ontario air standards for total reduced sulphur

Ontario Air Standard

For

Total Reduced Sulphur

June 2007

Standards Development Branch Ontario Ministry of the Environment

Ontario

Ontario Air Standards for Total Reduced Sulphur

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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. Total reduced sulphur 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 1977. 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 total reduced sulphur 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 total reduced sulphur. 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 total reduced sulphur.

Total reduced sulphur (TRS) is a mixture of reduced sulphur compounds, primarily composed of hydrogen sulphide (H2S), mercaptans (typically represented by methyl mercaptan), dimethyl sulphide (DMS), and dimethyl disulphide (DMDS). Hydrogen sulphide and methyl mercaptan are both colourless gases, with strong and unpleasant odour. Dimethyl sulphide and DMDS are colourless liquids, with strong unpleasant sulphur odours.

Hydrogen sulphide is used as an analytical reagent and an intermediate in the production of other reduced sulphur compounds, sulphuric acid, and in the precipitation of sulphides from metals. Other uses are as agricultural disinfectants, metallurgical applications, and large quantities of H2S are used in the production of heavy water, for use in nuclear power reactors. Hydrogen sulphide is also a by-product of various natural and industrial processes, including microbial degradation, the refining of oil and petroleum, and in the kraft process of producing wood pulp.


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Methyl mercaptan has been used as an odourant for natural gas, as an intermediate in the production of pesticides and jet fuel, and in the synthesis of methionine and plastics. It is produced as a by-product of the degradation of organic matter, and various industrial processes, including the kraft pulping process. Dimethyl sulphide is used as an intermediate in the synthesis of dimethyl sulphoxide, as a catalyst preactivator, as a gas odourant, and as a solvent for anhydrous mineral salts. Dimethyl disulphide is used as a sulphating agent for certain industrial catalysts and also as a food flavouring agent. Both DMS and DMDS are found in food products, and form as by-products of various industrial processes.

The National Pollutant Release Inventory (NPRI) did not require reporting on TRS or its components, except for hydrogen sulphide, prior to 2005. In 2005, Environment Canada started to report releases of TRS from Ontario facilities on the NPRI. Since 2000, industries have been required to report releases of hydrogen sulphide in Canada. The available data from the NPRI (2000 - 2005) indicate that the levels of hydrogen sulphide releases increased from 2000 to 2002 then declined back to the 2000 level. There was a significant increase of almost 40% in the national releases of hydrogen sulphide between 2000 and 2001, with an even greater increase observed in Ontario (260%). Ontario’s contribution to the national air releases of hydrogen sulphide had increased significantly being at 26% and 51% for 2000 and 2001, respectively. Since then, Ontario’s releases of hydrogen sulphide constituted approximately 20 - 30% of the national total releases. The hydrogen sulphide released in Ontario could be attributed mainly to activities from the pulp and paper industry. Environment Canada has summarized air emissions data of hydrogen sulphide submitted to the NPRI and TRS data submitted to MOE under O.Reg. 127/01. It was noted that in Ontario, approximately 60% of the reported TRS released were comprised of hydrogen sulphide and the rest was from other TRS compounds. Approximately 74% of the TRS were from the Pulp, Paper and Paperboard Mills sector and 25% were from the Iron and Steel Mills and Ferro-alloy Manufacturing sector. The findings of 60% of the Ontario TRS were comprised of hydrogen sulphide were consistent with those in the U.S.A where 65% of TRS were comprised of hydrogen sulphide.

In the last decade, a number of epidemiological studies have reported on the effects of exposure to TRS. The results of these studies suggest that exposure to TRS exhibits similar targets for adverse effects as that observed with exposure to H2S (e.g., irritation, respiratory and CNS effects). Before additional data concerning the adverse effects of exposure to TRS mixtures becomes available, the dose-response relationship of individual TRS compounds may be used to characterize the effects of exposure to TRS mixtures. With a lack of toxicological


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data for the TRS mixture and for the majority of the TRS compounds (i.e. methyl mercaptan, DMS, DMDS), H2S may provide an appropriate surrogate for the toxicological assessment and in the development of air quality standards for TRS.

Acute exposure to H2S has been reported in many occupational studies to cause irritation (eye, nose, respiratory tract) and CNS effects. Exposure to high concentrations has led to loss of consciousness (348 mg/m3) and even death (>1390 mg/m3), due to effects on the respiratory centre of the brain. Acute exposures to much lower concentrations (7-278 mg/m3) of H2S have been reported to cause dose-dependent increases in irritation to the eyes and mucous membranes. Asthmatics acutely exposed (15-30 minutes) to low levels (3-14 mg/m3) of H2S have been noted to experience bronchial constriction, while healthy volunteers exhibited a decrease in oxygen uptake in the blood, but only with exposure to 14 mg/m3. Studies examining acute effects with exposure to 7 mg/m3 of H2S reported a shift in metabolism in muscle from aerobic to anaerobic.

Chronic low-level exposures to individuals close to sources of H2S have remained a focus of recent research, with some epidemiological studies reporting an association between exposure and respiratory effects. However, the quality of the available toxicological data concerning chronic low-level exposures is poor as many of the studies have inadequately characterized the exposure and have small sample sizes.

The World Health Organization (WHO) updated its air guideline for H2S in 2000; however, no reassessment was performed. The WHO’s guideline of 150 µg/m3 was developed in 1987 based on data from the 1982 study of Savolainen that reported eye irritation in exposed workers. Since the 1982 report of Savolainen, a number of studies have reported effects at H2S concentrations below the LOAEL of 15 mg/m3 in the Savolainen study.

In view of the poor data quality of the available human studies, animal data have been used to derive air quality guidelines. The U.S. Environmental Protection Agency (U.S. EPA) derived its chronic inhalation Reference Concentration (RfC) of 2 µg/m3 based on lesions in the olfactory mucosa of rats. The California Environmental Protection Agency (CalEPA) developed its chronic inhalation Reference Exposure Level (REL) of 10 µg/m3 based on inflammation of the nasal mucosa in mice. The data used by the U.S. EPA and the CalEPA would appear to present the most scientifically relevant evidence for deriving a health-based guideline, as the two studies identify adverse health effects similar to those observed in humans in response to exposure to H2S.


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At present, health-based guidelines have been derived to protect communities from the risk of chronic exposure to H2S. Total reduced sulphur and its components of reduced sulphur compounds are malodorous compounds and hence the potential for adverse odour effects for these compounds is an important consideration in the development of air quality standards. In many cases, the reported odour threshold values for the individual TRS compounds fall below the concentrations of these compounds that may result in adverse health effects. In the development of odour-based air standards for TRS, the issue of simultaneous exposure to multiple odorous sulphidic compounds, each of which may have a range of reported odour thresholds, has also been addressed.

The Ministry of the Environment has reviewed and considered air quality guidelines and standards used by leading agencies worldwide. After reviewing additional toxicological and odour property information and considering stakeholder comments the Ministry has developed effects-based standards and odour-based air standards and guidelines for TRS and its component compounds.

Considering the stakeholders’ comments and the vast health database for hydrogen sulphide, a surrogate compound approach is the most appropriate method to develop health-based air standards for TRS. Hydrogen sulphide is determined to be the surrogate in view of the toxicology and the Ontario air release data from various sectors.

In terms of the health effects of hydrogen sulphide, the Ministry has considered that the poor data quality of available epidemiological studies does not provide sufficient confidence for air standards derivation. The endpoint of nasal lesions observed in the key animal studies, determined by the U.S. EPA and the CalEPA to derive their respective jurisdictional guidelines for H2S, is considered a consistent adverse effect in exposure to low doses of this reduced sulphur compound. The key study (Brenneman et al., 2000) determined by the U.S. EPA is considered to provide a more reliable basis than that of the CalEPA since a more recent study of quality was used and a low NOAEL of 13.9 mg/m3 for olfactory lesions was identified.

The U.S. EPA has derived an RfC of 2 µg/m3. However, the Ministry considers that the uncertainty factor of 10, employed by the U.S. EPA, for the extrapolation from the subchronic to chronic exposure is excessive. The Ministry is in agreement with many jurisdictions that an uncertainty factor of 3 (101/2) for the extrapolation of subchronic to chronic exposure is sufficient. Therefore, after adjustments to the identified NOAEL of 13.9 mg/m3, for continuous exposure and conversion to a human equivalent concentration (HEC), a total uncertainty factor of 100 is applied to the NOAELHEC of 0.64 mg/m3 to yield a criterion (after


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rounding) of 7 µg/m3. This value of 7 µg/m3 becomes the recommended 24-hour AAQC for H2S.

Summary of Recommended Air Standards and Guidelines

Several standards and guidelines have been developed for TRS and its compounds. As noted above, because of the extensive toxicological data base for hydrogen sulphide, this compound is being used as the surrogate for the TRS health-based standards. Two sectoral TRS standards are developed, based on the composition of hydrogen sulphide in the TRS emissions. For the other common TRS compounds (i.e., DMS, DMDS and mercaptans), due to insufficient health effects data for a quantitative analysis, no health-based standards have been developed.

For the highly offensively odourous substances, odour standards (i.e., for TRS, H2S and methyl mercaptan) or guidelines (i.e. for DMS and DMDS), have also been developed. Odour thresholds of the most prominent (i.e.,H2S) and the most odourous (i.e., methyl mercaptan) species in TRS mixtures provide the primary basis for the TRS odour standards. Half-hour standards have been derived from odour-based limits (i.e., from 10 minute average odour-based limits), rather than derived from chronic health effect-based limits (i.e., from 24-hour average health-based limits), because the odour-based derivation yielded slightly lower values for standards, and therefore, are considered to be protective for both health and odour effects.

As noted above, inhalation studies in animals, identifying adverse effects on the respiratory system, including toxicological effects on the nasal and olfactory mucosa, are considered to be the most appropriate basis for air quality standards development for H2S.

Based on an evaluation of the scientific rationale of air guidelines from leading jurisdictions, an examination of current toxicological research and odour information and, comments from stakeholders, the Ministry has derived the following air quality standards for hydrogen sulphide:

• A 24-hour average Ambient Air Quality Criterion (AAQC) of 7 µg/m3 (micrograms per cubic metre of air) for hydrogen sulphide based on the adverse effects on the respiratory system (nasal lesions) of this compound;

• A 10-minute average AAQC of 13 µg/m3 (micrograms per cubic metre of air) for hydrogen sulphide based on odour effects; and


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• A half-hour standard of 10 µg/m3 (micrograms per cubic metre of air) for hydrogen sulphide based on both odour and health effects of this compound.

Also based on current toxicological review on the properties of hydrogen sulphide, odour information, composition of hydrogen sulphide in TRS emissions from various industrial sectors and, comments from stakeholders, the Ministry has derived the following air quality standards for Total Reduced Sulphur (TRS):

For the Pulp and Paper sector:

• A 24-hour average AAQC of 14 µg/m3 (micrograms per cubic metre of air) for TRS based on the adverse effects on the respiratory system (nasal lesions) of this mixture;

• A 10-minute average AAQC of 13 µg/m3 (micrograms per cubic metre of air) for TRS based on odour effects; and

• A half-hour standard of 10 µg/m3 (micrograms per cubic metre of air) for TRS based on both odour and health effects of this mixture.

For all other sectors (including sectors such as Iron & Steel; Petroleum Refineries, Municipal Sewage Treatment Plants):

• A 24-hour average AAQC of 7 µg/m3 (micrograms per cubic metre of air) for TRS based on the adverse effects on the respiratory system of this mixture;

• A 10-minute average AAQC of 13 µg/m3 (micrograms per cubic metre of air) for TRS based on odour effects; and


Also, based on an evaluation of the scientific rationale of air guidelines from leading jurisdictions, an examination of current toxicological research and odour information and, comments from stakeholders, the Ministry has derived the following air quality standard for mercaptans (as methyl mercaptan):

• A 10-minute AAQC of 13 µg/m3 (micrograms per cubic metre of air) for mercaptans (as methyl mercaptan) based on odour effects; and


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• A half-hour standard of 10 µg/m3 (micrograms per cubic metre of air) for mercaptans (as methyl mercaptan) based on odour effects.

In addition, based on an evaluation of the scientific rationale of air guidelines from leading jurisdictions, an examination of current toxicological research and odour information and, comments from stakeholders, the Ministry has derived the following air quality guidelines for DMS and DMDS:

• A 10-minute AAQC of 30 µg/m3 (micrograms per cubic metre of air) for DMS based on odour effects; and

• A 10-minute AAQC of 56 µg/m3 (micrograms per cubic metre of air) for DMDS based on odour effects.

Notes to TRS standards:

• Any facility releasing only one specific species of the four major components of TRS will not be considered for the release of TRS; rather the respective standard or guideline for this specific species will apply.

• For any facility releasing a mixture (i.e., more than one species of the four major components of TRS), the TRS standard will apply and the standards and guidelines of the components of TRS will not.

• More information on the application of odour-based standards is set out in O. Reg. 419/05.

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 (except for the 10 minute odour-based AAQCs for DMS and DMDS) will be incorporated into Schedule 3 of O. Reg. 419/05; the half-hour standards 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 the above standards are 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:


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• “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).

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...............................................................................................ix

Listing of Tables ...............................................................................................xii 1.0 Introduction ..............................................................................................1

2.0 General Information .................................................................................3 2.1 Physical and Chemical Properties of TRS Compounds..........................3 2.2 Uses of TRS Compounds .......................................................................7 2.3 Sources and Levels of TRS Compounds................................................8 2.4 Environmental Fate of TRS Compounds ..............................................10 2.4.1 H2S 10

2.4.2 Methyl Mercaptan .................................................................................10

2.4.3 DMS and DMDS ...................................................................................11

3.0 Toxicology of TRS Compounds............................................................13 3.1 Acute Toxicity .......................................................................................13 3.2 Subchronic and Chronic Toxicity of TRS ..............................................13 3.2.1 Effects in Humans ................................................................................13

3.2.2 Effects on Animals................................................................................15 3.3 Developmental and Reproductive Toxicity............................................15 3.4 Genotoxicity..........................................................................................15 3.5 Carcinogenicity .....................................................................................15 3.6 Toxicology of H2S .................................................................................15 3.6.1 Mode of Toxicity ...................................................................................16

3.6.2 Acute Toxicity .......................................................................................16

3.6.3 Subchronic and Chronic Toxicity of H2S ...............................................19

3.6.4 Developmental and Reproductive Toxicity............................................23

3.6.5 Genotoxicity..........................................................................................24

3.6.6 Carcinogenicity .....................................................................................24 3.7 Toxicology of Methyl Mercaptan ...........................................................25 3.7.1 Acute Toxicity .......................................................................................26

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3.7.2 Subchronic and Chronic Toxicity ..........................................................26


3.7.4 Genotoxicity..........................................................................................27

3.7.5 Carcinogenicity .....................................................................................27 3.8 Toxicology of DMS and DMDS .............................................................27 3.8.1 Acute Toxicity .......................................................................................28

3.8.2 Subchronic and Chronic Toxicity ..........................................................28


3.8.4 Genotoxicity..........................................................................................28

3.8.5 Carcinogenicity .....................................................................................29 3.9 Environmental Effects...........................................................................29 3.9.1 Vegetation ............................................................................................29

3.9.2 Terrestrial and Aquatic Wildlife .............................................................29

4.0 Review of Existing Air Quality Criteria .................................................31 4.1 Overview...............................................................................................31 4.1.1 Overview of TRS Guidelines.................................................................39

4.1.2 Overview of H2S Guidelines .................................................................39

4.1.3 Overview of Methyl Mercaptan Guidelines ...........................................40

4.1.4 Overview of DMS and DMDS Guidelines .............................................41 4.2 Evaluation of Existing Criteria...............................................................41

5.0 Responses of Stakeholders to the Information Draft .........................47

6.0 Responses of Stakeholders to the Rationale Document ....................48

7.0 Considerations for the Development of an Ambient Air Quality Criterion for Total Reduced Sulphur ...............................................................52

8.0 Decision ..................................................................................................54

9.0 References..............................................................................................62

10.0 Appendix A: Agency-Specific Reviews of Air Quality Guidelines ....79 10.1 Agency-Specific Summary: Government of Canada ............................79 10.2 Agency-Specific Summary: Federal Government of the United States 81 10.3 Agency-Specific Summary: State of California .....................................85 10.4 Agency-Specific Summary: Commonwealth of Massachusetts ...........89 10.5 Agency-Specific Summary: State of Michigan .....................................94 10.6 Agency-Specific Summary: State of North Carolina ............................96


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10.7 Agency-Specific Summary: State of Texas.........................................100 10.8 Agency-Specific Summary: World Health Organization (WHO).........102

11.0 Appendix B: Acronyms, Abbreviation, and Definitions....................104

12.0 Appendix C: Summary of Toxicity Data .............................................108 12.1 Toxicity Data for Total Reduced Sulphur (TRS)..................................108 12.2 Toxicity Data for Hydrogen Sulphide (H2S).........................................112 12.3 Toxicity Data for Methyl Mercaptan ....................................................136 12.4 Toxicity Data for Dimethyl Sulphide (DMS).........................................139 12.5 Toxicity Data for Dimethyl Disulphide (DMDS) ...................................140

13.0 Appendix D: Relevant Toxicity Data For H2S.....................................141

14.0 Appendix E: References (Appendicies C & D)...................................157


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L isting of Tables

Table 1: Physical and Chemical Properties of H2S ...............................................4

Table 2: Physical and Chemical Properties for Methyl Mercaptan........................5

Table 3: Physical and Chemical Properties for DMS ............................................6

Table 4: Physical and Chemical Properties for DMDS..........................................7

Table 5: Summary of Existing Air Quality Guidelines1 for TRS and/or TRS Compounds ............................................................................................32

Table 6: Summary of Accepted Odour Detection Thresholds of TRS................46

Table 7: Air Releases of TRS and H2S in Ontario ..............................................57

Table C. 1: Summary of Subchronic/Chronic Toxicity Data for TRS.................108

Table C. 2: Summary of Acute Toxicity Data for Hydrogen Sulphide (H2S) ......112

Table C. 3: Summary of Short-Term Toxicity Data for Hydrogen Sulphide (H2S).............................................................................................................122

Table C. 4: Summary of Sub-Chronic/Chronic (Non-Cancer) Toxicity Data for H2S ......................................................................................................124

Table C. 5: Summary of Reproductive and Developmental Toxicity Data for H2S.............................................................................................................131

Table C. 6: Summary of Acute Toxicity Data for Methyl Mercaptan..................136

Table C. 7: Summary of Short-Term Toxicity Data for Methyl Mercaptan.........137

Table C. 8: Summary Sub-Chronic/Chronic (Non-Cancer) Toxicity Data for Methyl Mercaptan.................................................................................138

Table C. 9: Summary of Acute Toxicity Data for DMS ......................................139

Table C.10: Summary of Acute Toxicity Data for DMDS...................................140


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Table D. 1: Human Acute Lethality Data...........................................................141

Table D. 2: Human Non-lethal Toxicity Case reports ........................................144

Table D. 3: Epidemiological Studies .................................................................147

Table D. 4: Human Experimental Studies .........................................................149

Table D. 5: Animal Mortality Studies .................................................................151

Table D. 6: Animal Non-Lethal Studies .............................................................154


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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, 2005a). 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.

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

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


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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)

Total reduced sulphur 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 2006a) 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 total reduced sulphur. 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 of TRS Compounds

Total reduced sulphur (TRS) refers to compounds containing sulphur in its reduced state. Total reduced sulphur is a mixture of reduced sulphur compounds, primarily composed of hydrogen sulphide (H2S), mercaptans (typically represented by methyl mercaptan), dimethyl sulphide (DMS), and dimethyl disulphide (DMDS). Other reduced sulphur compounds may include substances such as carbon disulphide, carbonly sulphide, thioesters or alkyl sulphides and are less common, and differ in chemical and physical properties (NPRI, 2006). For the purpose of discussions in this document, total reduced sulphur will be defined as a mixture of two or more of the following: hydrogen sulphide, methyl mercaptan, dimethyl sulphide and dimethyl disulphide. Each substance is discussed separately within this section, as each has distinct physical and chemical properties. Summaries of the physical and chemical properties of H2S, methyl mercaptan, DMS and DMDS are provided in Table 1, Table 2, Table 3 and Table 4, respectively.

Hydrogen sulphide is described as a colourless gas, with a strong, unpleasant “rotten egg” odour (Collins and Lewis, 2000; IPCS, 1981). Hydrogen sulphide is soluble in water, alcohol, ether, glycerol, and in solutions of amines, alkali carbonates, bicarbonates, and hydrosulphides (IPCS, 1981). The odour threshold values range from 1.6 µg/m3 (0.001 ppm) to 270 µg/m3 (0.19 ppm) (AIHA, 1989; Devos et al., 1990, Nagy, 1991). A geometric mean value of 16.1 µg/m3 can be calculated.

Methyl mercaptan is a colourless gas, with a strong unpleasant “rotten cabbage” odour. It is soluble in water, alcohol, ether, petroleum and naptha (ATSDR, 1992). The odour threshold values range from 2 µg/m3 (0.001 ppm) to 81 µg/m3 (0.041 ppm) (AIHA, 1989; Devos et al., 1990, Nagy, 1991). A geometric mean value of 11 µg/m3 (0.0056 ppm) can be calculated.

Dimethyl sulphide is a colourless liquid, with a strong unpleasant sulphur odour. It is soluble in water, alcohol and ether (HSDB, 2004b). The odour threshold for DMS ranges from 6 µg/m3 (0.0023 ppm) to 88 µg/m3 (0.034 ppm) (HSDB, 2004b; Devos, 1990, Nagy, 1991). A geometric mean value of 30 µg/m3 (0.0116 ppm) can be calculated.

Dimethyl disulphide is also a colourless liquid, and is insoluble in water, and soluble in both alcohol and ether (HSDB, 2004c, Devos et al., 1990). The available odour thresholds for DMDS are 48 and 66 µg/m3 (Devos et al., 1990; Nagy, 1991). An arithmatic mean value of 57 µg/m3 can be calculated.


