:

The screening levels are health-based screening levels for non-carcinogenic effects under Michigan’s air toxic rules. These values are only used as a tool for the evaluation of ambient air impacts from new or modified air emission sources when a permit is requested. These values are not considered as general ambient air quality levels nor are they considered standards. The air toxics rules require that each source must apply the best available control technology for toxics (T-BACT) and the maximum ambient concentration of each toxic air contaminant cannot exceed its screening level. Some exceptions to the T-BACT requirement include processes emitting small amounts of low potency carcinogens or non-carcinogens that have relatively low toxicity.


MDEQ. 1998. Addendum: 97-033EQ. Air pollution control rules. Part 2. Air use approval. R 336.1224 to R 336.1232 and R 336.1299. Effective date: November 10, 1998. Michigan Department of Environmental Quality (MDEQ), Air Quality Division, Lansing, MI.

MDEQ. 1999. List of screening levels (ITSL, IRSL and SRSL). Verification date: July 6, 1999. Michigan Department of Environmental Quality (MDEQ), Air Quality Division, Lansing, MI.

US EPA. 1995. Chlorine dioxide. Oral RfD assessment last revised January 1994. Inhalation RfC assessment last revised November 1990. Carcinogenicity assessment last revised November 1995. Integrated Risk Information System (IRIS) on-line database. United States Environmental Protection Agency (US EPA), Cincinnati, OH. URL: http://www.epa.gov/iris/subst/index.html

Key Reference(s):


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Paulet, G., and Desbrousses, S. 1970. [Effect of a weak concentration of chlorine dioxide on laboratory animals.] Arch Mal Prof Med Trav Secur Soc 31(3):97-106.

Paulet, G., and Desbrousses, S. 1972. Toxicology of chlorine dioxide. Arch Mal Prof Med Trav Secur Soc 33(1-2):59-61. Cited In: US EPA, 1995.


No information.


Current. An updated list of screening levels that have been revised or newly established is produces every two months while a complete list of all screening levels is published at the beginning of each year.


The IRIS RfC of 0.2 µg/m3 was adopted as the 24-hour ITSL


These considerations are performed separately by the permitting section. No other specific information is available for this chemical assessment.


No information.


No information.


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10.6 Agency-Specific Summary: North Carolina


2. Agency: Department of Environment and Natural Resources



4. Application:

This acceptable ambient air level is a product of initial recommendations by the Scientific Advisory Board (SAB) from which averaging times are assigned by the staff of the Toxics Protection Branch. These toxic air pollutant values are considered guidelines only and apply to all facilities that emit a toxic air pollutant that are required to have a permit under 15A NCAC 2Q.0700 of North Carolina Air Quality Rules. A facility shall not emit any toxic air pollutant under North Carolina Air Quality Rules in such quantities that may cause or contribute beyond the premises (adjacent property boundary) to any significant ambient air concentration that may adversely affect human health (NC DEHR, 1999).


No information.

Key Reference(s):

Not applicable.


Not applicable.


No information.


Not applicable.



51

Not applicable.


No information.


No information.


52

10.7 Agency-Specific Summary: World Health Organization (WHO)


2. Agency: World Health Organization - Protection of the Human Environment (WHO-PHE) World Health Organization - Europe (WHO-Europe)



4. Application:

Two separate documents have or will be established. The European publication consists of the WHO Air Quality Guidelines for Europe (2000) and the WHO-UEH will contain globally-applicable air quality guidelines.


WHO. 1994a. Methodology and format for updating and revising the air quality guidelines for Europe. Report on a WHO Working Group. Bilthoven, Netherlands, 20-22 September 1993. EUR/ICP/CEH 230/A Rev.1.

WHO. 1994b. Update and revision of the air quality guidelines for Europe. Report on a WHO Planning Meeting. Bilthoven, Netherlands, 11-13 January 1993. EUR/ICP.CEH 230.

WHO. 1996. Updating and revision of the air quality guidelines for Europe. Report on a WHO Working Group on Volatile Organic Compounds. Brussels, Belgium, 2-6 October 1995.

WHO. 2000. Air quality guidelines for Europe. World Health Organization (WHO), Regional Office for Europe, Copenhagen. WHO regional publications.

Key Reference(s):

Not applicable.


Not applicable.



53

Not applicable.


Not applicable.


Not applicable.


Not applicable.


Not applicable.


54

11.0 Acronyms, Abbreviations, and Definitions

AAL Allowable Ambient Level (Massachusetts) or Acceptable Ambient Level (North Carolina)

AAQC Ambient Air Quality Criteria - used by the Ontario Ministry of the Environment to define the potential for causing an adverse effect

AAS Ambient Air Standard (Louisiana)

ACGIH American Conference of Governmental Industrial Hygienists - a non-governmental organization which establishes occupational safety exposure limits for workers

AGC Annual Guideline Concentration (New York State)

ATSDR Agency for Toxic Substances and Disease Registry - an agency of the US Department of Health and Human Services

BMC05 Benchmark Concentration - a statistical lower confidence limit (5%) on the dose producing a predetermined, altered response for an effect

bw body weight

CAPCOA California Air Pollution Control Officers Association

CAS Chemical Abstracts Service - ascribes a unique, identification (registry) number to each chemical to help clarify multiple listings for the same chemical structure

CCME Canadian Council of Ministers of the Environment

CEIL Ceiling Value - used by ACGIH for the concentration that shall not be exceeded during any part of the working exposure