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Table 1: Physical and Chemical Properties of H2S

CAS # 7783–06-4

RTECS # MX1225000

UN # 1053

Conversion Factors 1 ppm = 1.39 mg/m3, 1 mg/m3 = 0.7 ppm

Melting Point -85.5°C

Boiling Point -60.4°C

Flash Point -82.4°C

Water Solubility 1 g/187 mL at 10°C, 1 g/242 mL at 20°C

Log Kow -1.38 (calculated)

Chemical Formula H2S

Molecular Weight 34.08

Vapour Density (air=1) 1.19

Vapour Pressure 18.75 x 105 Pa at 20°C, 23.9 x 105 Pa at 30°C

Common Synonyms Sulphur Hydride, Sulphuretted Hydrogen, Stink Damp

Sources: ARB, 1997; HSDB, 2004a; Lewis, 1992; Windholz, 1976


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Table 2: Physical and Chemical Properties for Methyl Mercaptan

CAS # 74-93-1

RTECS # PB4375000

UN # 1064

Conversion Factors 1 ppm= 1.96 mg/m3, 1 mg/m3= 0.509 ppm

Melting Point -123°C

Boiling Point 6°C

Henry’s Law Constant 3.85 x 10-3 atm-m3/mol

Flash Point -17.78°C, open cup

Water Solubility 23.3 g/L at 20°C, 15.4 g/L at 25°C

Log Kow 0.78 (calculated)

Chemical Formula CH4S



Vapour Pressure 1520 mm Hg at 26.1°C

Common Synonyms Mercaptomethane, Methanethiol, Thiomethyl alcohol, Thiomethanol

Sources: HSDB, 2004d; Lewis, 1992


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Table 3: Physical and Chemical Properties for DMS

CAS # 75-18-3

RTECS # PV5075000

UN # 1164

Conversion Factors 1 ppm = 2.58 mg/m3, 1 mg/m3 = 0.39 ppm

Melting Point -98.3°C

Boiling Point 37.3°C

Henry’s Law Constant 1.61 x 10-3 atm-m3/mol

Flash Point -16°C

Water Solubility 22 g/L at 25°C

Log Kow 0.92

Chemical Formula C2H6S



Vapour Pressure 502 mm Hg at 25°C

Common Synonyms Dimethylmonosulphide, Dimethyl thioether, Methyl monosulphide, Methane thiomethane

Sources: HSDB, 2004b; Lewis, 1992; Windholz., 1976


7

Table 4: Physical and Chemical Properties for DMDS

CAS # 624-92-0

RTECS # JOI927500

UN # 2381

Conversion Factors 1 ppm= 3.84 mg/m3, 1 mg/m3= 0.26 ppm

Melting Point -85°C

Boiling Point 109.8°C

Henry’s Law Constant 1.21 x 10-3atm-m3/mol

Flash Point 24°C

Water Solubility Insoluble

Log Kow 1.77

Chemical Formula C2H6S2



Vapour Pressure 28.6 mm Hg at 25°C

Common Synonyms Methyl disulphide, Methyldithiomethane

Sources: HSDB, 2004c; Lewis, 1992

2.2 Uses of TRS Compounds

Hydrogen sulphide is used as an analytical reagent and intermediate in the production of other reduced sulphur compounds, sulphuric acid, and in the precipitation of sulphides from metals. Other uses are as agricultural disinfectants, for metallurgical applications, and large quantities of H2S are used in the production of heavy water, for use in nuclear power reactors (ATSDR, 1999; Collins and Lewis, 2000; IPCS, 1981).

Methyl mercaptan has been used as a gas odourant for natural gas, as an intermediate in the production of pesticides and jet fuel, and the synthesis of methionine and plastics (ACGIH, 2001b; ATSDR, 1992). Methyl mercaptan has also been used in the synthesis of flavours and food adjuvants (HSDB, 2004d).

Dimethyl sulphide is used as an intermediate in the synthesis of dimethyl sulphoxide, as a catalyst preactivator, as a gas odourant, and as a solvent for anhydrous mineral salts (HSDB, 2004b).


8

2.3

Dimethyl disulphide is used as a sulphating agent for certain industrial catalysts (HSDB, 2004c). DMDS is also permitted by the U.S. Food and Drug Administration for direct use on food as a flavouring agent (HSDB, 2004c).

Sources and Levels of TRS Compounds

Information relating to the source and concentration of TRS mixtures was very limited. Alternatively, information for the primary components of TRS mixtures has been summarised.

Hydrogen sulphide occurs naturally in volcanic gases, and may be produced from the degradation of plant and animal protein or the direct reduction of sulphate by bacteria or fungi (HSDB, 2004a; IPCS, 1981). It can be formed whenever elemental sulphur or sulphur-containing substances are in contact with organic materials at high temperatures (IPCS, 1981). Industrially, H2S is produced as a by-product from desulphurisation processes in oil and gas industries, rayon production, sewage treatment, leather tanning, and some power plants (Collins and Lewis, 2000). Hydrogen sulphide may also be generated by the production of coke from sulphur-containing coal, the refining of crude oil, and in the Kraft process of producing wood pulp (HSDB, 2004a).

In Canada, 10% of total atmospheric emissions of H2S are anthropogenic in origin (CCME, 1992). Hydrogen sulphide has been detected at levels between 0.07 and 53 mg/m3 in Finnish wastewater treatment plants, and at 0 to 28 mg/m3 in Finnish Kraft and sulphite mills (Nordic Expert Group, 2001).

Until 2005, the National Pollutant Release Inventory (NPRI) did not require reporting on TRS or its components, except for hydrogen sulphide. In 2005, Environment Canada started to report annual emission of TRS from industries in Ontario (Environment Canada, 2005). Since 2000, industries have been required to report releases of hydrogen sulphide in Canada. The available data from the NPRI (2000, 2001, 2002, 2003, 2004, and 2005) indicate that the levels of hydrogen sulphide releases are increasing. National air release amounts for 2000, 2001, 2002, 2003, 2004, and 2005 were 3332, 4599, 5210, 4907, 4295, and 3215 tonnes, respectively. The increase from 2000 to 2001 resulted in a 40% increase in the national releases of hydrogen sulphide. Since 2002, releases of H2S have been declining. Similarly, the on-site releases to the air in Ontario had increased significantly between 2000 and 2001. In 2000, releases of 883 tonnes were reported. In 2001, 2356 tonnes were booked. Since 2001, steady decreases in the release of hydrogen sulphide were noticeable. The air releases of H2S in 2002, 2003, 2004, and 2005 were 1615, 1377, 862, and 776 tonnes, respectively. Approximately, 20 to 31 percent of the national releases were contributed by industries in Ontario, except for the year of 2001, half (51%) of the national releases was from Ontario. In Ontario, a majority of the hydrogen sulphide releases were attributed to activities from the pulp and paper industry.

Under the Ontario Regulation 127/01, industries are required to report annual emissions of TRS and related compounds. In 2003, there were a total of 1,594


9

tonnes of TRS released in Ontario, as reported under O. Reg. 127/01 and 1,357 tonnes of hydrogen sulphide released. In Ontario, 85% of the total TRS releases were comprised of hydrogen sulphide and 15% as the other TRS compounds (e.g. methyl mercaptans, DMS and DMDS). However, if only Ontario facilities that reported both H2S and TRS were analysed, a total of 1,461 and 873 tonnes of TRS and H2S, respectively, were released from three major sectors including the Pulp, Paper and Paperboard Mills (NIACS 3221; 496 tonnes), the Iron and Steel Mills and Ferro-Alloy Manufacturing (NAICS 3311; 355 tonnes) and the Petroleum and related operations (NAICS 3241; 22 tonnes). Approximately 74% of the TRS were from the Pulp, Paper and Paperboard Mills sector and 25% were from the Iron and Steel Mills and Ferro-alloy Manufacturing sector. For releases of these three sectors, releases of H2S from the Pulp, Paper & Paperboard Mills contributed to approximately 46% of the TRS releases from this sector. For the other two industrial sectors, almost all (>96%) of the TRS releases were comprised of H2S. Thus, for these three major sectors, 60% of the released TRS were comprised of H2S. This observation that 60% of the TRS released from the major industrial sector in Ontario were comprised of hydrogen sulphide was consistent with that in the U.S.A where 65% of TRS were comprised of hydrogen sulphide. (Environment Canada, 2006).

Methyl mercaptan is naturally present in animal tissues, certain foods, and is also produced from decaying organic matter (HSDB, 2004d). It is also produced commercially by methanol condensation with H2S (ATSDR, 1992). Methyl mercaptan is also a by-product of kraft pulp mills and oil refineries, and is a component of coal tar, petroleum distillates and sour gas. It has been detected in the air of sulphite pulp mills at levels ranging from 0 up to 29.4 mg/m3 (15 ppm) (HSDB, 2004d).

Dimethyl sulphide is produced in the natural environment by organisms, particularly marine organisms (HSDB, 2004b). It is found in crude oil, natural gas and emissions from some types of vegetation. Dimethyl sulphide has been detected in effluent from kraft paper mills, petroleum refineries, sewage treatment plants, fish processing plants, leather manufacturing plants, sulphur dioxide scrubbing and starch manufacturing plants (HSDB, 2004b). Levels of DMS found in different occupational settings including, Kraft pulp mills and sewage treatment, were found to range from <129 µg/m3 (<0.05 ppm) to 508,300 µg/m3 (197 ppm) (HSDB, 2004b). Dimethyl sulphide is also found in foods such as Beaufort cheese, fresh strawberries, mutton, chicken, beef, pork and dried legumes (Dirinck et al., 1984; Dumont and Adda, 1978; Shahidi et al., 1986). It is also formed in some food items (e.g., beer) during fermentation of yeast and occurs in natural unrefined peppermint oil used in flavouring of chewing gum and mouthwash (Reed, 1984; Rogers, 1981).

Dimethyl disulphide is released naturally by soil, plants, microbes, and animal wastes. Other sources of DMDS include effluent from wastewater treatment plants, fish processing plants, starch and whiskey manufacturing plants, pulp mills, sulphur dioxide scrubbing operations and gasoline combustion (HSDB, 2004c). Levels of DMDS found in different occupational settings including, kraft pulp mills and sewage treatment, were found to range from <192 µg/m3 (<0.05 ppm) up to 5,760 µg/m3 (1.5 ppm) (HSDB, 2004c). Dimethyl disulphide also plays a predominant role in the natural flavour of vegetables including onions, garlic, peas, cabbage, rutabaga,


10

2.4

potato, sprouts, cauliflower and tomato (Furia and Bellanca, 1975). It has also been identified in oysters and roasted peanuts (Furia and Bellanca, 1975).

Environmental Fate of TRS Compounds

2.4.1 H2S

When released to the atmosphere, H2S exists as a vapour with residence time affected by ambient temperatures, humidity, sunlight and the presence of other pollutants (HSDB, 2004a). Hydrogen sulphide disperses, and can remain in the atmosphere from one day to over forty days, depending upon seasonal and atmospheric conditions (ATSDR, 1999; HSDB, 2004a). Hydrogen sulphide does not undergo photolysis or photochemical reaction with oxygen but, it is transformed by oxidation through reaction with hydroxyl radicals to form sulfhydryl radical (·SH), and eventually sulphur dioxide and sulphate compounds (HSDB, 2004a). The sulphate compounds are then removed from the atmosphere by plant absorption, soil adsorption or through precipitation (ATSDR, 1999).

Hydrogen sulphide in water will partition to air depending on several factors including temperature, humidity and pH (ATSDR, 1999). Volatilization of H2S is significantly influenced by increasing temperature and low pH (ATSDR, 1999). Ionization in water may occur depending upon pH, with the dominant form being H2S, under typical environmental conditions and the SH- radical with increasing pH (ATSDR, 1999).

Hydrogen sulphide may enter soil through atmospheric deposition and environmental release during manufacture, transport and storage of H2S. Hydrogen sulphide is water-soluble and as such, it easily migrates in moist soils and in aquatic environments (ATSDR, 1999; HSDB, 2004a). The presence of clay and organic matter may enhance the soil sorption of H2S (ATSDR, 1999; HSDB, 2004a). Hydrogen sulphide in soil and water may undergo microbial degradation by oxidation-reduction reactions, which oxidises H2S to elemental sulphur (HSDB, 2004a).

Hydrogen sulphide is not expected to bioconcentrate or biomagnify in the food chain (ATSDR, 1999; HSDB, 2004a).

2.4.2 Methyl Mercaptan

Methyl mercaptan in air is degraded by photochemical and nitrate radical reactions (ATSDR, 1992; HSDB, 2004d). In water, the primary fate process is volatilisation, with some oxidation and mineralisation occurring, depending on the pH and the presence of oxidants and metal catalysts in the water (HSDB, 2004d). Methyl mercaptan will adsorb to soil and may oxidise if it is released as vapour. Dilute solutions of methyl mercaptan in soil are less likely to adsorb to the same degree as the vapour form (HSDB, 2004d).

The predominant fate of atmospheric methyl mercaptan is through oxidization reactions with photochemically-generated hydroxyl radicals (half-life of 11.6 hrs) (HSDB, 2004d). Under photochemical smog conditions, the atmospheric loss is


11

much faster with a half-life of 2 hours (HSDB, 2004d). The photo-oxidative transformation of methyl mercaptan is catalysed by nitrogen oxides, yielding sulphur dioxide, nitric acid, formaldehyde, methyl nitrate, methanesulphonic acid, inorganic sulphate, DMDS, and nitric oxide (ATSDR, 1992).

Reactions with the nitrate radical (NO3) may be the dominant atmospheric degradation process for methyl mercaptan under certain conditions, with a calculated atmospheric lifetime of 1.2 hours for methyl mercaptan (ATSDR, 1992). This is less than the estimated atmospheric lifetime of 8.4 hours based on methyl mercaptan reaction with the hydroxyl radical (ATSDR, 1992).

Gaseous methyl mercaptan will adsorb to soil and may oxidise (HSDB, 2004d). Sorption capacities of 6 air-dried soil samples ranged from 2.4 to 3.1 mg methyl mercaptan per gram of soil (ATSDR, 1992). Methyl mercaptan may be degraded by methanogenic bacteria in soil, but limited information is available (ATSDR, 1992).

When present in water, methyl mercaptan will be lost through volatilisation (estimated half-life is 2 hours for volatilisation from a model river 1 m deep with a 1 m/s current and 3 m/s wind speed), the rate of which is dependent upon temperature, relative humidity, air currents, and the extent of mixing of the solution (ATSDR, 1992; HSDB, 2004d).

Bioconcentration in aquatic organisms is not considered to be significant based on a low estimated Bioconcentration Factor (BCF) of about 1 to 2 (ATSDR, 1992) and a low calculated octanol/water partition coefficient (Kow) of approximately 19 (log Kow 1.28).

Methyl mercaptan was rapidly mineralized when incubated in anaerobic lake sediments from Lake Mendota, Wisconsin for 4 hours (HSDB, 2004d). Addition of methyl mercaptan to sediment slurries from seven chemically different anoxic aquatic environments (including two estuarine salt marshes, a freshwater lake, and two hypersaline alkaline lakes) stimulated methane production without any noticeable lag (HSDB, 2004d).

2.4.3 DMS and DMDS

Dimethyl sulphide and DMDS are expected to exist primarily as vapours in the atmosphere due to their high vapour pressures at 25ºC (HSDB, 2004b and 2002c). In air, DMS and DMDS are degraded by photochemically produced hydroxyl and nitrate radical reactions (HSDB, 2004b and 2004c). Based on their high Henry’s Law Constants, volatilisation is expected to be the primary route of removal from water and soil (HSDB, 2004b and 2004c). Dimethyl sulphide and DMDS are not expected to bind to sediment or solids in water to any significant degree based on their low estimated organic carbon partitioning coefficients (Koc) values (HSDB, 2004b and 2004c). The potential for DMS and DMDS to bioconcentrate in aquatic organisms is low, based on their low estimated bioconcentration factors (HSDB, 2004b and 2004c).


12

Dimethyl sulphide and DMDS vapours in the atmosphere are degraded primarily through photochemical reactions (HSDB, 2004b and 2004c). Atmospheric degradation of DMS occurs by reaction with hydroxyl radicals (estimated half-life of 3.5 days), reaction with atomic oxygen (estimated half-life of 6.2 days); and reaction with NO3 radicals (estimated half-life of several hours or less) (HSDB, 2004b). Atmospheric degradation of DMDS is primarily by photochemical reactions with hydroxyl radicals (estimated half-life of 4 hours), direct photolysis (estimated half-life of 3.2 to 4.6 hours at full sunlight), and reaction with NO3 radicals (estimated half-life of 1.1 hour at night) (HSDB, 2004c).

When released in soil, DMS and DMDS are expected to be mobile in soil, based on their low estimated Koc of 75 and 220 for DMS and DMDS, respectively (HSDB, 2004b and 2004c). Dimethyl sulphide and DMDS loss through volatilisation is anticipated to be significant given their high Henry’s Law Constants (1.61 x 10-3 atm-m3/mole and 1.21 x 10-3 atm-m3/mole for DMS and DMDS, respectively) and vapour pressure (502 mm Hg and 28.6 mm Hg at 25ºC for DMS and DMDS, respectively) (HSDB, 2004b; 2004c). Dimethyl disulphide loss in soil through photolysis is also anticipated to be a major fate mechanism as DMDS absorbs UV light in the environmental spectrum and has been shown to photolyse rapidly (in gas phase) in sunlight. Although photolysis rates in soil have not been measured, the surface half-life (for full sunlight exposure) are likely similar to the several hour half-life observed in the gas phase (HSDB, 2004c).

When released in water, DMS and DMDS will be lost through volatilisation (HSDB, 2004b; 2004c). Estimated volatilisation half-lives for DMS in a model river and model lake are 3 hours and 3 days, respectively (HSDB, 2004b). For DMDS, estimated volatilisation half-lives for a model river and model lake are 3 hours and 4 days, respectively (HSDB, 2004c). Photodegradation of DMDS is also expected to be a major fate process in near-surface waters as DMDS absorbs UV light in the environmental spectrum and has been shown to photolyse rapidly (in gas phase) in sunlight. Although photolysis rates in water have not been measured, the near-surface half-life (for full sunlight exposure) may be similar to the several hour half-life observed in the gas phase (HSDB, 2004c). Based on low estimated organic carbon partitioning coefficients (Koc) of 75 and 220 for DMS and DMDS, respectively, both sulphide organics are not expected to adsorb to suspended solids and sediment in water (HSDB, 2004b; 2004c).

Bioconcentration in aquatic organisms is not considered to be significant for either DMS or DMDS based on low estimated BCFs of 3 and 13, respectively, and low calculated log Kow values of 0.92 and 1.77, respectively.


13

3.0 Toxicology of TRS Compounds

There are limited studies available that examine the health effects of exposure to TRS as a mixture. However, numerous studies are available which are focussed on the health effects associated with individual constituents of the TRS mixture, primarily H2S. Hydrogen sulphide is the most extensively studied of the TRS compounds because H2S is a leading cause of sudden death in the workplace according to the National Institute for Occupational Safety and Health (NIOSH) (1977). A summary of available toxicology information for TRS and its constituents is provided below.

3.1

3.2

Acute Toxicity

No acute studies following inhalation exposure to TRS were identified in humans and/or animals.

Subchronic and Chronic Toxicity of TRS

3.2.1 Effects in Humans

There are limited subchronic and chronic toxicity studies of TRS identified that focused on the health effects in humans. These studies are described below and summarized in, Table C. 1 (page 106). There are no subchronic and chronic toxicity studies of TRS identified for animals.

Excess mortality from cardiovascular disease and coronary heart disease was observed in Finnish sulphate mill workers exposed to TRS (Jappinen and Tola, 1990). The study involved male workers (4179 person years) employed at the plant for at least 1 year between 1945 and 1961 that were potentially exposed to H2S levels between 0 and 28 mg/m3 (0 and 20 ppm). Methyl mercaptan concentrations varied from 0 to 29 mg/m3 (0 to 15 ppm) and the highest levels of DMS and DMDS were 31 mg/m3 (12 ppm) and 6 mg/m3 (1.5 ppm), respectively (Kangas et al., 1984).

There are three Finnish community studies described below that were part of the South Karelia air pollution study. All three studies found higher occurrence of eye and respiratory symptoms, nasal symptoms, cough, headaches or migraines in the exposed populations when compared to reference or unexposed populations (Marttilla et al., 1995; Marttilla et al., 1994; Partti-Pellinen et al., 1996).

An epidemiologic study to examine the association of respiratory symptoms in children and long-term exposure to a mixture of H2S, methyl mercaptan and methyl sulphides from pulp mills (which used a sulphate method) were conducted in three communities in south eastern Finland (Marttilla et al., 1994). Two of the communities were in close proximity to pulp mills, while the third community was considered to be unimpacted by the pulp mills and served as a reference population. The parents of 134 children living in a severely polluted (n=42), moderately polluted (n=62) and rural


14

non-polluted (n=30) community responded to a cross-sectional, self-administered questionnaire that focussed on occurrence of eye and respiratory symptoms, and headache or migraine in children on the previous 4 weeks and 12 months. The study questionnaire had an overall response rate of 83%. The annual mean concentrations for H2S and methyl mercaptan were reported as 1 to 8 µg/m3 (0.7 to 6 ppb) and <1 to 5 µg/m3 (<0.5 to 3 ppb), respectively. The study findings indicated higher occurrence, but not statistically significant increase, of eye and nasal symptoms, cough and headache among children for both the 4-week and the 12-month intervals. The study concluded that the long-term exposure to relatively small concentrations of malodourous sulphur compounds may increase eye irritation and respiratory symptoms in children (Marttilla et al., 1994).

The relationship between daily exposures to TRS from pulp production and the intensity of health effects (i.e., eye, respiratory and CNS symptoms) was examined in a small industrial town located in southeast Finland (Marttilla et al., 1995). TRS, sulphur dioxide (SO2), nitrogen oxides (NOx), and total suspended particles (TSP) were monitored daily during a 15-month period from September 1988 to November 1989. Daily mean TRS concentrations varied from 0 to 82 µg/m3, and monthly mean concentrations varied from 3 to 19 µg/m3. Eighty-one (81) participants responded to a baseline survey that was carried out in October 1988 during a low exposure. These participants (n=81) were included in a study cohort that involved five (5) follow-up questionnaires that were carried out, immediately after a day(s) of exposure (81% response rate). The exposure day(s) is classified into three different categories based on the measured daily mean TRS concentrations in the ambient air: reference (<10 µg/m3), medium exposure (10 to 30 µg/m3), and high exposure (> 30 µg/m3). The questionnaire focused on the occurrence of eye and respiratory symptoms, headaches and nausea. The study found a dose-related increase in the intensity of eye and respiratory symptoms, and headaches for medium (10 to 30 µg/m3) and high (> 30 µg/m3) exposures to TRS (Marttilla et al., 1995).

Another population study was conducted to assess the eye irritation, respiratory tract and CNS symptoms in adults associated with low-level exposure to TRS in a small pulp and paper mill town in central Finland (Partti-Pellinen et al., 1996). Two communities were studied; one exposed population within 1 km from the pulp and paper mill, and one unexposed community. Air monitoring data were collected during March and December 1992. The mean annual TRS concentrations in the exposed community were 2 to 3 µg/m3, the 24-hour average concentrations varied between 0 to 56 µg/m3, and the maximum 1-hour concentration was 155 µg/m3. Questionnaires were randomly distributed to the exposed community (n=336) and to the reference community (n=380), and focused on the occurrence of eye and respiratory symptoms, headache or migraine during the previous 4 weeks and 12 months. The study findings indicated increased occurrence of cough, respiratory infections, and headaches for both the 4-week and the 12-month intervals in the exposed community. A strong association was observed between exposure to low-level TRS and higher occurrence of headaches in the exposed populations for the preceding 4-week and the 12-month intervals. Also, the study found a strong association between low-level TRS exposure and higher occurrence of coughs in the exposed populations for the preceding 12-month interval.


15

3.3

3.4

3.5

3.6

3.2.2 Effects on Animals

There is currently no information available on effects of TRS in animals.

Developmental and Reproductive Toxicity

No studies of developmental and reproductive toxicity following inhalation exposure to TRS were identified in humans and/or animals.

Genotoxicity

No studies of genotoxicity following inhalation exposure to TRS were identified in humans and/or animals.

Carcinogenicity

No studies of carcinogenicity following inhalation exposure to TRS were identified in humans and/or animals.

Toxicology of H2S

Case reports of accidental deaths from acute occupational exposures indicate that H2S can be readily absorbed through the lungs. This observation is supported by experimental studies that found that H2S can be absorbed through the skin, respiratory and digestive tract lining, with the respiratory tract being the primary site of absorption (Booth, 1982; Sullivan, 1992). Skin absorption appears to be minimal, however, exposure to pure H2S gas over large areas of the skin was lethal in guinea pigs after a 45-minute exposure period (Beauchamp et al., 1984;Deng, 1992).

Following absorption into the blood, H2S partly dissociates into HS- anion, while some remains as free H2S. Hydrogen sulphide is distributed to the brain, liver, kidneys, pancreas, and small intestine (Deng, 1992; Voigt and Muller, 1955).

Metabolism of H2S occurs by oxidation to sulphate, methylation, and reaction with metallo- or disulphide-containing proteins (Beauchamp, 1984). The major metabolic or detoxification pathway is the oxidation of sulphide to sulphate (Ammann, 1986).

Urinary excretion as free sulphate or conjugated sulphate is the predominant elimination pathway (Deng, 1992; Savolainen, 1982). Measurable amounts of thiosulphate have been found in the urine of men after exposure to an 8-hour Time-Weighted Average (TWA) concentration of <14 mg/m3 (<10 ppm ) H2S (Kangas and Savolainen, 1987).


16

3.6.1 Mode of Toxicity

Hydrogen sulphide inhibits metalloenzyme activity, such as cytochrome oxidase, causing cellular hypoxia (Collins and Lewis, 2000; Dorman et al., 2000; Dorman et al., 2002; Nicholson et al., 1998; Roth and Skrajny, 1997). Cytochrome oxidase is the critical enzyme of the mitochondrial respiratory chain, where it transfers electrons and hydrogen ions to oxygen to form water. If cytochrome oxidase inhibition occurs, or oxygen is lacking as the final electron acceptor, the electron transport down the chain is stopped. In that case, oxidative metabolism, which is the primary energy source for mammalian cells, ceases leading to membrane leakage, edema, release of cellular enzymes, and disturbance in ionic gradients (Nicholson et al., 1998).

There are studies that suggest that H2S toxicity may not result from a single biochemical interaction, but rather from complex interactions with a number of different enzyme systems, supporting the concept that H2S is a broad-spectrum toxicant (Nicholson et al., 1998; Roth and Skrajny, 1997).

3.6.2 Acute Toxicity

Appendix C, Table C. 2 (page 112) and Table C. 3 (page122) present a partial summary of the acute and short-term toxicity data for humans and experimental animals, respectively. In addition, the Massachusetts Department of Environmental Protection (MADEP, 2001) summarized relevant reviewed toxicity data for humans and experimental animals. The MADEP summary tables are included in Appendix D.

Effects in Humans

There are numerous reports of accidental deaths from acute exposures to H2S, primarily in occupational settings (ATSDR, 1999; HSDB, 2004a; Nordic Expert Group, 2001; U.S. EPA, 2004; WHO, 2000).

Accidental exposures to high concentrations of H2S (greater than 1,000 ppm or 1,390 mg/m3) for very brief periods have been reported to directly affect the respiratory centre, causing respiratory paralysis, cessation of autonomous breathing, and death (ACGIH, 1991; Arnold et al., 1985; Beauchamp et al., 1984; Mehlman, 1994; Milby, 1962).

Acute exposure to H2S directly affects the respiratory centre and leads to reversible unconsciousness; this can occur so rapidly that it is called a “knockdown” (Guidotti, 1996; Hessel and Melenka, 1999; Milby et al., 1999; Struve et al., 2001). Levels estimated at 348 mg/m3 (250 ppm) resulted in unconsciousness in three workers after several minutes of exposure (McDonald and McIntosh, 1951). Workers who experienced a knockdown were more likely to report shortness of breath and wheezing with chest tightness. These symptoms may indicate that these workers are at higher risk of developing reactive airways dysfunction syndrome (Hessel and Melenka, 1999; Milby et al., 1999). Low-level acute exposures to H2S cause irritation throughout the entire respiratory tract, resulting in rhinitis, pharyngitis, laryngitis, bronchitis, and pneumonia (Sullivan et al., 1992). Cough, sore throat, hoarseness, runny nose, and chest tightness are the most common symptoms and signs of H2S


17

exposures between 70 mg/m3 (50 ppm) and 348 mg/m3 (250 ppm) (Sullivan et al., 1992).

Acute exposures to H2S concentrations between 695 mg/m3 (500 ppm) and 1,390 mg/m3 (1000 ppm) are life threatening following exposures of 30 minutes or longer (NIOSH, 1977). Symptoms and signs associated with acute intoxication include sudden fatigue, headache, dizziness, intense anxiety, loss of olfactory function, nausea, abrupt loss of consciousness, disturbances of the optic nerves, hypertension, insomnia, mental disturbances, pulmonary edema, coma, convulsions, and respiratory arrest, followed by cardiac failure (Burnett et al. 1977; Frank, 1986; Thoman, 1969).

Hydrogen sulphide is a potent eye and mucous membrane irritant. The H2S concentrations at which eye irritation occurred (exposure duration not specified) and the severity of the effects observed varied from 7 mg/m3 (5 ppm) to 278 mg/m3 (200 ppm) (HSDB, 2004a; Nordic Expert Group, 2001; U.S. EPA, 2002; WHO, 2000). However, irritant effects of H2S at exposure levels below 28 mg/m3 (20 ppm) are not well documented (Nordic Expert Group, 2001).

An acute study was conducted to assess the effects of low concentrations of H2S on respiratory function (Jappinen et al., 1990). The study involved 7 women (mean age 44.1 years, range 31 to 61 years) and 3 men (mean age 40.7 years, range 33 to 50 years) with bronchial asthma. The asthmatic subjects were exposed for 30 minutes to H2S concentration of 2.8 mg/m3 (2 ppm) and the airway resistance, specific airway conductance and ventilatory capacity were measured. Three of the 10 asthmatic subjects complained of headaches. In addition, on average the airway resistance increased and the specific airway conductance decreased, although, these changes were not statistically significant.

There is limited research in humans on health effects associated with low-level exposures to H2S (Bhambani, 1999; Nordic Expert Group, 2001; Roth et al., 1995). The limited available data provides no evidence of pulmonary function effects in healthy men and women following inhalation of 2.8 to 14 mg/m3 (2 to 10 ppm) of H2S for 15 to 30 minutes; although some asthmatics may experience bronchial constrictions following exposure to 2.8 mg/m3 (2 ppm) H2S for 30 minutes (Bhambani, 1999). In healthy volunteers, exposure to14 mg/m3 (10 ppm) for 15 minutes during submaximal exercise revealed no significant changes in routine pulmonary function variables (Bhambani et al., 1996b). Studies examining the acute effects of 7 mg/m3 (5 ppm) and 14mg/m3 (10 ppm) H2S exposure on physiological responses during exercise demonstrated no significant cardiovascular or metabolic responses (Bhambani et al., 1996a; Bhambani, 1999; Nordic Expert Group, 2001). The only effect observed was a tendency for muscle lactate to increase and citrate synthase activity to decrease, which is an effect not observed at 2.8 mg/m3 (2 ppm) (Bhambani et al., 1991). In another study, it was also observed that inhalation of 14 mg/m3 (10 ppm) H2S reduced oxygen uptake in the blood during exercise, most likely by inhibiting the aerobic capacity of the exercising muscle (Bhambani, 1999; Bhambani et al., 1997; Nordic Expert Group, 2001). Common symptoms associated with H2S exposure, such as headaches, nausea, eye and throat irritation, were not observed in the above noted studies. This was presumed to be due to the mode of administration


18

(via oral inhalation using a close bag system), which prevented nasal and ocular exposure to the gas (Bhambani, 1999). However, in 1964, residents at Terre Haute, Indiana exposed to H2S at concentrations between 0.022 – 0.125 ppm (0.03 – 0.174 µg/m3) for seven consecutive hours had been described to report odour complaints, nausea, vomiting, diarrhoea, abdominal cramps, shortness of breath, choking, coughing, sore throat, chest pain, headache, burning eyes, fainting, awakening at night, loss of sleep, acute asthma attacks, anorexia and weight loss (MOL, 1978).

Exposure to high concentrations of H2S (duration not specified) causes paralysis of olfactory nerves which leads to loss of sense of smell or ‘olfactory fatigue’ (HSDB, 2004a). Olfactory fatigue is noted as H2S concentrations approach 139 mg/m3 (100 ppm) (HSDB, 2004a). At these levels, the gas disrupts cellular respiration and may cause profound respiratory depression as well as cardiac dysrhythmias (HSDB, 2004a).

The CNS is one of the principal targets of H2S and neurological effects, such as lethargy, fatigue and memory loss, have been observed following acute exposures to H2S (Roth and Skrajny, 1997). The neurobehavioral effects associated with acute exposures (in minutes to hours) to H2S were compared in 11 healthy subjects, 2 years to 6 years following exposure (ATSDR, 1999; HSDB, 2004a; Kilburn, 1997). Neurophysiological symptoms and frequencies, described as percent predicted adjusted for age, sex, educational achievement, and other factors, was compared with those in an unexposed population. Frequencies were elevated for 31 of 33 symptoms. Symptoms included impaired balance, prolonged simple choice reaction times, decreased visual field performance, abnormal colour discrimination, decreased hearing, cognitive disability, reduced perceptual motor speed, impaired verbal recall and remote memory, and abnormal mood status (ATSDR, 1999; HSDB, 2004a; Kilburn, 1997).

Effects in Animals

Short-term exposure of animals to high concentrations of H2S may result in lethality. Median Lethal Concentrations (LC50's) observed in acute inhalation studies of varying duration in various animal species ranged from 24 mg/m3 (17 ppm) to 1,500 mg/m3 (1,050 ppm) (see Appendix C, Table C. 2).

Health effects observed in laboratory animals are consistent with those in humans. Acute H2S intoxication in rhesus monkeys resulted in brain edema, degeneration and necrosis of the cerebral cortex and the basal ganglia (Savolainen, 1982). Exposure to a H2S concentration of 150 mg/m3 (107 ppm) for 2 hours resulted in inhibition of brain protein synthesis in mice within 48 hours, with the effect being normalized within 72 hours (Savolainen, 1982). It has been reported that the cerebral biochemical effects caused by repeated acute subclinical H2S intoxications are cumulative in mice (Savolainen, 1982).

Ocular and mucous membrane irritation appeared after 1 hour with exposure to 278 - 417 mg/m3 (200 to 300 ppm) of H2S. Exposure to 70 to 139 mg/m3 (50 to 100 ppm) of H2S for several hours or days produced reversible irritation of the corneal epithelium in dogs, cats, rabbits and guinea pigs (Grant, 1986). Studies on several


19

experimental animals indicated that exposure to H2S concentrations of 139 to 209 mg/m3 (100 to 150 ppm) for several hours produced local irritation of the eyes and the throat (Nordic Expert Group, 2001).

Another study of local effects in rats showed that a 4-hour H2S exposure at >280 mg/m3 (> 200 ppm) induced detectable histologic lesions in the nasal cavity (Lopez et al., 1988). Nasal lesions are the most sensitive endpoint identified to date in animal studies (Dorman et al., 2002). Studies in laboratory rats indicated extensive loss of olfactory neurons and basal cell hyperplasia following single exposures to H2S concentrations of 42 to 556 mg/m3 (30 ppm to 400 ppm) (Dorman et al., 2002). Localised lesions in the olfactory mucosa were observed following H2S exposures of 112 mg/m3 (80 ppm) or higher (Dorman et al., 2002). In addition, studies indicated that the distribution of nasal lesions in rats was influenced by the duration of exposure (Dorman et al., 2002; Moulin et al., 2002). A single 3-hour exposure to H2S at 112 mg/m3 (80 ppm) or higher resulted in olfactory lesions that were localised in the olfactory mucosa, whereas repeated 5-day exposures to 112 mg/m3 (80 ppm) H2S or higher resulted in lesions that were more extensive and involved approximately 70% of the rat nasal olfactory mucosa (Dorman et al., 2002).

Similar health effects reported in humans are also observed in the canary, cat, dog, goat, guinea pig, rabbit and rat following H2S exposure: at 150 to 225 mg/m3 (108 to 162 ppm), signs of local irritation of eyes and throat after many hours of exposure; at 300 to 400 mg/m3 (216 to 288 ppm), eye and mucous membrane irritation in 1 hour and slight general effects with longer exposure; at 750 to 1,000 mg/m3 (540 to 719 ppm), slight systemic symptoms in less than 1 hour and possible death after several hours; at 1,350 mg/m3 (971 ppm), grave systemic effects within 30 minutes and death in less than 1 hour; at 2250 mg/m3 (1,619 ppm), collapse and death within 15 to 30 minutes; and at 2,700 mg/m3 (1,942 ppm), immediate collapse, respiratory paralysis and death (WHO, 2000).

3.6.3 Subchronic and Chronic Toxicity of H2S

Effects in Humans

Limited information is available on the mortality of humans following chronic H2S exposure (ATSDR, 1999). There is also limited information on adverse health effects from chronic, low-level exposures (Legator et al., 2001). While several epidemiological and occupational studies indicate that exposure to hydrogen sulphide results in adverse effects, the characterization of the exposure and the resulting effects have been reported subjectively in many cases or not reported at all. Therefore, determining a valid dose-response relationship with respect to hydrogen sulphide exposure has been difficult. Appendix C, Table C. 4 summarizes the subchronic/chronic toxicity data for humans and experimental animals. Appendix D, Tables 2, 3, and 6 summarize toxicity data for humans and animals (MADEP, 2001).

Workers in sour gas plants who were exposed for prolonged periods (exposure duration not specified) to what was described as “relatively low concentrations” of H2S experienced “gas eye” or keratoconjunctivitis, a superficial inflammation of the cornea and conjunctiva (ACGIH, 2002a; Beauchamp, 1984; Nordic Expert Group,


20

2001; Reiffenstein, 1992). Symptoms include blepharospasm, tearing and photophobia (Guidotti, 1996). This inflammatory reaction can be accompanied by reversible chromatic distortion and visual disturbances. Exposure to H2S at concentrations in excess of 70 mg/m3 (50 ppm) causes eye irritation including initial lacrimation, and changes in visual acuity and perception (HSDB, 2004a; U.S. EPA, 2002). Prolonged exposure to H2S at concentrations in excess of 70 mg/m3 may result in inflammation and ulceration in the eyes, with the possibility of permanent scarring of the cornea in severe cases (HSDB, 2004a; U.S. EPA, 2002. Occupational exposures in viscose rayon workers resulted in eye irritation effects following 6 to 7 hours of exposure to 14 mg/m3 (10 ppm) H2S, or after 4 to 5 hours of exposure to 18 mg/m3 (13 ppm) H2S (Nesswetha, 1969). ). There were no reported eye irritation effects in workers at a heavy water plant exposed to H2S levels below 14 mg/m3 (10 ppm ) (Poda, 1966).

A common effect following prolonged H2S exposure is pulmonary edema at concentrations in the order of 348 to 834 mg/m3 (250 to 600 ppm) (ACGIH, 1991; Beliles and Beliles, 1993; Milby et al., 1999; WHO, 2000). Patients who survived loss of consciousness due to H2S poisoning often suffered from pulmonary edema (Milby et al., 1999; Schneider et al., 1998; Tvedt et al., 1991; Vuorela et al., 1987; Wasch et al., 1989). Post-mortem findings for 5 of 8 sewer workers who died of H2S intoxication included pulmonary edema, myocarditis, hemorrhagic gastric mucosa, and a greenish colour of the brain and the upper region of the intestine (Gregorakos et al., 1995).

Levels of carbon disulphide (CS2) and H2S were measured in a viscose rayon factory using stationary and personal monitoring equipment (Vanhoorne et al., 1991). Personal samples were collected gradually over 5 years. The background level of H2S in the factory was determined to be 9.8 mg/m3 (7 ppm). The average exposures for the different jobs within the plant ranged from 3 to 147 mg/m3 for CS2 and 0 to 9 mg/m3 for H2S. The study findings reported eye pain experienced by exposed workers in the viscose rayon industry but, the observed effects could have been due to simultaneous exposures to several chemicals also present in the factory including lead, sulphuric acid (H2SO4) (Vanhoorne et al., 1991).

The Pennsylvania Department of Health conducted a health survey at an elementary school in response to complaints about H2S odours believed to be associated with mushroom-composting operations in south eastern Pennsylvania (Logue et al., 2001). The survey assessed whether exposures to H2S were associated with an increased incidence of adverse health effects among students from the exposed school compared to students from the unexposed control school. Daily ambient air levels for H2S were collected and H2S concentrations ranged from 17 to 82 µg/m3 (12 to 59 ppb) in outdoor air, and <14 to 95 µg/m3 (<10 ppb to 68 ppb) in indoor air. Two surveys were conducted; one from April 20 through June 5, 1998 and the other survey from August 31 through October 30, 1998. Both surveys were carried out while school was in session. Questionnaires were distributed to students that focussed on H2S-related symptoms including eye, skin and throat irritation, tightness in the chest, asthma, cough, wheezing, dizziness, headache, nausea or vomiting, etc. No association was found between the H2S exposures experienced by the students and adverse health effects. As such, the authors concluded that the students


21

attending the elementary school near the mushroom-composting operations were not exposed to any significant public health hazard (Logue et al., 2001).

A panel study was conducted by the Agency for Toxic Substances and Disease Registry (ATSDR) to investigate whether odour and air pollutants emanating from the Fresh Kills Municipal Landfill, located on Staten Island, New York, were associated with respiratory health effects among residents diagnosed with asthma (ATSDR, 2000; White et al., 1999). The 6-week study period involved a group of 148 persons, aged 15 to 65 years, who had been diagnosed with asthma and who lived near the landfill. During the study period, participants were asked to complete a daily diary to record respiratory symptoms (wheeze, cough and shortness of breath) experienced and any changes in participant’s peak air flow (a measure in lung function) between morning and evening. In addition, ambient air measurements were taken in their residential area, with H2S, wind direction and odour selected as indicators of landfill emissions. During the study period, the 15-minute maximum for H2S per day ranged from < 2.8 µg/m3 (2 ppb) to 45.9 µg/m3 (33 ppb), averaging 9 µg/m3 (6.6 ppb). The study findings indicated that H2S concentrations were not related to either respiratory symptoms (e.g., wheeze) or lung function. However, there was a significant association between odour perception (as reported in daily diaries by study participants) and measures of respiratory symptoms, peak air flow and medication usage. This relationship was stronger among certain subgroups of participants, such as persons aged 30 to 49 years of age and persons who worked on Staten Island (White et al., 1999).

Health effects from chronic, low-level exposure to H2S were examined in two exposed communities in the U.S., located in close proximity to industrial sources of H2S; one in Odessa, Texas and the second in Puna, Hawaii (Legator et al., 2001). Symptoms of adverse respiratory and CNS effects that were reported in the two exposed communities were compared to three unexposed communities that were used as a reference. The H2S annual average concentrations in Odessa, Texas ranged from 3 to 40 µg/m3 (7 to 27 ppb), and the H2S concentrations in Puna, Hawaii ranged from 278 to 695 µg/m3 (200 to 500 ppb). The health survey results indicated a significant increase in the incidence of CNS symptoms (i.e., fatigue, restlessness, depression, short-term and long-term memory loss, balance, difficulty sleeping, anxiety, lethargy, headaches, dizziness, tremors and change in senses) in the exposed populations in comparison to the unexposed, reference populations. Also, the study reports a significant increase in the incidence of respiratory symptoms (i.e., wheezing, shortness of breath, persistent cough, bronchitis, pneumonia, lung disease) in the exposed populations compared to the unexposed, reference populations. When the two exposed communities were compared, 6 of the 14 CNS-related symptoms (long-term memory loss, lethargy, anxiety, balance, depression and fatigue) in the Puna, Hawaii community were significantly elevated from the Odessa, Texas community. The reason for this difference was not known. The author suggested that it may not be related to chemical exposures. The respiratory symptoms (i.e., wheezing, shortness of breath, persistent cough, and wheezing) were not significantly different when the two exposed communities were compared. The authors identified limitations of the health survey findings, the most significant being the susceptibility of the results to response enhancement bias (i.e., increase in


22

reported symptoms as a result of respondent awareness of, and sensitization to, the fact that they are exposed).

The neurobehavioral effects associated with chronic exposures to H2S were compared in 5 subjects with exposure durations of 11 to 22 years (Kilburn, 1997). These subjects were downwind of either a crude oil collection tank or H2S-emitting oil refineries. One subject worked in a sewage treatment plant and smelled H2S for 11 years. Neurophysiological symptoms and frequencies, described as percent predicted adjusted for age, sex, educational achievement and other factors were compared with those in an unexposed population. Frequencies were elevated for 31 of 33 symptoms including impaired balance, prolonged simple choice reaction times, decreased visual field performance, abnormal colour discrimination, decreased hearing, cognitive disability, reduced perceptual motor speed, impaired verbal recall and remote memory, and abnormal mood status (Kilburn, 1997). However, as exposure was not characterized in this study, no conclusions can be made concerning the concentration of H2S exposure and the observed adverse health effects.