CEPA Canadian Environmental Protection Act

DEC Department of Environmental Conservation - Department in state agency of New York

DEL Department of Environment and Labour - Department in provincial agency of Newfoundland


55

DENR Department of Environment and Natural Resources - Department in state agency of North Carolina

DEP Department of Environmental Protection - Department in state agencies of Massachusetts, New Jersey, and Florida

DEQ Department of Environmental Quality - Department in state agencies of Michigan and Louisiana

ENEV Estimated No-Effects Value - similar to a NOAEL, it is used by CCME for derivation of environmental quality guidelines

ESL Effects Screening Level (Texas)

GLC Ground Level Concentration - the concentration of contaminant predicted by dispersion modelling

HEAST Health Effects Assessment Summary Tables - prepared by US EPA’s Office of Health and Environmental Assessment. HEAST contains risk assessment information on chemicals that have undergone reviews, although generally not as extensive as the reviews conduced under IRIS

HEC Human Equivalent Concentration

IARC International Agency for Research on Cancer

IHRV Inhalation Risk Value - used by Minnesota for carcinogens

IRIS Integrated Risk Information System - a database published by the US EPA containing risk assessment information on a wide range of chemicals

IRSL Initial Risk Screening Level - a limit corresponding to a one in a million lifetime risk of cancer used by Michigan for screening new sources of emissions

ITSL Initial Threshold Screening Level - similar to the IRSL, however, derived from the RfC for non-carcinogens

LC50 Median Lethal Concentration - the concentration of a substance in the medium (e.g., air, water, soil) to which a test species is exposed, that will kill 50% of the population of that given species


56

LD50 Median Lethal Dose - the dose of a substance given to a test species, that will kill 50% of the population of that given species

LOAEL Lowest-Observed-Adverse-Effect Level

LOEC Lowest-Observed-Effect Concentration

LOEL Lowest-Observed-Effect Level

MAC Maximum Acceptable Concentration

MACT Maximum Achievable Control Technology

MAGLC Maximum Acceptable Ground-Level Concentration (Ohio)

MOEE Ontario Ministry of the Environment and Energy - as known between 1993 and 1997, which is now known as OMOE or Ontario Ministry of the Environment

MRL Minimal Risk Level - a term used by ATSDR, which defines a daily exposure (either from an inhalation or oral route) not likely to induce adverse non-carcinogenic effects within a given time period, i.e., acute, intermediate, or chronic

NAAQS National Ambient Air Quality Standards (US EPA)

NIEHS National Institute of Environmental Health Sciences (USA)

NIOSH National Institute for Occupational Safety and Health (an agency of the US Department of Health and Human Services)

NOAEL No-Observed-Adverse-Effect Level

NOEC No-Observed-Effect Concentration

NOEL No-Observed-Effect Level

NPRI National Pollutant Release Inventory

NTP National Toxicology Program (USA)

OEHHA Office of Environmental Health Hazard Assessment (California EPA)

OEL Occupational Exposure Limit


57

OSHA Occupational Safety and Health Association - a branch of the US Department of Labour

PEL Permissible Exposure Limit (OSHA air standard)

POI Point of Impingement - used in conjunction with dispersion modelling to define the area in which the maximum ground level concentration (GLC) of a contaminant is predicted to occur

RD50 Median Respiration Rate Decrease - the dose at which respiration rate is decreased 50%

REL Either Reference Exposure Limit as used by the California EPA which defines the concentration at or below which no adverse health effects are expected in the general population or Recommended Exposure Limit used by both NIOSH and ATSDR

RfC Reference Concentration - an estimate of a daily inhalation exposure not likely to induce adverse health effects during a lifetime

RfD Reference Dose - an estimate of a daily exposure to the human population that is likely to be without appreciable risk of deleterious non-cancer effects during a lifetime

RGDR Regional Gas Dose Ratio (US EPA)

RTECS Registry of Toxic Effects of Chemical Substances - database maintained by NIOSH

SGC Short-term Guideline Concentration (New York State)

SRSL Secondary Risk Screening Level - a limit corresponding to one in one-hundred-thousand lifetime risk of cancer used by Michigan for screening new sources of emissions

STEL Short-term Exposure Limit

T-BACT Best Available Control Technology for Toxics

TC Tolerable Concentration - used by Health Canada to define the airborne concentration to which a person can be exposed for a lifetime without deleterious effects (for non-carcinogens)


58

TC01 Tumorigenic Concentration - the concentration of a contaminant in air generally associated with a 1% increase in incidence or mortality due to tumours

TC05 Tumorigenic Concentration - the concentration of a contaminant in air generally associated with a 5% increase in incidence or mortality due to tumours

TD05 Tumorigenic Dose - the total intake of a contaminant generally associated with a 5% increase in incidence or mortality due to tumours

TEL Threshold Effects Exposure Level (Massachusetts)

TLV Threshold Limit Value - an exposure concentration that should not induce an adverse effect in a work environment

TWA Time-Weighted-Average - allowable exposure averaged over an 8-hour workday or 40-hour work week

UF Uncertainty Factor

US EPA United States Environmental Protection Agency

WHO World Health Organization

ppm parts per million

ppb parts per billion

m3 cubic metres

mg a milligram, one thousandth of a gram

μg a microgram, one millionth of a gram

ng a nanogram, one billionth of a gram