Effects in Animals

A 90-day vapour inhalation toxicity study was conducted using B6C3F1 mice exposed to H2S vapour (CIIT, 1983a). Three groups of mice consisting of 10 males and 12 females were exposed to H2S at TWA concentrations of 14.1 mg/m3 (10.1 ppm), 42.5 mg/m3 (30.5 ppm), and 110 mg/m3 (80 ppm). A control group consisting of 10 males and 12 females were exposed to clean air. The duration of exposures was 6 hours/day, 5 days/week for 90 days. During the exposure period, the mice were examined twice daily for mortality and clinical signs. The mice were examined and weighed weekly. Prior to necropsy, the eyes were examined and an evaluation of neurological functions (posture, gait, facial muscle tone, and reflexes) was conducted. Urine and blood samples were collected from the mice and the following tissues and organs were examined during necropsy: external surfaces, orifices and organs, cranial cavity, carcass, brain, spinal cord, thoracic, pelvic and abdominal cavities and their viscera, cervical tissues and organs. At a H2S concentration of 110 mg/m3 (80 ppm), there was a significant depression of body weight gain in both sexes. Examination of the eyes revealed no abnormalities. Urine and blood data showed no significant differences in comparison to the controls. At necropsy, no gross lesions were identified that were attributed to exposure to H2S. However, as part of the histopathology study, an exposure-related lesion was identified in the high exposure group (110 mg/m3 or 80 ppm). The lesion was observed in 8/9 male and 7/9 female mice. The lesion was generally minimal to mild in severity and was located in the anterior portion of the nasal structures, primarily in the squamous portion of the nasal mucosa, but extended to areas covered by the respiratory epithelium. This lesion was not observed in any animals in other exposure groups. Therefore, for mice, 110 mg/m3 (80 ppm) is considered a Lowest-Observed Adverse Effect Level (LOAEL) for nasal inflammation, and 42.5 mg/m3 (30.5 ppm) is the No-Observed Adverse Effect Level (NOAEL) (CIIT, 1983a).


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In a similar, but more recent study by Brenneman et al. (2000), hydrogen sulphide was administered via inhalation to groups (12/dose) of 10-week old male CD rats at concentrations of 0, 13.9, 42 or 111 mg/m3 (0, 10, 30 or 80 ppm) H2S for 6 hours/day, 7 days/week for 10 weeks. After euthanisation, a histological evaluation of the nasal cavity was conducted to identify exposure-related lesions. Nasal lesions related to H2S exposure were limited to the olfactory mucosa and consisted of multifocal, bilaterally symmetrical olfactory neuron loss and basal cell hyperplasia affecting the lining of the dorsal medial meatus and the dorsal and medial regions of the ethmoid recess. Exposure-related effects to the olfactory mucosa were observed at 42 mg/m3 (30 ppm) and 111 mg/m3 (80 ppm), affecting approximately 50% and 70% of the species tested. Changes in the olfactory epithelium in the control group and the group exposed to 13.9 mg/m3 (10 ppm) were similar. Therefore, the authors concluded that the NOAEL for the observed olfactory lesions was 13.9 mg/m3 (10 ppm) (Brenneman et al., 2000). The U.S. EPA used the NOAEL of 13.9 mg/m3 (10 ppm) to derive their Reference Concentration (RfC) of 2 µg/m3.

3.6.4 Developmental and Reproductive Toxicity

Based on the limited information available in humans and laboratory animals, H2S does not appear to induce developmental effects (U.S. EPA, 2002). Appendix C, Table C. 5 (page 131) summarizes the available reproductive and developmental toxicity data for H2S.

Effects in Humans

Some evidence suggests that H2S exposure may be associated with an increase rate of spontaneous abortions (ATSDR, 1999). Increased risk of spontaneous abortions among women employed in rayon textile jobs and paper product jobs was noted in an industrial community in Finland. Increased rate of spontaneous abortions (p<0.1) was noted in all socioeconomic classes in areas where the mean annual level of H2S exceeded 4 µg/m3 (3 ppb). However, the difference was not statistically significant (Hemminki & Niemi, 1982).

Effects in Animals

Pregnant rats (n = 7-9) administered 0, 69.7, 139 or 209 mg/m3 H2S (0, 50, 100 or 150 ppm, respectively) for 6 hours/day during Gestational Days (GD) 6 to 20 experienced reduced maternal body weight gain at 209 mg/m3 (150 ppm) and reduced fetal body weight gain in all exposed groups (Saillenfait et al., 1989). In dams exposed to 139 or 209 mg/m3 (100 or 150 ppm), reduced absolute weight gain and increased implantations and live fetuses were observed. No maternal toxicity or adverse effects on the developing fetus were observed in a follow-up experiment whereby 20 pregnant female rats were exposed to 139 mg/m3 (100 ppm) H2S for 6 hours/day on GD6 to 20 (Saillenfait et al., 1989).

Female Sprague-Dawley rats and pups exposed to 27.9, 69.7 or 105 mg/m3 H2S (20, 50 or 75 ppm, respectively) for 7 hours/day from GD 1 to postnatal day 21 reported significantly elevated maternal blood glucose in all exposed groups at day 21


24

postpartum (Hayden et al., 1990a). No effects on blood glucose were noted in the offspring (Hayden et al., 1990a).

In another study by Hayden et al. (1990b), female Sprague-Dawley rats were exposed to 27.9, 69.7 or 105 mg/m3 of H2S (20, 50 or 75 ppm, respectively) from GD 6 to postnatal day 21. The study reported no observed effects in examining a number of developmental parameters including: gestation length, litter size, viability, pup body and organ weights, maternal weights, liver or brain content of protein, DNA or cholesterol. Increased delivery time was noted to be in a concentration-related manner, but differences in time of ear detachment and hair development was not (Hayden et al., 1990b).

Changes in several amino acids (aspartate, glutamate and taurine) were measured on postnatal days 7, 14 and 21 in rat pup cerebrum and cerebellum after exposure to 105 mg/m3 (75 ppm) H2S for 7 hours/day from GD 5 to postnatal day 21 (Hannah et al., 1989). Although changes in aspartate, glutamate and taurine were recorded, the adverse effect in brain levels of neurotransmitters is unclear. A follow-up study with a similar experimental design, reported maternal blood taurine levels were significantly increased on the day of parturition and on postnatal day 21 after exposure to 69.7 mg/m3 (50 ppm) H2S (Hannah et al., 1990).

Sprague-Dawley rats exposed to 0, 27.9, or 69.7 mg/m3 H2S (0, 20 or 50 ppm, respectively) for 7 hours/day, from GD 6 to postnatal day 21 reported significant effects on the number, symmetry and length of dendritic branches of cerebellar Purkinje cells at both dose levels (Hannah and Roth, 1991). The significance of these neuronal changes remains to be studied.

3.6.5 Genotoxicity

No studies of genotoxicity following inhalation exposure to H2S were identified in humans.

A negative result for mutagenicity was observed with H2S gas in Ames/salmonella assays using TA97, TA98, and TA100 strains, either with or without metabolic activation using S9 liver fractions from male Syrian golden hamsters or Sprague-Dawley rats that had been induced with 500 mg/kg Aroclor 1254 (U.S. EPA, 1984).

One study (Gocke et al., 1981) reported that H2S was a weak mutagen in Salmonella typhimurium TA1535 and that this response was abolished by the addition of an S9 microsomal fraction from the liver of Aroclor-pre-treated rats.

3.6.6 Carcinogenicity

Effects in Humans

A retrospective epidemiologic study evaluated the risk of cancer to known target organ systems for H2S toxicity in residents of Rotorua, New Zealand (Bates et al., 1998). The city of Rotorua uses geothermal energy for industrial and domestic heating purposes, and there were human health concerns related to H2S and


25

mercury exposures from geothermal sources. There were no H2S levels presented in the study but, the most reliable monitoring data available from the area taken in 1978 reported median H2S concentrations of 20 µg/m3, with 35% over 70 µg/m 3 and 10% over 400 µg/m 3 (Bates et al., 1997). Based on the cancer registry data, there was a significant increase risk of developing nasal cancer in Rotorua residents in comparison to the rest of the population of New Zealand. However, this conclusion was based only on the incidence of four cancers. Due to the higher percentage of Maori population in Rotorua compared to the rest of New Zealand, the authors examined their data stratified by ethnicity and sex, and found a significantly increased risk of cancers of the trachea, bronchus and lung among female Maoris in Rotorua compared to female Maoris in the rest of New Zealand. The authors concluded that there was a lack of exposure information related to smoking history between the two populations which did not permit findings of causal relationship between H2S and cancer incidence (Bates et al., 1998).

Effects in Animals

There are no studies on the possible carcinogenic effect of H2S identified in animals following inhalation exposure.

3.7 Toxicology of Methyl Mercaptan

There is limited toxicity information in humans and experimental animals following inhalation exposure to methyl mercaptan (ATSDR, 1992). Most studies of occupational exposure to methyl mercaptan in the pulp industry also involve exposure to other sulphur-containing compounds such as H2S, DMS, and sulphur dioxide as well as to methyl mercaptan (ATSDR, 1992). Appendix C, Tables A.6 through A.8 summarize the acute, short-term, and subchronic/chronic toxicity data for methyl mercaptan, respectively.

The toxicokinetics of methyl mercaptan following inhalation exposure has not been well studied. Adverse effects reported as hemolysis, methemoglobinemia, coma and death were noted following inhalation exposure by a 53-year old worker (Shults et al., 1970). A 15-minute exposure of rats to methyl mercaptan during an acute inhalation toxicity study resulted in the induction of comas in rats (Zieve et al., 1974). The results from these studies suggest that methyl mercaptan is well absorbed and distributed through the blood following inhalation exposure (ATSDR, 1992). Methanethiol binds to protein and erythrocyte and is subsequently metabolized by serving as a methyl, sulphur or methylthiol donor for the synthesis of amino acids and proteins. Non-metabolized free thiol is exhaled through the respiratory system along with the biosynthesized material and other gaseous products. When the level of methanethiol exceeds metabolizable capacity, it binds to protein and erythrocytes and indirectly decreases vascular oxygen-carrying capacity (Clayton and Clayton, 1981; 1982).

The toxicokinetics of methyl mercaptan has been studied following the intra-peritoneal injection of 14C or 35S labelled methyl mercaptan into rats. After 6 hours, the radioactivity was distributed to the plasma proteins (22.7%), liver (17.8%),


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intestinal mucosa (16.7%), lungs (11.5%), kidneys (11.4%), spleen (9.8%) and testes (8.5%) (Canellakis and Tarver, 1953). No radioactivity was identified as being distributed to the erythrocytes. Methyl mercaptan was identified as metabolising to carbon dioxide and sulphur-containing compound. Carbon dioxide and volatile sulphur-containing compounds were expired in the breath. Eight hours after administration of 35S- methyl mercaptan, 32% of the 35S- was excreted as sulphur compounds in the urine. In a separate study involving the IP injection of rats with 35S- methyl mercaptan, 94% of 35S- was excreted as sulphate in the urine within 21 hours (Derr and Draves, 1983).


There was one report of a fatality resulting from occupational exposure to methyl mercaptan involving a 53-year old male worker who was emptying tanks containing methyl mercaptan for approximately one week. No information regarding the exposure level was available, but it was assumed that both inhalation and dermal exposure occurred. The man was hospitalised in a coma, developed hemolytic anemia and methemoglobinemia, and died 28 days after admission. The immediate cause of death was determined to be a massive embolus that occluded both main pulmonary arteries (Shults et al., 1970).

Exposure to low levels of methyl mercaptan (approximately 8 mg/m3 for several hours) has resulted in nausea and headaches in humans (Sandmeyer, 1981). Other signs and symptoms reported following low-level exposures include eye and mucous membrane irritation, headaches, dizziness, staggering gait, nausea and vomiting (HSDB, 2004d).

Acute inhalation assays of varying duration in rats (strain and gender unspecified) gave LC50 values which ranged from 1,323 to 3,261 mg/m3 (675 to 1,664 ppm) (Reed, 1983; Tansy et al., 1981). One study reported an LC50 of 1,323 mg/m3 (675 ppm) for male and female rats exposed to methyl mercaptan for 4 hours (Tansy et al., 1981). However, no deaths occurred in 10 rats exposed to 784 mg/m3 (400 ppm) for 4 hours, while 100% mortality was reported at 1,372 mg/m3 (700 ppm) and above (ATSDR, 1992). In another study, 15 minutes of exposure to 2,744 mg/m3 (1,400 ppm) of methyl mercaptan produced lethargy or coma in rats (Zieve et al., 1974).

Exposures to higher concentrations of methyl mercaptan have been identified from animal studies as resulting in lethargy at 1,372 mg/m3 (700 ppm) (Ljunggren and Norberg, 1943); comas and alveolar hemorrhaging at 2794 to 2,940 mg/m3 (1,400 to 1,500 ppm) (Ljunggren and Norberg, 1943; Zieve et al., 1974) and convulsions, CNS depression, paralysis of locomotor muscles, mucous membrane irritation and death at 19,600 mg/m3 (10,000 ppm) (Ljunggren and Norberg, 1943).

3.7.2 Subchronic and Chronic Toxicity

One case study investigated the relationship between exposure to organic sulphides and effects in erythrocytes and heme synthesis in 18 exposed workers (gender not specified) at a pulp and paper facility in Sweden (Klingberg et al., 1988). Three sulphides were analysed including DMS, DMDS and methyl mercaptan. No changes


27

in erythrocyte number or morphology were observed, and levels of haptoglobin and hemoglobin did not differ significantly between the exposed and control groups. The concentrations of iron and transferrin were found to be elevated, while the concentration of ferritin was found to be low compared to the controls, indicating a disturbance of iron metabolism. As part of the study, six workers were assessed 2 days and 10 days after their involvement in a clean-up following an explosion. The level of serum iron was significantly increased in the workers at 2 days compared to 10 days post exposure. The authors speculated based on their results that exposure to low levels of organic sulphides could inhibit the intracellular uptake of iron in the reticuloendothelial system. However, due to concomitant exposure to DMS and DMDS, it is impossible to attribute the effects to any one compound.

In toxicity studies of subchronic exposure, male rats (31/dose) were exposed to 0, 4, 34 and 114 mg/m3 of methyl mercaptan for 7 hours/day, 5 days/week for 3 months (Tansy et al., 1981). At 114 mg/m3, a significant decrease in body weight gain was observed. Histological alterations in the liver were also noted, but the authors did not state whether the changes were related to methyl mercaptan exposure.


No developmental and reproductive toxicity data following inhalation exposure to methyl mercaptan were identified.

3.7.4 Genotoxicity

No genotoxicity data following inhalation exposure to methyl mercaptan were identified.


No carcinogenicity data following inhalation exposure to methyl mercaptan were identified.

3.8 Toxicology of DMS and DMDS

There is limited toxicity information in humans and experimental animals following inhalation exposure to DMS and DMDS. The most probable routes of human exposure are through ingestion of foods, as DMS and DMDS are naturally occurring, and through occupational exposures (HSDB, 2004b and 2004c).

Appendix C, Tables A.9 and A.10 summarise the acute toxicity data for DMS and DMDS, respectively.

Data regarding the toxicokinetics of DMS or DMDS is limited. Inhalation or ingestion of low quantities of methyl sulfide into the mammalian systems is reported as being readily metabolized (Clayton and Clayton, 1981; 1982). Exposure to DMDS via the intraperitoneal route has resulted in the expiration of DMS in laboratory mice (Susman et al., 1979). In addition, exposure of rats to a non-comatogenic dose of


28

methyl mercaptan through the colon showed elevated levels of DMS and DMDS in expired breath of rats (Blom et al., 1990).


The reported LC50's for DMS following acute inhalation assays of varying duration in mice and rats (strain and gender unspecified) were 32 mg/m3 and 103,845 mg/m3 (12.5 ppm to 40,250 ppm), respectively (RTECS, 2002; Tansy et al., 1981). Appendix C, Table C. 9 (page 139) summarizes the acute toxicity data for DMS following inhalation, oral and dermal exposures. Symptoms following low-level (duration not specified) inhalation exposures to DMS include severe eye irritation as well as irritation of the nose and throat (HSDB, 2004b). Inhalation exposures to DMS have generally been reported to result in little systemic toxicity (HSDB, 2004b).

The reported LC50's for DMDS following acute, 2-hour inhalation exposures in mice and rats (strain and gender unspecified) were 12 and16 mg/m3 (3 to 4 ppm), respectively (Lewis, 1992). Appendix C, Table C.10 (page 140) summarizes the acute toxicity data for DMDS following inhalation exposures. The reported symptoms following acute exposure have included nausea and headaches followed by olfactory fatigue with prolonged exposure (HSDB, 2004c). Exposure of laboratory rats to 3,091 mg/m3 (805 ppm) of DMDS for 4 hours did not result in mortality, with some evidence of microscopic liver damage on histopathologic examination (HSDB, 2004c). Laboratory rats exposed to 7.1 to 26 mg/L of DMDS by inhalation for 30 to 35 minutes exhibited pulmonary irritation with lung ecchymoses and convulsions (HSDB, 2004c).

3.8.2 Subchronic and Chronic Toxicity

Data regarding the subchronic or chronic toxicity associated with DMS exposures in animals were not identified. A single study in rats reported microscopic liver damage following inhalation exposure to 8 mg/m3 (2 ppm) of DMDS for a period of three months (HSDB, 2004c).

As previously discussed in terms of methyl mercaptan toxicity (see Section 3.3.2), the study by Klingberg et al. (1988) noted effects on blood iron, transferrin and ferritin concentrations in individuals exposed to a mixture of methyl mercaptan, DMS and DMDS.


No developmental and reproductive toxicity data following inhalation exposure to DMS or DMDS were identified.

3.8.4 Genotoxicity

No genotoxicity data were identified for DMS or DMDS.


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3.9


No carcinogenicity data following inhalation exposure to DMS or DMDS were identified.

Environmental Effects

3.9.1 Vegetation

Sulphur is an essential element for plant growth. When exposed to air pollution that contains sulphur compounds, sulphur acts as either a “fertilizer” or as a toxic agent (Noggle et al., 1986). When gaseous uptake of sulphur exceeds the demands from sulphur metabolism and the rate of detoxification, accumulation of sulphur-containing compounds in vegetation can occur (Herschbach et al., 1995; Maas, 1987). In addition, de Kok et al. (1997) demonstrated that there is a strong interaction between atmospheric and soil sulphur nutrition as plants are able to grow in the absence of sulphate with H2S as the sole source of sulphur. In general, there is a lack of dose-response models for individual TRS compounds other than H2S for a variety of vegetation species and environmental conditions. However, a LOEL and NOEL have been identified for H2S.

The National Research Council of Canada (NRCC, 1981) completed a review of the scientific literature and concluded that vegetation was relatively insensitive to short-term exposure to high concentrations of H2S. Impairment to plant growth and physiological processes generally begins at 350 µg/m3 and higher concentrations of H2S for several plant species (Buwalda et al., 1993; de Kok et al., 1989, 1997; Herschbach et al., 1995; Khalil et al., 1996; Kord et al., 1993a, b; Kord and Abbass, 1993; Maas et al., 1987, 1988; Taylor and Selvidge, 1984; Thompson and Kats, 1978). It has been suggested that long-term exposures to concentrations of less than 392 µg/m3 of H2S generally stimulate plant growth whereas long-term exposures at higher concentrations can result in growth inhibition, reduced biomass yield and/or visible injury to foliage (de Kok et al., 1983a, 1986; Thompson et al., 1979; Thompson and Kats, 1978; NRCC, 1981). The lowest observable effect concentration (LOEC) for H2S has been identified as 350 µg/m3 (Buwalda et al., 1993; de Kok et al., 1989, 1997; Herschbach et al., 1995; Khalil et al., 1996; Kord et al., 1993a,b; Kord and Abbass, 1993; Maas et al., 1987, 1988; Taylor and Selvidge, 1984; Thompson and Kats, 1978) and the no observable effect concentration (NOEC) has been reported as being 140 µg/m3 for a variety of long-term exposure periods (de Kok et al., 1983a,b; Maas et al., 1988).

3.9.2 Terrestrial and Aquatic Wildlife

As with the effects on vegetation, little information is available concerning the effects of either TRS or methyl mercaptan, DMS and DMDS. A number of studies have examined the effect of H2S on both terrestrial and aquatic wildlife. The minimal concentration of H2S associated with lethality reported in a number of animal studies has been identified as generally being 700 mg/m3 (Haggard et al., 1922; Lund and Wieland, 1966; U.S. EPA, 1993). Adverse nasal, eye and respiratory irritation have


30

been observed in animals exposed to air concentrations of H2S being generally greater than 14 mg/m3 (Beauchamp et al., 1984). However, concentrations of H2S as low as 0.014-4.9 mg/m3 have been reported to increase the likelihood of eye and respiratory irritation in cattle (cows and calves) (Beauchamp et al., 1984). There are currently insufficient data to identify the potential effects to wildlife and livestock due to chronic exposure to H2S. The sensitivity of different species of terrestrial animals to exposure to H2S has been identified through a comparison of both laboratory and field studies. While only eye and nasal irritation have been identified with exposure of cattle to H2S greater than 14 mg/m3 (Beauchamp et al., 1984), deaths have been reported to occur in wild birds, bats, owls and mice exposed to an estimated maximum H2S concentration of 18 mg/m3 (Newman, 1985).

Very little data is available concerning the potential effects of exposure to H2S on aquatic organisms. Acute toxicity data suggests that species variability is a major factor in sensitivity to H2S exposure. Results from a number of studies have reported a range of 96-hour LC50 values of 0.007 mg/L for walleye (Stizostedion vitreum) up to 95 mg/L for goldfish (Carassius auratus) (Adelman and Smith, 1972; Smith and Oseid, 1970; Smith et al., 1976a,b). Results from one chronic toxicity study examining several different aquatic species suggest that species sensitivity is less of a factor with chronic exposure to H2S. The range of reported highest no observable adverse effect levels from the study were 0.0007 mg/L (bluegill – Lepomis macrochirus) up to 0.01 mg/L for goldfish (Smith and Oseid, 1975).


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4.0 Review of Existing Air Quality Criteria

The current 1-hour AAQC for TRS in Ontario is 40 μg/m3, and the half-hour POI guideline is 40 μg/m3. These criteria were developed based on the available information on the odour effects of TRS in 1977. The current 1-hour AAQC for H2S in Ontario is 30 μg/m3, and the half-hour POI standard is 30 μg/m3. These criteria were developed based on the available information on the odour effects of H2S in 1974. The current 1-hour AAQC for methyl mercaptan in Ontario is 20 μg/m3, and the half-hour POI standard is 20 μg/m3. These criteria were developed based on the available information on the odour effects of methyl mercaptan in 1974. The current 1-hour AAQC for DMS in Ontario is 30 μg/m3, and the half-hour POI standard is 30 μg/m3. These criteria were developed based on the available information on the odour effects of DMS in 1974. The current 1-hour AAQC for DMDS in Ontario is 40 μg/m3, and the half-hour POI standard is 40 μg/m3. These criteria were developed based on the available information on the odour effects of DMDS in 1974.

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, specifically: the Canadian Federal Government and provinces; the U.S. EPA, many of the U.S. states, the World Health Organization (including WHO-Europe), the Netherlands, the Swedish Institute of Environmental Medicine and the United Kingdom. For TRS and its compounds, this report reviews the scientific basis for air quality guidelines and standards for those jurisdictions that have air quality standards or guidelines for TRS. A brief summary of available criteria is presented in Table 5. An overview of the basis of the guideline values and how they relate to other agency and jurisdiction values are provided in Section 4.1. Agency- specific summaries of several of the guidelines are presented in Section 10.

In reviewing the air quality guidelines and exposure limits presented in Table 5 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 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.

4.1 Overview

Information concerning air quality guidelines was obtained from a number of agencies and is summarized in Table 5. An overview of the basis of the guideline values for TRS, H2S, methyl mercaptan, DMS and DMDS and how they relate to other agency and jurisdiction values are provided below.


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Table 5: Summary of Existing Air Quality Guidelines1 for TRS and/or TRS Compounds

Agency

Guideline Value Basis of Guideline Date2 Comments

Canada

(CEPA)

No guideline is listed. Draft values documented in 1992 were not finalized. TRS has not been scheduled for Canada-Wide Standard development.

TRS (as H2S)

40 µg/m3

(half-hour average, POI)

1982 Point of Impingement Guideline

40 µg/m3

(1-hour, AAQC)

Odour* 1982 Ambient Air Quality Criterion

H2S

30 µg/m3


Odour 1978 Point of Impingement Standard

30 µg/m3

(1-hour, AAQC)

Odour 1978 Ambient Air Quality Criterion

DMS

30 µg/m3


Odour

1978 Point of Impingement Standard

30 µg/m3

(1-hour, AAQC)


DMDS

40 µg/m3


Odour

1978 Point of Impingement Standard

Ontario

(MOE)

40 µg/m3

(1-hour, AAQC)



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Agency


Mercaptans (as Methyl mercaptan)

20 µg/m3


Odour 1978 Point of Impingement Standard

20 µg/m3

(1-hour, AAQC)

Odour

1978 Ambient Air Quality Criterion

H2S

14 µg/m3

(1-hour AQG)

Odour

1975 Ambient Air Quality Criterion

4 µg/m3

(24-hour AQG)


Alberta

Static H2S

0.10 mg/SO3 equivalent/day/100 cm2 as a 1-month accumulated loading

Not available Not available

Ambient Air Quality Criterion

TRS (Derived for Forest Products Industry)

7 µg/m3

(1-hour average)

Odour

1977

Ambient Air Quality Guidelines

Maximum Desirable Criterion

28 µg/m3

(1-hour average)

Odour 1977 Maximum Acceptable Criterion

3 µg/m3

(24-hour average)

Odour 1977 Maximum Desirable Criterion

6 µg/m3

(24-hour average)

Odour 1977 Maximum Acceptable Criterion

British Columbia

H2S

7.5-14 µg/m3

(1-hour averaging, MDC)

Not available

1974/1975

Maximum Desirable Criterion


34

Agency


28-45 µg/m3

(1-hour averaging, MAC)

Not available 1974/1975 Maximum Acceptable Criterion

42-45 µg/m3

(1-hour averaging, MTC)

Not available 1974/1975 Maximum Tolerable Criterion

4 µg/m3

(24-hour averaging, MDC)

Not available 1974/1975 Maximum Desirable Criterion

6-7.5 µg/m3

(24-hour averaging, MAC)

Not available 1974/1975 Maximum Acceptable Criterion

7.5-8 µg/m3

(24-hour averaging, MTC)

Not available 1974/1975 Maximum Tolerable Criterion

H2S

1400 µg/m3

(1 hour average, MTLC)

Undue annoyance from odour

1985 Maximum Tolerable Level Concentration Guideline

15 µg/m3

(1 hour average, MALC)


1985 Maximum Acceptable Level Concentration Guideline

5 µg/m3

(24-hour average, MALC)


1985 Maximum Acceptable Level Concentration Guideline

Manitoba

1 µg/m3

(1-hour average, MDLC)


1985 Maximum Desirable Level Concentration Guideline

New Brunswick

H2S

15 µg/m3

(1-hour average)

Odour 1979 Air Quality Objectives


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Agency


5 µg/m3

(24-hour average - Ground Level Concentration)

Odour 1979 Air Quality Objectives

H2S

15 µg/m3

(1-hour average)

Odour

1989

Clean Air Regulations

Saskatchewan

5 µg/m3

(24-hour average)

Odour 1989 Clean Air Regulations

U.S. EPA

(IRIS)

H2S

2 µg/m3

(RfC)

nasal lesions of the olfactory mucosa

(Brenneman et al., 2000)

2003 RfC for Inhalation

H2S

42 µg/m3

(Acute REL)

Odour

(California State Dept. Of Public Health, 1969)

1999 Acute Reference Exposure Level

California

(OEHHA)

10 µg/m3

(Chronic REL)

Nasal histological changes in mice

(CIIT, 1983a)

2000 Chronic inhalation Reference Exposure Level

H2S

84 µg/m3 (0.06 ppm)

(3-minute average)

Not available

1981

Ambient Air Quality Standards

Delaware

42 µg/m3 (0.03 ppm)

(1-hour average)

Odour

(based on California’s acute REL)

1981 Ambient Air Quality Standards

Kentucky

H2S

14 µg/m3

(1-hour average)

Based on odour threshold

1960's/

1970's

Ambient Air Quality Standard


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Agency


Louisiana

(LDEQ)

H2S

330 µg/m3

(8-hour average)

Based on the ACGIH TLV-TWA value of

14 mg/m3

1992 Ambient Air Standard

The value was derived by dividing the ACGIH TLV-TWA value by 42.

H2S

10 µg/m3

(Subchronic TEL)

Inflammation of nasal mucosa

(CIIT, 1983a)

2002 Threshold Effects Level

93 µg/m3

(30-minute Acute TEL)

Bronchial obstruction and headache in asthmatics


Massachusetts

(MADEP)

10 µg/m3

(1-24 hour Acute TEL)

Reduction in body weight gain


Michigan

(MDEQ)

H2S

1 µg/m3

(24-hour average, ITSL)

Based on the

U.S. EPA’s RfC

1995 Initial Threshold Screening Level

New Jersey

(NJDEP)

H2S

1 µg/m3

(RfC)

Based on the

U.S. EPA’s RfC

2001 RfC for Inhalation

H2S

14 µg/m3

(1-hour SGC)

Odour

1972 Short-term Guideline Concentration

New York

(NYDEC)

1 µg/m3

(annual, AGC)

Based on the

U.S. EPA’s RfC

2000 Annual Guideline Concentration

North Carolina

(NCDENR)

H2S

2.1 mg/m3

(1-hour average)

Acute irritant

(N.C. SAB, 2001)

1990

Acceptable Ambient Level


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Agency


56 µg/m3 (0.056 mg/m3)

(1-hour recommended AAL)

Triggering of asthma symptoms

(Jappinen et al., 1990)

2001 Proposed - Acceptable Ambient Level

Under review

120 µg/m3 (0.12 mg/m3) to

33 µg/m3 (0.033 mg/m3)

(24-hour recommended AAL)

Nasal toxicity to

eye pain and visual disturbances.

(Brenneman et al., 2000 and Vanhoorne, 1991)

2001 Proposed - Acceptable Ambient Level

Under review

Methyl Mercaptan

50 µg/m3 (0.05 mg/m3)

1-hour

Based on the ACGIH TLV-TWA of 1 mg/m3

1990

Acceptable Ambient Level

1120 µg/m3

(30-minute average)

Odour 1968 Texas Administrative Code

Allowable Emissions.

Emission of H2S cannot exceed 1120 µg/m3 (based on a 30-min average) if residential, business of commercial properties are downwind.

TNRCC is TCEQ (Texas Commission for Environmental Equality)

Texas

(TNRCC)

1680 µg/m3

(30-min average)

Odour 1968 Texas Administrative Code

Allowable Emissions

Emission of H2S cannot exceed 1680 µg/m3 (based on a 30-min average) if industrial and vacant tracts and rangelands not normally occupied by people are downwind.


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Agency


Methyl Mercaptan

2 µg/m3 (short-term ESL)

0.2 µg/m3 (ESL, annuals)

2003

Short-term 1-hour Effect Screening Level (ESL)

Long-term annual ESL)

Texas

TCEQ

Dimethyl Sulphide

3 µg/m3 (short-term ESL)

0.3 µg/m3 (long-term ESL)

2003

Short-term 1-hour ESL

long-term annual ESL

The Netherlands No guidelines listed for TRS or H2S.

Sweden No guidelines listed for TRS or H2S.

H2S

7 µg/m3

(30-minute average)

Odour

2000

Air Quality Guidelines for Europe

WHO

(Europe and

PHE)

150 µg/m3

(24-hour average)

Eye irritation

(Savolainen, 1982)

1987 Air Quality Guidelines for Europe

and

Air Quality Guidelines (WHO-PHE)

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 U.S. 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.

* Takes into account technical difficulties of control, dispersion, enforcement and measurement.


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4.1.1 Overview of TRS Guidelines

The provinces of Ontario, British Columbia and Newfoundland are the only agencies with guidelines for TRS. These values were set in the 1970's and 1980's and were developed mainly for the purpose of odour control. The values range from 28 to 100 µg/m3 for a 1-hour average. In addition, British Columbia has a maximum desirable criterion of 7 µg/m3, a level considered reasonable for polluted areas to aim for and to achieve. When the TRS value was developed by the MOE, a theoretical assessment indicated that concentrations of TRS compounds should not exceed 26 µg/m3 for any individual components in TRS and 23 µg/m3 when TRS is measured collectively. Due to the difficulties in the control, dispersion, enforcement and measurement of TRS, a value of 40 µg/m3 was established.

4.1.2 Overview of H2S Guidelines

The majority of the agencies reviewed have guidelines for H2S. Many have guidelines developed in the 1970's and 1980's that were derived to protect against odour annoyance. More recent guidelines also address health concerns related to H2S exposure. The U.S. Department of Health and Human Services, under the Agency for Toxic Substances and Disease Registry (ATSDR), has developed inhalation Minimal Risk Levels (MRL) of 0.07 ppm (97 µg/m3) for acute exposures and of 0.03 ppm (42 µg/m3) for intermediate exposures (ATSDR, 1999).

Guidelines Developed based on Health Effects

Subchronic inhalation studies in rodents have been used by a number of agencies in developing their guideline values for H2S. A mouse subchronic inhalation study, conducted by CIIT (1983a) identified a NOAEL of 42 mg/m3 for inflammation of nasal mucosa. Massachusetts used this NOAEL in developing their guideline values of 1 µg/m3. Both Michigan (24-hour Initial Threshold Screening Level [ITSL]) and New Jersey (Reference Concentration for Inhalation [RfC]) derived their respective air quality guidelines of 1 µg/m3 based on the previous U.S. EPA’s RfC of 1 µg/m3. California’s chronic REL of 10 µg/m3 was developed from the CIIT (1983a) study, using the NOAEL of 42 mg/m3. The U.S.EPA has recently updated its RfC to 2 µg/m3 from 1 µg/m3, using the NOAEL of 13.9 mg/m3 for effects of nasal lesions of the rat olfactory mucosa, from the study of Brenneman et at. (2000).

Air guidelines, based on health effects of H2S reported in humans, commonly address symptoms involving the eyes and respiratory tract. The current North Carolina 1-hour AAL of 2.1 mg/m3 is based on the ACGIH’s recommended Short Term Exposure Limit (STEL) for occupational settings of 21 mg/m3 (15 ppm). The ACGIH’s STEL was developed to minimize the potential for eye and respiratory tract irritation, symptoms of fatigue, headache, and dizziness, and CNS effects such as paralysis of the respiratory center and sudden death (ACGIH, 2001c). The North Carolina Scientific Advisory Board (N.C. SAB) has recently suggested that the 1-hour AAL be adjusted to 56 µg/m3 (0.04 ppm) based on human respiratory effects observed by Jappinen et al. (1990), however their review has not yet been completed (N.C. SAB, 2003). The acute MRL of 97µg/m3 the ATSDR has been derived from the


40

study of Jappinen et al. (1990). The WHO has a guideline of 150 µg/m3 to protect against eye irritation. Louisiana has established an 8-hour average guideline of 330 µg/m3 based upon the ACGIH-TWA. The current ACGIH Threshold Limit Value-Time Weighted Average (TLV-TWA) is 14,000 µg/m3 (10 ppm) for an 8-hour workday and a 40-hour workweek. The value was set in 1966 to minimise the potential for eye and respiratory tract irritation, symptoms of fatigue, headache, and dizziness, and CNS effects such as paralysis of the respiratory centre and sudden death (ACGIH, 2001c). However, a notice of intended change has been issued to revise the TLV-TWA to 7,000 µg/m3 (5 ppm) based on biochemical studies between 1991 to 1997 that showed a shift in metabolism in muscle from aerobic to anaerobic following brief controlled exposures at 7,000 µg/m3 (5 ppm) in humans (Bhambhani et al., 1997; Bhambhani et al., 1996a; Bhambhani et al., 1996b; Bhambhani et al., 1994; Bhambhani and Singh, 1991). A shift in metabolism from aerobic to anaerobic is thought to decrease the rate at which chemical energy can be produced in the muscle cell, thereby resulting in fatigue (Bhambhani, 1999). The ACGIH currently has a STEL of 21,000 µg/m3 (15 ppm) that was set in 1976 to protect against eye irritation. This STEL is to be withdrawn upon adoption of the new TLV-TWA value.

Odour Based Guidelines

The provinces of Ontario, Alberta, B.C., Manitoba, Newfoundland, New Brunswick and Saskatchewan have guideline values for H2S that were developed to reduce odour annoyance. Their 1-hour values range from 14 µg/m3 to 45 µg/m3 (10 to 32 ppb). In addition, B.C. has 1-hour Maximum Desirable Criteria of 7.5 µg/m3 to 14 µg/m3 (5 to 10 ppb) and Manitoba has a 1-hour Maximum Tolerable Level Concentration of 1400 µg/m3 (980 ppb). The 24-hour values for B.C. range from 4 µg/m3 to 8 µg/m3 (3 to 6 ppb). California has developed a 1-hour Acute Reference Exposure Level (REL) of 42 µg/m3 (29 ppb) based on odour, which was subsequently adopted by Delaware as an Ambient Air Quality Standard. Kentucky and New York each has an ambient air quality standard of 14 µg/m3 (10 ppb) based on odour. The WHO established a 30-minute average guideline of 7 µg/m3 (5 ppb) to prevent substantial complaints of odour (WHO, 2000). Instead of an air quality guideline, Texas has established property line standards. Emissions of H2S cannot exceed net ground level concentrations of 115 µg/m3 (80 ppb) (30-min averaging) if residential, business or commercial properties are downwind and 173 µg/m3 (121 ppb) (30-min average) if industrial and vacant tracts and rangelands not normally occupied by people are downwind.

4.1.3 Overview of Methyl Mercaptan Guidelines

Ontario, Newfoundland and North Carolina are the only jurisdictions that have established ambient air quality guidelines for methyl mercaptan. The values range from 20 to 50 µg/m3 (1-hour average). The value established by Newfoundland is likely based upon the guideline set by Ontario. The value of 0.05 mg/m3 used by North Carolina was obtained by adjusting the ACGIH TLV-TWA (Threshold Limit Value-Time Weighted Average) value of 1 mg/m3 (0.5 ppm) by a factor of 20 to take into account variation in susceptibility and the severity of the effect.


41

The ACGIH and the Occupational Safety and Health Association (OSHA) both established an 8-hour TLV-TWA for methyl mercaptan of 1 mg/m3 (0.5 ppm). The ACGIH developed its TLV-TWA in 1970 to prevent odour annoyance and at higher, but still low-level exposure, headache, nausea, eye and mucous membrane irritation, and possible CNS effects (ACGIH, 2001b). OSHA developed its Permissible Exposure Limit (PEL) in the 1980's to protect against acute sensory effects and possible organ damage (OSHA, 1989). NIOSH set the same level of 1 mg/m3 (0.5 ppm) as a 15-minute Ceiling Limit. NIOSH set a 15-minute Ceiling Limit in 1978 for a group of thiols that included methyl mercaptan, based on a study by Gobbato and Terribile (1968) that describes olfactory fatigue and mucosal irritation with exposure to ethyl mercaptan at a concentration of 8 mg/m3 (4 ppm), but not at 0.8 mg/m3 (0.4 ppm) (NIOSH, 1978). Acute inhalation studies have indicated that methyl mercaptan is of approximately the same order of toxicity as ethyl mercaptan (NIOSH, 1978).

4.1.4 Overview of DMS and DMDS Guidelines

With a lack of toxicological data for DMS and DMDS, Ontario and Newfoundland are the only provinces with guidelines for DMS and DMDS based on odour considerations. The Newfoundland guideline values for DMS and DMDS are based upon the guidelines set by the MOE.

4.2 Evaluation of Existing Criteria

A review of the basis of agency air standards and guidelines for TRS and reduced sulphur compounds indicated that health and odour concerns are the two major effects considered. Toxicological data concerning the potential for adverse health effects with exposure to methyl mercaptan, DMS and DMDS are lacking. The lack of toxicological data for these TRS components is evidenced in their lack of health-based air quality guidelines from a number of jurisdictions and agencies. Therefore, deriving a health based guideline for TRS based on the potential for adverse effects with exposure to these components of TRS is currently not possible. The toxicological effects of H2S from inhalation exposure have been extensively investigated and many jurisdictions and agencies have developed health-based air guidelines for this compound. Therefore, an effects-based air quality standard for H2S may be used as a surrogate to derive effects-based air quality standards for TRS.

Odour is characteristic of the sulphidic compounds of TRS and adverse impact from exposure to these odorous substances could lead to undesirable health effects. Odour-based guidelines have been derived for all of the individual components of TRS. The difficulty in deriving an odour-based air standard is the inconsistent proportion of each of the components within the TRS mixture, as reported odour thresholds (50% detection) for each component vary widely with values ranging anywhere from 3.0x10-3 µg/m3 up to 270 µg/m3.

Considering the odour and adverse health effects of the sulphidic compounds of TRS, effects-based air standards for TRS can be derived based on two approaches:


42

odours impact and adverse health concerns. The two approaches will be discussed in the following:

Health-based Approach for TRS Air Quality Guideline Development

The odour effects of TRS and related sulphidic compounds in general were described to occur and their odour thresholds were reported at concentrations below adverse health effect thresholds for these compounds. On the basis of these observations, most of the agencies have focussed on guidelines to avoid the odour effects of TRS compounds for short-term exposures. The State of Massachusetts was the only jurisdiction who has developed a short-term (30-minute) health-based guideline value for H2S based on the human study by Jappinen et al. (1990). The study reported bronchial obstruction and headaches in the asthmatic subjects. The authors noted that the observed results should be considered preliminary. In view of this caution, the study of Jappinen et al. (1990) is not considered suitable for the development of a health-based criterion for H2S and TRS.

Most of the agencies reviewed do not have health-based guidelines for TRS for long-term, low-dose environmental exposures. Instead, guidelines have been derived based on the long-term health effects of H2S. The U.S. EPA has recently updated its RfC to 2 µg/m3 from 1 µg/m3 (U.S EPA, 2004). The U.S. EPA derived its updated RfC from the NOAEL of 13.9 mg/m3 of the study of Brenneman et al. (2000). The NOAEL was converted into a human equivalent concentration (NOAELHEC) of 0.64 mg/m3 after adjusting for exposure duration and for difference in the gas respiratory effect in the extrathoracic region between rats and humans. A total uncertainty factor of 300 was applied. The uncertainty factors included: 3 for interspecies extrapolation; 10 for subchronic exposure; 10 for sensitive individuals.

Most of the U.S. State agencies have adopted the old U.S. EPA’s RfC of 1 µg/m3 which was based on the animal study of the CIIT (1983a). The World Health Organization (WHO) examined the conclusions of the study of Savolainen (1982) on the development of an occupational exposure limit for H2S. This study was updated in 2001 by the Nordic Expert Group (2001). From this study, both the WHO (2000) and the Nordic Expert Group (2001) considered the identified LOAEL of 15 mg/m3 for eye irritation for criteria determination. The WHO applied an uncertainty factor of 100 (10 to extrapolate from a LOAEL to a NOAEL and 10 for intraspecies variability [sensitive individuals within the population]) to derive its guideline value of 150 µg/m3. Since the publication of the study by Savolainen in 1982 a number of human and animal studies have identified critical effects at H2S concentrations below the study’s LOAEL of 15 mg/m3. Therefore, it is possible that an air quality guideline derived based on this study would not be protective against adverse effects in humans exposed to H2S and TRS. Also the study had a number of limitations (e.g., those with severe pre-existing conditions were excluded, small sample size, very short-exposure duration) including the lack of control conditions reduce the value of this study.

The State of California derived its chronic REL of 10 µg/m3 from the animal study of CIIT (1983a). A number of state agencies (e.g. Michigan, Massachusetts, New Jersey and New York) adopted the U.S. EPA’s previous RfC value as their respective


43

air quality guidelines. The key endpoint, nasal inflammation, has been observed in other animal studies as well as in humans following low level exposure to H2S (Brenneman et al., 2000; HSDB, 2004a).

The CalEPA used the NOAEL identified in the CIIT (1983a) study to calculate and obtain human equivalent concentration to the NOAEL (NOAELHEC). The CalEPA applied a total uncertainty factor of 100 by incorporating an uncertainty factor of 3 to adjust from subchronic to chronic exposure, a factor of 3 for interspecies conversion, and a factor of 10 for intraspecies differences (see section 7.3 for details).

The Office of Environmental Health Hazard Assessment (OEHHA) of the CalEPA considered that the extrapolation of exposure durations to be related to the average lifetime of the species in the determination of an appropriate uncertainty factor. In the study of CIIT (1983a), mice were exposed for 90 days which represents 12% of an average lifespan of two years, an expected lifetime of this species, thus a 3-fold uncertainty was adequate (OEHHA, 2000). The OEHHA used a 3-fold uncertainty factor to account for interspecies difference in susceptibility since an extrapolation of the NOAEL to an NOAELHEC had been performed.

It is evident that from the review of agency guidelines, a health-based criterion for TRS is not available. Most of the available health-based guidelines for reduced sulphur compounds were established for H2S using either animal or human data. These H2S guidelines vary within a wide spectrum of concentrations, e.g., from 1 µg/m3 of some of the U.S. state agencies to 1680 µg/m3 of the State of Texas. These criteria apparently are below concentrations reported to cause effects in humans (e.g. 2.8 mg/m3; irritation and change in muscle metabolism from aerobic to anaerobic) (Bhambani, 1996a & 1999; Jappinen et al., 1990). However, since respiratory effects in sensitive populations have been reported at TRS concentrations close to the odour thresholds of reduced sulphur compounds (Marttilla et al., 1995; Marttilla et al., 1994; Partti-Pellinen et al., 1996), the odour and health effects will have to be weighed together in the development of air standards for TRS.

Odour-based Approach for TRS Air Quality Guideline Development

In Canada, ambient air standards and guidelines for TRS are based primarily on the odour property. Before commenting on the available odour guidelines, the possible impacts of odour will need to be examined. Conventional perception of odour effects is related to the aesthetic nature of odorous substances. Characterizing odour effects as simply a nuisance effect may understate the possible health impacts of odours on individual and community health. It has been suggested that people who notice odour more frequently are more likely to report health symptoms than those who sense odour less frequently (Sider et al., 1994). The relationship between odour perception, annoyance and reported symptoms, however, can be complex. Cavalini (1994) found that individuals who perceived odours may become annoyed and some of these annoyed individuals reported health complaints. Those reported health complaints may represent a small sensitive sub-population.

It has been suggested that odourants may stimulate the trigeminal nerve and can increase the cortical blood flow, which may be partly responsible for the headaches


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that are one of the complaints associated with environmental exposure to odours (Major and Silver, 1999). Since some exposed individuals are likely to experience appreciable discomfort, sensory response to odours may result in changes of behavioural components (Dick and Ahlers, 1998). As well, long-term exposure to odourants may produce persistent, although reversible, reduction in perception of that odour (Cavalini, 1994). The adverse health outcomes, consistent self-reporting of such health outcomes and the decrease in a sense of well-being in communities impacted by odours suggest that persistent exposure to unpleasant odours can have a significant impact on social behaviour and community health.

Another complicating factor is risk perception. Other than the unpleasant smell, odorous air is often perceived as a health risk to humans. This is likely to be the case with odours from industrial sources as there is a strong perception that in general industrial pollutants are associated with health risks (Cavalini, 1994; Dalton and Wysocki, 1996; Leonards et al., 1969; Sider et al., 1994). Nonetheless, there appears to be a commonly observed relationship between the presence of odours in a community and incidents of reports of specific symptoms such as headaches, nausea, irritation of the eyes and throat, as well as worsening of conditions of asthmatics.

The determination of odour thresholds, whether detection, recognition or complaint, is no simple task since olfaction is a biological response and subject to individual sensibility variations. There is so far no agreed method for olfactometry. The commonly used method relies on an odour panel of individuals to evaluate and report the “50% detection threshold” since it provides the median of estimates of individual sensitivity to the odour being studied. Few studies provide sufficient information to define a 5% or 10% response level. A large number of odour thresholds for the TRS compounds are available from two source categories: one from the review papers (e.g. AIHA, 1989; Amoore and Hautala; Ruth, 1986) and one from original studies on odour threshold determination (e.g. Nagy, 1991). Most of the review papers quote the odour threshold values determined from a number of original studies to provide either a range or the geometric mean of a range of odour thresholds for different TRS chemicals. Although literature reviewed provides odour threshold values from more than one report, most of these original studies have never been critically reviewed to assess the validity of the methods used. One exception is the AIHA (1989) that critically reviewed the quality of the reported odour thresholds of 360 original papers for different chemicals and provides certain degree of confidence in odour threshold determination. The odour threshold values from the AIHA report (1989), the Nagy (1991) study and the Devos et al. (1990) publication may provide a basis for odour-based air quality standards development for the TRS compounds (See Table 6: Summary of Accepted Odour Detection Thresholds of TRS ). Table 6: Summary of Accepted Odour Detection Thresholds of TRS also provides geometric mean values of odour thresholds for each respective TRS compound. The odour threshold of 0.0003 µg/m3 (Williams, 1977) was not used in the calculation of the geometric mean of odour thresholds for methyl mercaptan for the fact that this is a very low odour threshold reported for this odourous compound, strongly suspected to be an outlier in light of the orders of magnitude difference compared to other odour threshold determinations. This level is also far less than the level (>1 µg/m3) measured by current method of detection for TRS.


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TRS exists as mixtures of reduced sulphur compounds and deriving an ambient air standard for TRS mixtures based on odour requires information pertaining to the mixture’s specific chemical composition and the odour thresholds of the individual TRS components. For most mixtures consisting of similar compounds, the perceived odour intensity is approximately equivalent to or slightly less than the sum of the odour intensities of the individual components of the mixture (CARB, 1985; NRC, 1979).


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Table 6: Summary of Accepted Odour Detection Thresholds of TRS

TRS Compound Odour Detection Threshold (µg/m3)

Reference*

6.5 Adams (1968)

10 Cederlof (1966)

180 Katz (1930)

74 Nishida (1979)

1.6 Thiele (1979)

270 Williams (1977)

2.7 Winneke (1979)

9.3 Young (1966)

5.5 Nagy (1991)

Hydrogen Sulphide

23 Devos et al. (1990)

Geometric mean 16.1

81 Katz (1930)

38 Nishida (1979)

0.0003 ** Williams (1977)

2.4 Nagy (1991)

Methyl Mercaptan


Geometric mean 11

88 Nishida (1979)

51 Nagy (1991)

DMS


Geometric mean 30

66 Nagy (1991) DMDS


Geometric mean 56.3

* See AIHA (1989) for bibliographic information on individual references, excepting Nagy (1991).

** Not used in the geometric mean determination (See text for explanation)


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5.0 Responses of Stakeholders to the Information Draft

In August 2005, the Ministry posted Information Draft documents for 12 chemicals, including TRS, 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 inhalation toxicological information examined by the Ministry; the rationale of the other jurisdiction guidelines that the Ministry considered appropriate for the development of air quality standards; specifically the issues on the development of short-term odour-based and long-term health-based air quality standards for TRS; the most appropeiate rationale for odour-based TRS air standards and for the component compounds of TRS; the appropriateness of using hydrogen sulphide as the surrogate compound for the development of health-based air standards for TRS; and whether air standards for hydrogen sulphide, methyl mercaptan, DMS and DMDS need to be revised.

During the consultation period the Ministry received two submissions from stakeholders regarding the draft document for TRS. Representatives of the mining industry and the forestry industry association submitted comments.

In general, stakeholders supported the use of a surrogate compound for assessing the toxicity of TRS and for effects-based air standards development, and hydrogen sulphide appears to be the most appropriate for its vast toxicological database. However, opinions were different on odour-based TRS air standards. The opinion supporting odour-based TRS air standards cautioned about the appropriate representation of the odour thresholds associated with the varying composition of the TRS components in air standards setting. The opinion against odour-based TRS standards advocated the basis of standards setting under the O. Reg. 419/05 that emphasized effects (health)-based air standards. There were also comments on the development of air standards for TRS and for its components with respect to the nature of the toxicity and availability of toxicological information for individual TRS compounds.

There were comments addressing the ambient levels of TRS and compounds and their releases reporting under the NPRI. Release data on the NPRI and the O.Reg. 127/01 had been updated and incorporated. Comments addressing the process of air standards setting were not responded to in the Rationale Document but are addressed in this final version of the standards development supporting document.


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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 Total Reduced Sulphur” and requested public comments over a period of 91 days. The Ministry received comments on total reduced sulphur from ten stakeholders. Five submissions provided comments specific to the proposed TRS standards. Four submissions commented on the odour issues of TRS compounds. One submission commented on the general standards setting process. One submission did not specifically raise any issues with TRS. Highlights from five TRS-specific comments are summarized below.

Comments of a Technical Nature Specific to Total Reduced Sulphur (TRS):

Comment: One submission suggested using the odour recognition threshold, rather than the odour detection thresholds which are too stringent, for odour-based standards derivation. The odour recognition threshold better represents the point where an odour becomes a nuisance in the community. Another comment also suggested that the odour-based guideline should be based on an odour recognition threshold and scaled to 1-hour average value.

Response: In April 2005, the Ministry consulted on two options: (1) setting the standard based on the geometric mean of the best data set of odour detection (OD) thresholds or (2) adjust the value in option 1 by the complaint level determined in a certain percentage (e.g., 10%) of the population. The second option was to better address the point where odour becomes a serious nuisance in the community. Based on the outcome of the consultation, option (1) was selected for the development of odour-based standards and guidelines. Since even option 1 is based on the geometric mean from several data sets over a broad range of values, it is quite possible that for some more sensitive people, who identified the OD threshold in the ‘low end of the range study’ might find the OD threshold a nuisance from the ‘high end of the range study’. With regard to scaling a guideline to a 1-hour average value, the Ministry is still exploring various ways to implement odour standards and guidelines (see General Comments below). Comment: The use of H2S as a surrogate for the odour effects of TRS is not appropriate; the submission viewed TRS as a surrogate for the odourous substances in TRS. This submission explained that many sulphur-containing compounds measured by a TRS analyzer did not cause odours. An example was that in the pulp & paper mills sector, where TRS emissions contain many compounds other than H2S, and therefore, less stringent standards have been proposed for this sector. Response: The surrogate basis used for the odour effects of TRS were twofold: the most prominent component of TRS (i.e., H2S ) and the two most odorous substances


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of TRS (i.e., H2S and methyl mercaptan). In addition, stakeholders previously requested that it would be reasonable at the practical level to have a circumstance, where compliance with the odour-based AAQC/standard for each or several of the individual TRS compounds assured compliance with the odour-based AAQC/standard for the overall TRS mixture. For all these reasons the sectoral odour-based standards for TRS, and the odour-based standards for H2S and for methyl mercaptan are all identical. The less stringent standard proposed for the pulp and paper sector is based on health, which in turn is based on the H2S content of TRS in the emissions from this sector. The evaluation and consideration of sector-specific standards for TRS was performed based on information obtained from the emission inventory reported under the O. Reg 127 and previous NPRI data. The data from the recent 2005 NPRI report also support the current analysis on the sector-represented TRS and H2S emissions. Comment: One submission commented on the fact that the NPRI indicated that reported annual emissions of H2S are decreasing and questioned the basis for the revision of standards. Response: The prioritization of H2S for review of standards is based on factors other than emission quantities, such as the toxicology and possible impacts on health, and the guidelines update status of other jurisdictions. Despite the fact that the releases of H2S in Ontario may have decreased, recent research indicates that H2S may be toxic at low environmental concentrations (see text). Comment: There were two comments related to acute effects. One noted that, based on the availability of acute effects studies on H2S, no acute 1-hour average standards have been set for H2S or TRS. The other comment viewed the 24-hour AAQC as an acute effect-based standard and noted that the use of the uncertainty factor, for exposure duration extrapolation, is inappropriate in the derivation of the TRS standard. Response: The 24-hour average AAQC was not derived from acute toxicological data. This AAQC is based on chronic effects and is intended to protect against chronic exposures, as well as acute exposures, that could arise while still meeting the 24-hour average standard. The Ministry sets 1-hour average standards for acute effects only if these effects occur at such a low concentration that the chronic effects-based standard would not protect against them. Comment: New information from Health Canada and Environment Canada, as a result of listing TRS for NPRI reporting, may provide a reference of new information for TRS and H2S.


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Response: The evaluation and consideration of sector-specific standards for TRS was performed based on information obtained from the emission inventory reported under the O. Reg 127 and previous NPRI. The data from the recent 2005 NPRI report also support the current analysis on the sector-represented TRS and H2S emissions. Comment: The use of H2S as the surrogate chemical for TRS emissions may penalize the non-pulp and paper mill industries, e.g. in situations when H2S constitutes a small portion of their TRS emissions. Rather than creating different standards for the two industrial sectors, the 24-hour health-based TRS standard should be the same as the H2S standard and compliance will be based on the H2S composition of the TRS from each specific source at the facility (to avoid setting two standards). Response: While seemingly simple in having the same H2S and TRS standard, in practice this actually sets up a situation which would require the accurate determination of H2S in the TRS emissions for each source. In turn this approach in fact creates many site specific standards and, depending on the accuracy of composition determination at various sources, it potentially creates an uneven playing field for similar sources. Comment: There were also practical workability issues (i.e., simultaneous application of all the standards) of compliance for TRS, as a mixture, and for the individual components, based on odour. Response: In response to this comment, the recommendations for the applicability of the TRS standards have been clarified as follows in this document and will be clarified in O.Reg 419/05:

• Any facility releasing only one specific species of the four major components of TRS will not be considered for the release of TRS and the respective standards or guidelines for this specific species will apply.


• Implementation of odour-based limits is set out in O.Reg 419/05. Comment: Two comments suggested exemptions for valid reasons. In one case it was suggested that agricultural fumigation should be exempted from the air quality guideline for DMDS. DMDS is replacing a chemical having a far more severe environmental impact (Methyl Bromide). While banned as a result of the Montreal Protocol, Methyl Bromide remains in use today under exemption due to the absence of an environmentally and economically acceptable alternative. DMDS is


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such an alternative. DMDS’s use as an agriculture fumigant would be regulated under the Canadian Pest Control Products Act. In the other case it was noted that ethyl mercaptan, used as a warning odorant in mining ventilation systems, should be exempted from the TRS standards. Response: These have been taken into consideration in the amended O. Reg 419/05

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.

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

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

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


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7.0 Considerations for the Development of an Ambient Air Quality Criterion for Total Reduced Sulphur

The current ambient air quality criterion for TRS in Ontario is 40 μg/m3 (one-hour average) and the half-hour Point-of-Impingement guideline is 40 μg/m3; both were based on the odour effects of TRS from information available in 1977.

The current ambient air quality criteria for H2S and DMS in Ontario are both 30 μg/m3 (one-hour average) and the half-hour Point-of-Impingement standards are also 30 μg/m3; both were based on the odour effects of these compounds from information available in 1974.

The current ambient air quality criterion for DMDS in Ontario is 40 μg/m3 (one-hour average) and the half-hour Point-of-Impingement standard is 40 μg/m3; these were based on the odour effects of DMDS from information available in 1974.

The current ambient air quality criterion for methyl mercaptan in Ontario is 20 μg/m3 (one-hour average) and the half-hour Point-of-Impingement guideline is 20 μg/m3; both were based on the odour effects of methyl mercaptan from information available in 1977.

A review on the effects of TRS clearly indicates that adverse health effects on the CNS, respiration and respiratory system, and odour concerns are characteristic of reduced sulphur compounds. All of the reduced sulphur compounds of TRS are malodorous substances and that explains the odour concerns of TRS. In the last decade, a number of epidemiological studies have reported on the potential health effects of TRS. Results of these studies suggest that adverse effects developed in mid- and long-term exposure to TRS resemble those observed from exposure to H2S (e.g., irritation, respiratory and CNS effects). Data on acute exposure of humans or animals to TRS is not available. The few Finnish studies on small communities in Finland exposed to mixtures of reduced sulphur compounds from pulp mills reported that children exposed to low concentrations of TRS compounds over prolonged periods may be adversely affected with irritations to their eyes and the development of respiratory symptoms and cough and headaches (Marttilla et al., 1994; Marttilla et al., 1995; Partti-Pellinen et al., 1996). In one case, dose-related changes in the intensity of eye irritation, respiratory symptoms and headache for medium (10 to 30 µg/m3; daily mean concentrations) and high (>30 µg/m3) exposures were observed (Marttilla et al., 1995).

Data from these epidemiological studies may suggest a causal relationship between TRS exposure and the reported symptoms; however, with the constraints of experimental design, exposure information is inadequate for a detailed characterization of a dose-response relationship. The adverse effects of H2S have been extensively studied. With a lack of toxicological data for methyl mercaptan,


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DMS and DMDS, H2S may be the most appropriate surrogate compound for the development of health-based air standards for TRS.

Short-term exposure to H2S has been reported in many occupational studies to cause irritations to the eyes, nose, respiratory tract, and to induce CNS effects. Exposure to high concentrations has led to loss of consciousness (348 mg/m3) and may be death (>1390 mg/m3), likely a result of adverse effects on the respiratory centre in the brain. Acute exposures to much lower concentrations (7-278 mg/m3) of H2S have been reported to cause dose-dependent increases in irritation to the eyes and mucous membranes. Asthmatics acutely exposed (15 -30 minutes) to low levels (3-14 mg/m3) of H2S have been noted to experience bronchial constriction, while healthy volunteers exhibited a decrease in oxygen uptake in the blood, but only with exposure to 14 mg/m3. Studies examining acute effects with exposure to 7 mg/m3 of H2S reported a shift in metabolism in muscle from aerobic to anaerobic.

Epidemiological studies have reported that individuals exposed to low levels of H2S close to a source indicated an association between exposure and respiratory effects. However, the quality of these studies is poor as many of the studies have inadequately characterized the exposure and have small sample sizes. The WHO (1987) derived a health-based air guideline value of 150 µg/m3 based on the data from the study of Savolainen (1982) that reported eye irritation in exposed workers. The WHO updated their air guidelines in 2000 (WHO, 2000), however, no reassessment of the guideline value for H2S was conducted. Since the study of Savolainen (1982), a number of studies have reported observed adverse effects at H2S exposure concentrations below the LOAEL of 15 mg/m3 as reported in the Savolainen study (Savolainen, 1982).

Due to the poor data quality of the available human studies, data obtained from well controlled chronic animal studies, such as those of the CIIT (1983a) and Brenneman et al. (2000) have provided the basis for most of the health-based guidelines for H2S. The CIIT study (CIIT, 1983a) reported inflammation of the nasal mucosa in mice exposed to H2S for period of 90 days and identified a NOAEL of 42.5 mg/m3. The CalEPA has derived a health-based air guideline for H2S from the CIIT study (CIIT, 1983a). The U.S. EPA has derived a RfC from a NOAEL of 13.9 mg/m3 for nasal lesions of the olfactory mucosa in rats (Brenneman et al., 2000). These agencies rationalized the merits of the CIIT study (CIIT, 1983a) and the Brenneman et al. study (2000) in that the critical effect observed (nasal inflammation and lesions in the olfactory mucosa) had been noted in other animal studies as well as in humans following low level exposures to H2S. These clinical symptoms may be relevant to humans in low exposure situations.

Most of the observed adverse effects from acute H2S exposures occur at concentrations above the reported odour thresholds for this compound. This may account for the lack of acute health effect-based guidelines developed for H2S. The same may be true for methyl mercaptan, DMS and DMDS. It is likely that air standards developed based on the odour thresholds of reduced sulphur compounds may provide a sufficient margin of safety for the acute effects of TRS compounds.

Since TRS and its compounds are malodorous substances, and there are suggestions that odours may have psychological effects and neurological effects on


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sensitive individuals, odour-based guidelines should be developed to control the odour problems related to the emission of these compounds.

8.0 Decision

The development of health- and odour-based air standards for TRS is complex. There are several important factors that need to be considered when setting air standards for TRS and its compounds. First, components of reduced sulphur compounds in the TRS mixture have to be determined. Second, the composition is likely to vary depending on the nature of the industrial facilities (e.g., kraft pulp mills versus petrochemical plants). Hence, it may be reasonable to consider regional or source-specific conditions for TRS emissions in deriving air quality standards or in the implementation of these standards. Alternatively, in the situation where data concerning the composition of the TRS mixture is not available, one of the TRS compounds could be used as a surrogate to characterize the health and odour effects for TRS. The likely deficiency of this approach is the potential for either being overly conservative in assuming all of the TRS emissions are composed of this particular surrogate reduced sulphur compound, if using for example the odour threshold of methyl mercaptan (the TRS compound with the lowest odour threshold), or for underestimating the odour of the emissions by assuming all of the TRS emitted is due to one of the other TRS compounds (H2S, DMS, DMDS). A strategy to address the variability in the composition of reduced sulphur compounds can be developed by investigating the air release characteristics with information obtained from the NPRI and O. Reg. 127/01.

The Ministry of the Environment has reviewed and considered air quality standards and guidelines used by leading agencies worldwide. After reviewing additional toxicological and odour property information, the Ministry has developed effects-based standards and odour-based air standards and guidelines for TRS and its component compounds.

Health-based air standards

Considering the stakeholders’ comments and the vast database for hydrogen sulphide, a surrogate compound approach is the most appropriate method to develop health-based air standards for TRS and the various reduced sulphur compounds. Hydrogen sulphide is determined to be the surrogate in view of the Ontario air release data from the NPRI and emission inventory data reported under the O. Reg 127/01. The Ministry has considered that the poor data quality of available epidemiological studies does not provide sufficient confidence in air standards derivation. The endpoint of nasal lesions observed in the key animal studies, determined by the U.S. EPA and the CalEPA to derive their respective jurisdictional guidelines for H2S, is considered a consistent adverse effect in exposure to low doses of this reduced sulphur compound. The key study (Brenneman et al., 2000) determined by the U.S. EPA is considered to provide a more reliable basis than that of the CalEPA since a more recent study of quality was used and a low NOAEL of 13.9 mg/m3 for olfactory lesions was identified.


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The U.S. EPA has derived an RfC of 2 µg/m3. However, the Ministry considers that the uncertainty factor of 10, employed by the U.S. EPA, for the extrapolation from the subchronic to chronic exposure is excessive. The Ministry is in agreement with many jurisdictions that an uncertainty factor of 3 (101/2) for the extrapolation of subchronic to chronic exposure is sufficient. Therefore, a total uncertainty factor of 100 is applied to the NOAELHEC of 0.64 mg/m3 to yield a criterion of 7 µg/m3. This value of 7 µg/m3 becomes the 24-hour AAQC for H2S.

There is no sufficient toxicological data for the derivation of individual health-based air standards for methyl mercaptan, DMS or DMDS.

Sector-specific air standards for TRS

On the basis of available emission inventory information and source release characteristics, the Ministry is proposing to develop sector-specific air standards for TRS. The TRS air standards are developed for the pulp, paper and paper kraft mills (e.g. NAICS 3221) and for other industrial sources such as the iron and steel (NAICS 3311), petroleum and related products (NAICS 3241) and other sectors.


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Table 7 provides information on the release of TRS and H2S from major industrial sources in Ontario in the reporting year of 2003 (MOE, 2006b). There were 1,594 tonnes of TRS released to the air in Ontario from all sources. Considering only facilities that reported releases for both H2S and TRS, three major industrial sectors released a total of 1461.434 tonnes and accounted for approximately 92% of the total TRS released from all sectors. These three major sectors include the Pulp, Paper & Paperboard mills (NAICS 3221), Iron, Steel and Ferro-alloy (NAICS 3311) and the Petroleum & related products (NAICS3241). Approximately 60% of the total TRS releases from these three sectors were made up of H2S. Releases of H2S from the Pulp, Paper and Paperboard Mills sector contributed to approximately half (46%) of the TRS from this sector. Over 96% of the TRS releases were made up of H2S for the other two major sectors. Approximately 74% of the total TRS from these three major sectors were made up of releases from the pulp and paper kraft mills industry. On the basis of this air releases analysis, it is propsed to set TRS air standards for the pulp and paper kraft mills industry and the other industrial sources. For the pulp, paper and kraft mills industry, approximately half of TRS was made up of H2S, and based on the proposed H2S AAQC of 7 µg/m3, the 24-hour AAQC for TRS will become 14 µg/m3. For the other sectors, releases of TRS were almost totally comprised of H2S and therefore, the 24-hour AAQC of 7 µg/m3 for H2S will be used as the surrogate for the 24-hour AAQC for TRS.


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Table 7: Air Releases of TRS and H2S in Ontario

Industrial Sectors (NIACS) 2003 Reported Releases Iron, Steel and

Ferro-alloy (3311) Pulp, Paper & Paperboard mills (3221)

Petroleum & related products (3241)

Total of All 3 Major Sectors

H2S/TRS 355.348/362.47 495.699/1076.244 21.866/22.72 872.913/1461.434

% of H2S in TRS

98.04 46.06 96.24 59.73

Sector TRS/total TRS

362.348/1461.434 1076.244/1461.434 22.72/1461.434

% of Sector TRS/total TRS

24.8 73.64 1.55

Notes: Release quantities are presented in tonnes and only data from facilities reporting both TRS and H2S are used

Odour-based Air Standards and Guidelines

The Ministry has given careful consideration to two of five important factors which influence odour impacts, as a basis for recommending odour-based standards and guidelines. These two factors are intensity (referring to an individual’s perception of the odour strength or concentration) and offensiveness (which is a rating of the pleasantness or unpleasantness of an odour). They are two of five interacting factors, collectively known as FIDOL factors: Frequency, Intensity, Duration, Offensiveness and Location. The high offensiveness and high intensity factors are guiding the development of odour based standards (as opposed to guidelines) for TRS and some TRS compounds.

In addition, it is important to underline some important facts, observations and findings regarding the health effects of odour which emphasize that odour is not simply a nuisance effect. These are (discussed in more detail in Section 4.2, under the heading ‘Odour-based Approach for TRS Air Quality Guideline Development’) as follows:

• Characterizing odour effects as simply a nuisance effect may understate the possible health impacts of odours on individual and community health.

• It has been suggested that odourants may stimulate the trigeminal nerve and can increase the cortical blood flow, which may be partly responsible for the headaches that are one of the complaints associated with environmental exposure to odours.


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• The adverse health outcomes, consistent self-reporting of such health outcomes and the decrease in a sense of well-being in communities impacted by odours suggest that persistent exposure to unpleasant odours can have a significant impact on social behaviour and community health.

• Nonetheless, there appears to be a commonly observed relationship between the presence of odours in a community and incidents of reports of specific symptoms such as headaches, nausea, irritation of the eyes and throat, as well as worsening of conditions of asthmatics.

Air emissions of H2S and TRS from various sectors and the odour thresholds of the TRS components are the other factors used in developing odour-based standards and guidelines. Based on emission inventory data reported under Reg. 127 and from the NPRI, for the pulp, paper and kraft mills industry, approximately half of TRS was made up of H2S, and the rest of TRS is made up of methyl mercaptans, DMS and DMDS (Table 7). For the iron and steel sector and the petroleum and related compounds sector, most of the TRS is composed of H2S. The calculated geometric means of odour detection thresholds for H2S, methyl mercaptan, DMS and DMDS are 16.1, 11, 30 and 56.3, respectively. It is apparent that both H2S and methyl mercaptan (for mercaptans) are the two most odourous substances of TRS. Considering the emission inventory data and the odour thresholds of TRS compounds, the odour thresholds of H2S and methyl mercaptan provide the most appropriate basis for the development of odour standards for TRS. The geometric means of H2S and methyl mercaptan are used to calculate a combined geometric mean of 13.2 (or 13 with rounding) µg/m3. This combined geometric mean odour threshold of13 µg/m3 becomes the odour threshold for TRS. Thus, the 10-min odour-based standard for TRS is set to be 13 µg/m3 for all sectors.

In addition, as suggested by stakeholders, it would be reasonable at the practical level to have a circumstance, where compliance with the odour-based AAQC/standard for each or several of the individual TRS compounds assured compliance with the odour-based AAQC/standard for the overall TRS mixture. For this reason, the 10-min odour-based standards for H2S and mercaptans are also set at 13 µg/m3.

For DMS and DMDS, based on the geometric mean of the odour thresholds of the individual compounds, the 10-min odour-based guidelines are set at 30 and 56 µg/m3, respectively.

Summary of Recommended Air Standards and Guidelines

Several standards and guidelines have been developed for TRS and its compounds. Because of the extensive toxicological data base for hydrogen sulphide, this compound is used as the surrogate for the TRS health-based standards. Two sectoral TRS standards have been derived with reference to the amount of hydrogen sulphide in the TRS emissions. For some of the TRS compounds (i.e., DMS, DMDS


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and mercaptans), due to insufficient health information, no health-based standards are developed.

For these highly offensively odourous substances, odour standards (i.e., for TRS, H2S and mercaptans) or guidelines (i.e. for DMS and DMDS), have also been derived. Odour thresholds of the most prominent (i.e., hydrogen sulphide) and the most odourous (i.e., methyl mercaptan) species in TRS mixtures provide the primary basis for the TRS odour standards. Examining the half-hour standards derived from chronic health effects-based limits (i.e., from 24-hour health-based average limits) and from odour-based limits (i.e., from 10 minute odour-based average limits) found slightly lower values with the odour-based limits. Therefore, the half-hour standards derived from odour-based limits are considered to be protective for both health and odour effects.

Considering the toxicological information and the review of guidelines from other jurisdictions, adverse effects on the respiratory system such as lesions in the nasal and olfactory mucosa reported in inhalation animal studies are considered to be the most appropriate basis for recommending air quality standards for hydrogen sulphide. These animal studies also provided the basis of the United States Environmental Protection Agency’s guidelines for this substance.

Based on an evaluation of the scientific rationale of air guidelines from leading jurisdictions, an examination of current toxicological research and odour information and, comments from stakeholders, the Ministry is setting the following air quality standards for hydrogen sulphide:

• A 24-hour average Ambient Air Quality Criterion (AAQC) of 7 µg/m3 (micrograms per cubic metre of air) for hydrogen sulphide based on the adverse effects on the respiratory system (nasal lesions) of this compound; and

• A 10-minute average AAQC of 13 µg/m3 (micrograms per cubic metre of air) for hydrogen sulphide based on odour effects

• A half-hour standard of 10 µg/m3 (micrograms per cubic metre of air) for hydrogen sulphide based on both odour and health effects of this compound.

Also based on current toxicological research on the properties of hydrogen sulphide, odour information, amount of hydrogen sulphide in TRS emissions from various sectors and, comments from stakeholders, the Ministry is setting the following air quality standards for Total Reduced Sulphur (TRS):

For the Pulp and Paper sector:

• A 24-hour average AAQC of 14 µg/m3 (micrograms per cubic metre of air) for TRS based on the adverse effects on the respiratory system of this mixture; and


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• A 10-minute average AAQC of 13 µg/m3 (micrograms per cubic metre of air) for TRS based on odour effects


For all other sectors (includes sectors such as Iron & Steel; Petroleum Refineries, Municipal Sewage Treatment Plants):

• A 24-hour average AAQC of 7 µg/m3 (micrograms per cubic metre of air) for TRS based on the adverse effects on the respiratory system (nasal lesions) of this mixture; and

• A 10-minute average AAQC of 13 µg/m3 (micrograms per cubic metre of air) for TRS based on odour effects


Also, based on an evaluation of the scientific rationale of air guidelines from leading jurisdictions, an examination of current toxicological research and odour information and, comments from stakeholders, the Ministry is setting the following air quality standard for mercaptans (as methyl mercaptan):

• A 10-minute AAQC of 13 µg/m3 (micrograms per cubic metre of air) for mercaptans (as methyl mercaptan) based on odour effects

• A half-hour standard of 10 µg/m3 (micrograms per cubic metre of air) for mercaptans (as methyl mercaptan) based on odour effects

In addition, based on an evaluation of the scientific rationale of air guidelines from leading jurisdictions, an examination of current toxicological research and odour information and, comments from stakeholders, the Ministry is setting the following air quality guidelines for DMS and DMDS:

• A 10-minute AAQC of 30 µg/m3 (micrograms per cubic metre of air) for DMS based on odour effects

• A 10-minute AAQC of 56 µg/m3 (micrograms per cubic metre of air) for DMDS based on odour effects

Notes to TRS standards:

• Any facility releasing only one specific species of the four major components of TRS will not be considered for the release of TRS; rather the respective standard or guideline for this specific species will apply.



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• More information on the application of odour-based standards is set out in O. Reg. 419/05.

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 (except for the 10 minute odour-based AAQCs for DMS and DMDS) will be incorporated into Schedule 3 of O. Reg. 419/05; the half-hour standards 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 the above standards are 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);

• “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


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Smith, L.L. et al. 1976a. Toxicity of hydrogen sulfide to various life history stages of bluegill (Leopomis Macrochirus). Trans Amer Fish Soc 105(3):442-449. Cited In: CESARS, 2003.

Smith, L.L. et al. 1976b. Acute and chronic toxicity of hydrogen sulfide to the fathead minnow, Pimphales promelas. Environ Sci Technol 10(6):565-568. Cited In: CESARS, 2003.

Smith L.L. and Oseid, D. 1970. Toxic effects of hydrogen sulfide to juvenile fish and fish eggs. Proceeding of the 25th Industrial Waste Conference, May 5-7, 1970. Eng. Extension Series No. 137, Purdue University. Cited In: CESARS, 2003.

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10.0 Appendix A: Agency-Specific Reviews of Air Quality Guidelines

10.1 Agency-Specific Summary: Government of Canada

1. Name of Chemical:

Reduced Sulphur Compounds (CAS# N/A)

2. Agencies:

Canadian Environmental Protection Act (CEPA) under the auspices of Health Canada

3. Guideline Value(s):

No air quality guidelines for TRS or its primary components are listed in the Canadian Environmental Quality Guidelines (EQGs) (CCME, 1999). Draft values were derived in a 1992 document titled “Recommended Ambient Air Quality Objectives for Reduced Sulphur Compounds” (Federal-Provincial Advisory Committee on Air Quality, 1992); however, they were never finalized. No schedule has been identified for the finalization of the Air Quality Objectives for TRS.

Total reduced sulphur and its primary components have not been listed on the first Priority Substances List (PSL 1) or the second Priority Substances List (PSL 2). In addition, no health based tolerable daily intake values have been established for TRS or its primary components (Health Canada, 1996).

4. Application:

The Canadian EQGs, established by multi-jurisdictional groups as indicators of environmental quality, are intended to protect, sustain and enhance the quality of the Canadian environment. Provincial and territorial jurisdictions have the authority to implement the Canadian EQG’s. Implementation of the EQGs requires consideration of the local conditions.

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 PSL 1. Further to this, in 1995, PSL 2 was established and the 25 substances identified were scheduled to be evaluated over the upcoming years.

Some of the substances listed in Health Canada (1996) have Tolerable Daily Intake (TDI) values for non-carcinogenic effects, which are expressed on a body weight basis (e.g., mg/kg/day). These values are the total intake by ingestion, to


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5.

6.

which it is believed that a person can be exposed over a lifetime without deleterious effects.

Documentation Available:

No information.

Key Reference(s):

No information.

Peer Review Process and Public Consultation:

No information.

7.

8.

Status of Guideline:

Not applicable.

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

1.

Agency-Specific Summary: Federal Government of the United States

Name of Chemical:

Hydrogen Sulphide (CAS# 7783-06-4)

Agency:

U.S. Environmental Protection Agency (U.S. EPA)

Guideline Value(s):

An inhalation Reference Concentration (RfC) of 2 µg/m3 has been derived by the U.S. EPA.

Application:

The U.S. EPA, through the Integrated Risk Information System (IRIS), posts cancer and non-cancer exposure limits for the inhalation and oral routes of exposure which can be used towards the derivation of ambient air guidelines or standards by other jurisdictions. 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 that 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.


U.S. EPA. 2004. Integrated Risk Information System Hydrogen Sulfide. United States Environmental Protection Agency (U.S. EPA).

URL: http://www.epa.gov/iris/subst/0061.htm. Accessed: 8/5/2004.

Key Reference(s):

Brenneman, K.A., James, R.A., Gross, E.A., and Dorman, D.C. 2000. Olfactory neuron loss in adult male CD rats following subchronic inhalation exposure to hydrogen sulfide. Toxicol Pathol 28: 326-333.


Information provided in IRIS undergoes both internal and external peer review. The external review will range from letter reviews, to panel meetings, to SAB or other Federal Advisory Committee Act (FACA) review, based upon the judgment of the scientific complexity by the sponsoring Office. Although IRIS is not subject to notice and comment requirements of the Administrative Procedures Act, U.S. EPA posts the draft assessment on the internet for public viewing during the


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external peer review period. Any comments submitted are considered by the sponsoring Office. In some cases, U.S. EPA solicits public comment (e.g., prior to an SAB review, or for other program needs) when the assessment is posted.

A consensus review of IRIS Summaries and Toxicological Reviews is also conducted by senior health representatives of the Office of Research and Development, the U.S. EPA Program Offices and Regional Offices. The purpose of the consensus review is to obtain broad Agency consensus on: (1) whether a clear and logical explanation is given of how the conclusions and decisions in the assessment were reached; (2) how external peer review comments were addressed and incorporated; and (3) whether relevant U.S. EPA guidelines and science policy have been appropriately applied.

After incorporating comments from the consensus process and ensuring a scientifically complete and internally consistent set of documents, the sponsoring Office provides final draft documents for technical editing followed by a quality assurance approval by the IRIS Program Director and staff. The documents are then submitted to the IRIS webmaster for loading on IRIS.


Current.


The RfC is based on the assumption that thresholds exist for certain toxic effects. The inhalation RfC was derived from information provided in a 90-day vapour inhalation toxicity study in rats (Brenneman et al., 2000). A summary of the study and the derivation of the RfC are provided below. The LOAEL was determined to be 42 mg/m3 (30 ppm) for nasal lesions of the olfactory mucosa, and a NOAEL was determined to be 13.9 mg/m3 (10 ppm).

The NOAEL was obtained from a 10-week inhalation toxicity study conducted using 10-week old male CD rats. Twelve rats per group were exposed to H2S vapour for 6 hours/day, 7 days/week for 10 weeks at 0, 10, 30 or 80 ppm (0, 13.9, 42 or 111 mg/m3).

At the end of the 10-week exposure, animals were euthanized and nose cavities were examined a 6 different sectional levels for lesions. Lesions were graded in severity with a scale of 0 to 4, indicating normal to severe. No effects were observed in the control group or the 10 ppm dose group. Nasal lesions of the olfactory mucosa were noted at the 30 ppm and the 80 ppm dose groups. Lesions included multifocal, bilaterally symmetrical olfactory neuron loss and basal cell hyperplasia affecting the lining of the dorsal medial meatus and dorsal and medial region of the ethmoid recess. These lesions were rated mild to severe. Olfactory neuron loss was observed only at the 80 ppm dose in section level 3 of the nose where the most rostral margin of the olfactory epithelium is integrated with the rostral portion of the respiratory epithelium. Mild to moderate olfactory neuron loss occurred in section level 4 of the animals in the 30 ppm


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dose group; intensity of lesions increased to moderate to severe in the 80 ppm dose group.

Basal cell hyperplasia in section level 4 was noted in both the 30 and 80 ppm dose groups but more pronounced in the 30 ppm dose group. In section level 5 of animals of the 30 and 80 ppm dose groups, mild to moderate olfactory neuron loss and mild basal cell hyperplasia mainly affecting the nasal septum, dorsal nasal cavity and marginal ethmoturbinate were observed. The nasal septum was not affected in the 30 ppm dose group. In section level 6, similar pattern and severity of lesions were noted only in the 80 ppm dose group. None of these lesions was observed in the control or the 10 ppm dose groups.

The RfC was derived from the NOAEL that was adjusted to take into account species difference and uncertainty factors. In this inhalation study, the rats were exposed to H2S for 6 hours per day, 7 days per week for 10 weeks. The NOAEL was adjusted to represent a continuous exposure scenario (e.g., 24 hours per day, 7 days per week) using the following calculation:

NOAELADJ: 13.9 mg/m3 x 6 hours/24 hours x 7 days/7 days = 3.48 mg/m3

Given that the NOAEL was determined in rats, the NOAEL is multiplied by a regional gas dose ratio in the extrathoracic region of the respiratory tract (RGDRET) to determine the Human Equivalent Concentration (HEC). The NOAELHEC takes into account dosimetric differences between humans and rats for gases with respiratory effects.

The NOAELHEC was calculated as follows:

NOAELHEC = NOAELADJ x RGDRET = 0.64 mg/m3

Where:

RGDRET = (MVa/Sa)/(MVh/Sh) = 0.184

Minute ventilatory volume for experimental animal species (MVa) = 0.131 m3

MVh - Minute ventilatory volume for human (MVh) = 20 m3

Surface area of tracheobronchial region for experimental animal species (SaET) = 15.0 cm2 Surface area (in cm2) of extrathoracic region for human (ShET) = 200 cm2

A total uncertainty factor of 300 was applied to the NOAEL(HEC), including a factor of 10 to protect sensitive individuals, a factor of 10 to adjust from a subchronic to a chronic exposure, and a factor of 3 for interspecies conversion.

RfC = NOAELHEC/UF = 2x10-3 mg/m3 or 2 µg/m3

Therefore the inhalation RfC for H2S was set at 2 µg/m3.


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Key Risk Management Considerations:

The inhalation RfC is an estimate of a daily inhalation exposure of the human population, including sensitive subgroups that are likely to be without an appreciable risk of deleterious effects during a lifetime.

Multimedia Considerations of Guidelines:

The oral RfD of 3x10-3 mg/kg/day, based upon reported gastrointestinal disturbances in pigs when H2S was present in their diet, was withdrawn from IRIS in 2003 after re-evaluation of the key oral study in pigs. The key study of Wetterau et al. (1964) was considered to be marginal in its characterization of exposure and effects on pigs.

Other Relevant Factors:

The overall U.S. EPA confidence in the inhalation RfC is medium to high. The study was assigned a medium confidence rating because it was a subchronic study and only male animals were used. The confidence in the database was rated medium to high because it addresses reproductive and developmental effects as well as examines target tissues of H2S exposure such as neurological tissues and tissues at port-of-entry.


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10.3 Agency-Specific Summary: State of California

Name of Chemical: Hydrogen Sulphide (CAS# 7783-06-4)

Agency: California Air Resources Board (ARB), Office of Environmental Health Hazard Assessment (OEHHA)

Guideline Value(s):

An acute Reference Exposure Level (REL) of 42 µg/m3 has been established based on odour.

A chronic REL of 10 µg/m3 has been set based on nasal histological changes observed in mice.

An ambient air quality standards has been set at 0.03 ppm (42 µg/m3) for a 1-hour average by the ARB.

Application:

The reference exposure levels (RELs) were obtained from tables available on the OEHHA website. The development and application of the values are described in the OEHHA documents Air Toxics “Hot Spots” Program Risk Assessment Guidelines Part I: Technical Support Document for The Determination of Acute Reference Exposure Levels for Airborne Toxicants and Part III: Technical Support Document for The Determination of Chronic Reference Exposure Levels for Airborne Toxicants. The REL’s are used in the Air Toxic’s “Hot Spots” Program as indicators of the potential adverse health effects of chemicals. The REL’s are not air quality guidelines.


Collins, J. and Lewis, D. 2000. Hydrogen Sulfide: Evaluation of Current California Air Quality Standards with Respect to Protection of Children. Prepared for: California Air Resources Board, Hazard Assessment.

OEHHA. 1999. Air Toxics "Hot Spots" Program Risk Assessment Guidelines Part I: Technical Support Document for The Determination of Acute Reference Exposure Levels for Airborne Toxicants

OEHHA. 2000. Air Toxics "Hot Spots" Program Risk Assessment Guidelines Part III: Technical Support Document for The Determination of Chronic Reference Exposure Levels for Airborne Toxicants


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Key Reference(s):

Amoore, J.E. 1985. The perception of hydrogen sulfide odour in relation to setting an ambient standard. California Air Resources Board Contract A4-046-33. Cited In: OEHHA, 1999.

California State Department of Public Health. 1969. Recommended Ambient Air Quality Standards. HS-3. Cited In: OEHHA, 1999.

California Air Resources Board (CARB). 1984. Report of the committee regarding the review of the AAQS for hydrogen sulfide. Memorandum from CARB to G. Duffy. Cited In: OEHHA, 1999.

CIIT. 1983a. 90-Day vapor inhalation toxicity study of hydrogen sulfide in B6C3F1 mice. Cited In: OEHHA, 2000.

Reynolds, R.L. and Kamper, R.L. 1984/1985. Review of the State of California Ambient Air Quality Standard for Hydrogen Sulfide. Lakeport (CA): Lake County Air Quality Management District. Cited In: OEHHA, 1999.


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.


Current.


Acute REL

The acute REL (which is numerically equivalent to the California Ambient Air Quality Standard) for H2S was originally based on an olfactory perception study conducted by the California State Department of Public Health. The study involved exposing sixteen individuals to increasing concentrations of H2S until their odour threshold was reached (California State Department of Public Health, 1969). The range of odour thresholds was 0.012 - 0.069 ppm, with a geometric mean of 0.029 ppm. A value of 42 µg/m3 (0.03 ppm) was chosen as the REL, as no uncertainty factors were applied. However, the CalEPA notes that there have been reports of headaches and other symptoms at the level of the standard (42 µg/m3) (OEHHA, 1999). Therefore, California has concluded that this acute REL may need to be re-examined as more data becomes available.


Chronic REL

The chronic REL is derived from the results of a 90-day vapour inhalation toxicity study in mice (OEHHA, 2000).

Summary of 90-day Subchronic Inhalation Study

A 90-day vapour inhalation toxicity study was conducted using B6C3F1 mice exposed to hydrogen sulphide vapour (CIIT, 1983a). Three groups of mice consisting of 10 males and 12 females each were exposed to H2S at TWA concentrations of 14.1 mg/m3 (10.1 ppm), 42.5 mg/m3 (30.5 ppm), and 110 mg/m3 (80 ppm). A control group of 10 males and 12 females was exposed to clean air. All groups were exposed 6 hours/day, 5 days/week for 90 days.

During the exposure period, mice were observed twice daily for mortality and clinical signs. In addition, the mice were examined and weighed weekly. Prior to necropsy, the eyes were examined and an evaluation of neurological function (posture, gait, facial muscle tone, and reflexes) was conducted. Urine and blood samples were collected and the following tissues and organs examined during necropsy: external surfaces, orifices and organs, cranial cavity, carcass, brain, spinal cord, thoracic, pelvic and abdominal cavities and their viscera, cervical tissues and organs.

At a H2S level of 110 mg/m3 (80 ppm), there was a significant depression of body weight gain in both sexes. Examination of the eyes revealed no abnormalities. Urine and blood data showed no significant differences in comparison to the controls. At necropsy, no gross lesions were identified that were attributed to exposure to H2S. However, as part of the histopathology study, an exposure-related lesion was identified in the high exposure group (110 mg/m3). The lesion was observed in 8/9 male and 7/9 female mice and consisted of inflammation of the nasal mucosa in the anterior segments of the nose. The lesion was generally minimal to mild in severity and was located in the anterior portion of the nasal structures, primarily in the squamous portion of the nasal mucosa, but extended to areas covered by the respiratory epithelium. This lesion was not observed in any animals in other exposure groups. Therefore, in mice, 110 mg/m3 (80 ppm) is considered a LOAEL for nasal inflammation, and 42.5 mg/m3 (30.5 ppm) is a NOAEL.

Derivation of Chronic REL

In order to calculate the REL, the NOAEL is adjusted to take into account species difference and uncertainty factors. In the inhalation study, the mice were exposed to H2S for 6 hours per day, 5 days per week. The NOAEL was adjusted to represent a continuous exposure scenario (e.g., 24 hours per day, 7 days per week) using the following calculation:


Given that the NOAEL was determined in mice, the NOAEL is multiplied by a regional gas dose ratio in the extrathoracic region of the respiratory tract

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(RGDRET) to determine the Human Equivalent Concentration (HEC). The NOAELHEC takes into account dosimetric differences between humans and mice for gases with respiratory effects. The NOAELHEC was calculated as follows:


Where:




Surface area of tracheobronchial region for experimental animal species (SaET) = 3.0 cm2 Surface area (in cm2) of extrathoracic region for human (ShET) = 200 cm2

California applied an uncertainty factor of 100. The UF includes a factor of 3 to adjust from subchronic to chronic exposure, a factor of 3 for interspecies conversion and a factor of 10 for intraspecies conversion. As a result, the calculated chronic REL is 10 µg/m3.

Chronic REL = NOAELHEC/UF = 10 µg/m3


No information.


No information.


No information.

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10.4 Agency-Specific Summary: Commonwealth of Massachusetts


Agency: Massachusetts Department of Environmental Protection

Guideline Value(s):

The Threshold Effects Exposure Level (TEL) and Allowable Ambient Limit (AAL) derived by Massachusetts are 1 µg/m3.

A number of guideline values have been proposed by Massachusetts. A value of 10 µg/m3 has been proposed as the subchronic TEL. A value of 93 µg/m3 has been proposed as the acute TEL for a 30-minute period and 10 µg/m3 for a 1- to 24-hour period.

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.”


Office of Research and Standards. 1995. Memorandum. Revised Air Guidelines. Commonwealth of Massachusetts, Department of Environmental Protection.

Massachusetts Department of Environmental Protection (MADEP). 1995. Massachusetts Allowable Threshold Concentrations.

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MADEP. 2001. Hydrogen Sulfide (CAS Reg. No. 7783-06-04), Chronic, Subchronic and Acute Inhalation Exposure Guidelines, Draft Document. MADEP, Office of Research and Standards.

Key Reference(s):

U.S. EPA. 2002. Integrated Risk Information System Hydrogen Sulfide. United States Environmental Protection Agency (U.S. EPA). URL: http://www.epa.gov/iris/subst/0061.htm.


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 were employed in the development of the TEL and AAL values. Specifically, evidence from the International Agency for Research on Cancer (IARC), the American National Toxicology Program (NTP) and the U.S. EPA was used. As guidelines, the process used and values generated are not subject to the extensive review and consultation to which air quality standards would be subjected. However, external peer reviews on the Massachusetts methodology and guideline documentation have been carried out and public input was solicited at a minimum of two public meetings on the Massachusetts methodology and guideline document.


The guideline values identified for Massachusetts are current.


Chronic Threshold Effects Exposure Level (TEL) and Allowable Ambient Limit (AAL)

Study Summary

The chronic TEL and AAL were derived from the same study that was used by the U.S. EPA to develop a RfC. A summary of the study and the derivation of the TEL/AAL is provided below. The LOAEL was determined to be 110 mg/m3 (80 ppm) for nasal inflammation, and a NOAEL was determined to be 42.5 mg/m3 (30.5 ppm).

The NOAEL was obtained from a 90-day vapour inhalation toxicity study conducted using B6C3F1 mice exposed to hydrogen sulphide vapour. Three groups of mice consisting of 10 males and 12 females were exposed to H2S at TWA concentrations of 14.1 mg/m3 (10.1 ppm), 42.5 mg/m3 (30.5 ppm), and 110 mg/m3 (80 ppm). A control group consisting of 10 males and 12 females were exposed to clean air. The duration of exposures was 6 hours/day, 5 days/week for 90 days.

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During the exposure period, the mice were observed twice daily for mortality and clinical signs. The mice were examined and weighed weekly. Prior to necropsy, the eyes were examined and an evaluation of neurological functions (posture, gait, facial muscle tone, and reflexes) was conducted. Urine and blood samples were collected from the mice and the following tissues and organs were examined during necropsy: external surfaces, orifices and organs, cranial cavity, carcass, brain, spinal cord, thoracic, pelvic and abdominal cavities and their viscera, cervical tissues and organs.

At a H2S level of 110 mg/m3 (80 ppm), there was a significant depression of body weight gain in both sexes. Examination of the eyes revealed no abnormalities. Urine and blood data showed no significant differences in comparison to the controls. At necropsy, no gross lesions were identified that were attributed to exposure to H2S. However, as part of the histopathology study, an exposure-related lesion was identified in the high exposure group (110 mg/m3 (80 ppm)). The lesion was observed in 8/9 male and 7/9 female mice and consisted of inflammation of the nasal mucosa in the anterior segments of the nose. The lesion was generally minimal to mild in severity and was located in the anterior portion of the nasal structures, primarily in the squamous portion of the nasal mucosa, but extended to areas covered by the respiratory epithelium. This lesion was not observed in any animals in other exposure groups. Thus, for mice, 110 mg/m3 (80 ppm) is considered a LOAEL for nasal inflammation, and 42.5 mg/m3 (30.5 ppm) is a NOAEL.

Development of Chronic TEL/AAL

The methodology for deriving allowable ambient limits is summarized in a document developed by the Massachusetts Department of Environmental Protection entitled “The Chemical Health Effects Assessment Methodology and the Method to Derive Allowable Ambient Limits”.

In order to calculate the TEL/AAL, the NOAEL is adjusted to take into account species difference and uncertainty factors. In the inhalation study, the mice were exposed to H2S for 6 hours per day, 5 days per week. The NOAEL was adjusted to represent a continuous exposure scenario (e.g., 24 hours per day, 7 days per week) using the following calculation:


Given that the NOAEL was determined in mice, the NOAEL is multiplied by a regional gas dose ratio in the extrathoracic region of the respiratory tract (RGDRET) to determine the Human Equivalent Concentration (HEC). The NOAELHEC takes into account dosimetric differences between humans and mice for gases with respiratory effects. The NOAELHEC was calculated as follows:

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92


Where:




Surface area of tracheobronchial region for experimental animal species (SaET) = 3.0 cm2

Surface area of extrathoracic region for human (ShET) = 200 cm2

The HEC was then divided by the square root of 10 for an interspecies uncertainty factor adjustment. Further uncertainty factors of 10 to protect high-risk groups and 10 to adjust from subchronic to chronic exposure were also applied. To account for inadequacies in the database the value was then divided by the square root of 10.

Adjustment for uncertainty factors = 1.01 mg/m3 /(10 x 10 x square root of 10) = 0.00319 mg/m3

Adjustment for inadequacies in the database = 0.00319 mg/m3 / square root of 10 = 0.001 mg/m3 TEL = AAL = 1 µg/m3 (0.001 mg/m3)

Therefore, the inhalation TEL and AAL for H2S was set at 1 µg/m3.

The Chemical Health Effects Assessment Methodology and the methodologies used by the U.S. EPA were consistent, which resulted in the TEL, AAL and RfC being equal.

Proposed Subchronic Threshold Effects Exposure Level (TEL)

The subchronic TEL is derived from the same information and using the same methodology as the chronic TEL. However, a factor of 10 that was applied for the chronic TEL to adjust for subchronic to chronic exposure was not required, and therefore not applied, for the subchronic TEL.

Proposed Acute Threshold Effects Exposure Level (TEL)

The 30-minute acute TEL was based upon a study conducted to assess the effects of low concentrations of H2S on respiratory function (Jappinen et al., 1990). The study involved two groups. The first was comprised of 26 male pulp mill workers


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(mean age of 40.3 years, range of 22 to 60 years) with daily exposure to H2S usually at a concentration below 10 ppm. The second group included 7 women (mean age 44.1 years, range 31 to 61 years) and 3 men (mean age 40.7 years, range 33 to 50 years) with bronchial asthma. The respiratory function and bronchial responsiveness of the pulp mill workers was measured after at least one day off work and at the end of a workday. The asthmatic subjects were exposed for 30 minutes to a H2S concentration of 2.8 mg/m3 (2 ppm) and the airway resistance, specific airway conductance and ventilatory capacity were measured. No significant change in respiratory function or bronchial responsiveness related to exposure to H2S in the pulp mill workers was found. Three of the 10 asthmatic subjects complained of headaches. In addition, on average the airway resistance increased and the specific airway conductance decreased, although, these changes were not statistically significant.

Based upon this study, a LOAEL of 2.8 mg/m3 was determined for bronchial obstruction and headache in asthmatics. An uncertainty factor of 30 was applied, 10 for the use of the NOAEL and 3 for human variability to result in a value of 93 µg/m3. The value of 93 µg/m3 was chosen as a 30-minute acute TEL given that the study upon which the value was based exposed subjects for 30 minutes and those adverse effects were associated with exposure to 42 µg/m3 for a 1-hour duration.

Available data for short-term low-level exposure to H2S at various time points were considered to be insufficient to develop an acute 1- to 24-hour TEL. Therefore, the subchronic TEL of 10 µg/m3 has been adopted as the 1- to 24-hour TEL.


No information.


The ATC is typically equal to 5 times the TEL to eliminate the multi-media exposure factor. However, certain TELs (such as that for H2S) do not incorporate a multi-media exposure factor into the TEL and therefore, the TEL and ATC are equal. The TEL for H2S did not incorporate a multi-media exposure adjustment, as it was determined that the majority of exposures occur via inhalation [Based on information provided by Diane Manganaro, Department of Environmental Protection, by e-mail on October 15, 2002).


No information.


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10.5 Agency-Specific Summary: State of Michigan


Agency: Department of Environmental Quality (DEQ), Environmental Science and Services Division (previously known as the Air Quality Division’s Toxics Unit)

Guideline Value(s):

An Initial Threshold Screening Level (ITSL) of 1 µg/m3 is listed as a 24-hour value.

Application:

Screening levels are developed by the Air Quality Division’s Toxics Unit for the implementation of the Michigan’s air toxic rules. The air toxic rules apply to any new or modified process for which an application for a permit to install is required, and which emits a toxic air contaminant. The air toxics rules require that each source must apply the best available technology for toxics (T-BACT) and the maximum ambient concentration of each toxic air contaminant cannot exceed its screening level.


DEQ. 2002. Procedures for Developing Screening Levels.

DEQ. 2002. Michigan Air Toxics System. Initial Threshold Screening Level/Initial Risk Screening Level (ITSL/IRSL). December 2, 2002.

Key Reference(s):

U.S. EPA. 2002. Integrated Risk Information System Hydrogen Sulfide. United States Environmental Protection Agency (U.S. EPA).

URL: http://www.epa.gov/iris/subst/0061.htm


Not applicable.


The guideline is current.

http://www.epa.gov/iris/subst/0061.htm


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The ITSL is based upon the RfC developed by the U.S. EPA. When the U.S. EPA establishes a RfC, and there is no indication that the chemical is carcinogenic, then the ITSL is set at a value equal to the RfC and no further evaluation is done.


No information.


No information.


No information.


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10.6 Agency-Specific Summary: State of North Carolina

Name of Chemical: Hydrogen Sulphide (CAS# 7783-06-4) and Methyl Mercaptan (CAS# 74-93-1)

Agency: North Carolina Department of Environment and Natural Resources (NCDENR), Division of Air Quality (DAQ)

Guideline Value(s):

The H2S 1-hour acceptable ambient air level is set at 2.1 mg/m3.

The methyl mercaptan 1-hour acceptable ambient air level is set at 0.05 mg/m3.

Application:

The acceptable ambient air level is a product of initial recommendations by the North Carolina Scientific Advisory Board (N.C. SAB) from which averaging times are assigned by the staff of the Toxics Protection Branch. These toxic air pollutant values are considered to be 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.


North Carolina Scientific Advisory Board (N.C. SAB). 2001. Summary of the toxicity assessment of hydrogen sulfide conducted by the Secretary’s Scientific Advisory Board on Toxic Air Pollutants.

North Carolina Department of Environment and Natural Resources (NCDENR). 1986. Methyl Mercaptan Worksheet. Division of Air Quality.

Key Reference(s):

Brenneman, K., James, A., Gross, EA., and Dorman, D. 2000. Olfactory neuron loss in adult male CD rats following subchronic inhalation exposure to hydrogen sulfide. Toxicolc Pathol 28: 326-333.

Jappinen, P., Vilkka, V., Marttila, O. And Haahtela, T. 1990. Exposure to hydrogen sulphide and respiratory function. Br J Ind Med 47: 824-828.

Vanhoorne, M., Van den Berge, L., Devreese, A., Tutgat, E, Van Poucke, L. And Van Peteghem, C., 1991. Survey of chemical exposures in a viscose rayon plant. Ann Occup Hyg. 35(6):619-631.



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The N.C. SAB’s recommendations are passed to the NCDENR through the Toxics Protection Branch after allowing time for public comment. The proposed guidelines are then forwarded to the Rules Development Branch of the DAQ Planning Section for further public comment and eventual rule implementation.


The H2S Acceptable Ambient Level (AAL) is under review at the request of the NCDENR. The Secretary’s Scientific Advisory Board on Toxic Air Pollutants evaluated the toxicity of H2S and recommended the AAL based upon several health endpoints. The bases of the recommended AALs are discussed below.

The methyl mercaptan AAL was set in 1986 and has not been reviewed since.


Current Hydrogen Sulphide Guideline

The current 2.1 mg/m3 1-hour AAL is based on the ACGIH-STEL of 21 mg/m3 (15 ppm) for occupational exposures. The ACGIH-STEL was developed to minimize the potential for eye and respiratory tract irritation, symptoms of fatigue, headache, and dizziness, and central nervous system effects such as paralysis of the respiratory center and sudden death (ACGIH, 2001c).

The AAL was derived by applying a safety factor of 10 to the ACGIH-STEL. The health basis for the AAL is identified as acute irritant effects including respiratory irritation and eye effects (N.C. SAB, 2001).

Hydrogen Sulphide Guidelines Under Review

The N.C. SAB evaluated the toxicity of H2S and have recommended a 1-hour AAL guideline and two 24-hour AAL guidelines.

Recommended 1-Hour AAL

The recommended 1-hour AAL of 56 Fg/m3 (0.04 ppm) is based on observed human respiratory effects in a study conducted by Jappinen et al. (1990) (N.C. SAB, 2001).

This study assessed the effects of low concentrations of H2S on respiratory function. The study involved two groups. The first group was comprised of 26 male pulp mill workers (mean age of 40.3, range of 22 to 60 years) with daily exposure to H2S usually below 10 ppm. The second group included 10 individuals with bronchial asthma, seven women (mean age 44.1 years, range 31 to 61 years) and three men (mean age 40.7 years, range 33 to 50 years). The respiratory function and bronchial responsiveness of the pulp mill workers was measured after at least one day off work and at the end of a workday. The asthmatic subjects were exposed for 30 minutes to a H2S concentration of 2.8 mg/m3 (2 ppm) and the airway resistance, specific airway conductance and ventilatory capacity were measured. No significant changes in respiratory


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function or bronchial responsiveness related to exposure to H2S in the pulp mill workers were found. In the asthmatic subjects, on average the airway resistance increased and the specific airway conductance decreased, although, these changes were not statistically significant. A LOAEL was determined to be 2.8 mg/m3 (2 ppm).

Derivation of 1-Hour Guideline

The LOAEL was adjusted to account for the extrapolation from a LOAEL to a NOAEL (5), and inter-individual variability (10). The derived 1-hr value was calculated as follows:

2.8 mg/m3 / 50 = 0.056 mg/m3.

Recommended 24-Hour AAL’s

The high-end recommended 24-hour AAL of 120 µg/m3 (0.083 ppm) is based on the results of a subchronic rat inhalation exposure study by Brenneman et al. in 2000 (N.C. SAB, 2001).

Hydrogen sulphide was administered via inhalation to groups of 10-week old male CD rats at concentrations of 0, 14, 42 or 112 mg/m3 (0, 10, 30 or 80 ppm) H2S for 6 hours/day, 7 days/week for 10 weeks. Each group consisted of 12 rats. After euthanisation, a histological evaluation of the nasal cavity was conducted to identify exposure-related lesions. Nasal lesions related to H2S exposure were limited to the olfactory mucosa and consisted of multifocal, bilaterally symmetrical olfactory neuron loss and basal cell hyperplasia affecting the lining of the dorsal medial meatus and the dorsal and medial regions of the ethmoid recess. Exposure-related effects were observed at 42 mg/m3 (30 ppm) and 112 mg/m3 (80 ppm), affecting approximately 50% and 70% respectively, of the olfactory mucosa at these exposure concentrations. Changes in the olfactory epithelium in the control group and the group exposed to 14 mg/m3 (10 ppm) were similar. The NOAEL for olfactory lesions was determined to be 14 mg/m3 (10 ppm).

Derivation of High-End 24-Hour Guideline

The NOAEL was determined to be 14 mg/m3 (10 ppm). The NOAEL was adjusted to account for continuous exposure time (24/6), interspecies variability (3), and inter-individual variability (10). The 24-hr value was calculated as follows: 14 mg/m3/120 = 0.12 mg/m3.

The low-end recommended 24-hour AAL of 0.033 Fg/m3 is based on a study by Vanhoorne, 1991 of eye pain experienced by exposed workers in the viscose rayon industry (N.C. SAB, 2001).

Levels of CS2 and H2S were measured in a viscose rayon factory using stationary and personal monitoring equipment. Personal samples were collected gradually over 5 years. The background level of H2S in the factory was determined to be 9.8 mg/m3 (7 ppm).


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The LOAEL identified by the NCDENR of 13.7 mg/m3 (9.8 ppm) is not referenced in the Vanhoorne (1991) and may have been obtained from a different article that used information from the same study.

Derivation of Low-End 24-Hour Guideline

A LOAEL was determined to be 13.7 mg/m3 (9.8 ppm). The LOAEL was adjusted to account for discontinuous exposure (4.2), for the extrapolation from a LOAEL to a NOAEL (10), and inter-individual variability (10). The 24-hr value was calculated as follows: 14 mg/m3/420 = 0.033 mg/m3.

Methyl Mercaptan

In North Carolina, pollutants are categorized into 1 of 4 types based on toxicity - carcinogen, chronic, acute systemic or acute irritant. Methyl mercaptan was classified as an acute systemic toxicant. Given this classification, the AAL was developed by using the ACGIH TLV-TWA of 1 mg/m3. The TLV-TWA for methyl mercaptan was developed to protect against the objectionable odour of methyl mercaptan, as well as headache, nausea, eye and mucous membrane irritation and possible CNS effects.

The North Carolina AAL was derived by adding a factor of 10 to account for variation in susceptibility and a factor of 2 to take into account the severity of the effects. The derived AAL was calculated as follows:

1 mg/m3 /20 = 0.05 mg/m3.


In the development of the recommended AAL, odour was not considered as a basis for setting the AAL as odour nuisance regulations in North Carolina serve to protect citizens impacted by industrial emissions of H2S.


AALs are intended to be incremental exposure values and represent exposure values that would add to the “background” exposures that occur as a result of other natural or man-made processes.


No information.


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10.7 Agency-Specific Summary: State of Texas


Agency: Texas Natural Resource Conservation Commission (TNRCC)

Guideline Value(s):

Emissions of H2S cannot exceed net ground level concentrations of 115 µg/m3 (0.08 ppm) (30-min averaging) if residential, business of commercial properties are downwind. The emission of H2S cannot exceed net ground level concentrations of 173 µg/m3 (0.12 ppm) (30-min average) if industrial and vacant tracts and rangelands not normally occupied by people are downwind.

Application:

The TNRCC is involved in regulating the allowable off-property concentrations (ambient standards). Hydrogen sulphide controls are identified in the Texas Administrative Code, Title 30, Part 1, Chapter 112, Subchapter B, Rule 112.31-112.34. Under Rule 112.31 the emission of H2S cannot exceed net ground level concentrations of 0.08 ppm (30-min averaging) if residential or businesses of commercial properties are downwind. Under Rule 112.32 the emission of H2S cannot exceed net ground level concentrations of 0.12 ppm (30-min average) if industrial and vacant tracts and range lands not normally occupied by people are downwind. Rule 112.33 identifies the calculation methods by which the net ground level concentrations may be determined. Rule 112.34 indicates that Rules 112.31 to 112.34 are in force immediately.


Texas. 1976. Texas Administrative Code, Title 30 - Environmental Quality, Part 1 - Texas Commission on Environmental Quality, Chapter 112 - Control of Air Pollution from Sulfur Compounds, Subchapter B - Control of Hydrogen Sulfide, Rule 112.31, effective January 1, 1976.

TNRCC. 1999. TNRCC Regulatory Guidance. Hydrogen Sulfide.

Hydrogen Sulfide Rules. Undated. Provided by Alan Henderson in October, 2002. Texas Commission on Environmental Quality.

Key Reference(s):

No references.


Due to the date of the standard (1968), information pertinent to its development was not obtained.


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The guideline is current. In 1992, the Texas Air Control Board attempted to lower the odour based net ground level concentration from 115 µg/m3 to 14 µg/m3 (30-minute period), however the proposal was not adopted.


No information.


No information.


No information.


No information.


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


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

Guideline Value(s):

A 24-hour Time Weighted Average (TWA) of 150 µg/m3 has been set for effects other than cancer or odour/annoyance by both WHO-Europe and WHO-PHE. In addition to their 24-hour value, WHO-Europe has established a 30-minute average guideline of 7 µg/m3 to prevent substantial complaints of odour annoyance.

Application:

The objective of the WHO Guidelines for Air Quality is to help countries derive their own national air quality standards for protection of human health from air pollution. The guidelines are not intended to be standards.


WHO. 1999. Air quality guidelines. Protection of the Human Environment, World Health Organization, Geneva.

URL: www.who.int/peh/air/Airqualitygd.htm

WHO. 2000. Air quality guidelines for Europe. World Health Organization (WHO), Regional Office for Europe, Copenhagen. 2nd Edition. WHO regional publications, European Series, #91.

or URL: http://www.who.dk/air/Activities/20020620_1

Key Reference(s):

Savolainen, H. 1982. Nordiska expertguppen for gransvardesdokumentation. 40. Dihyrgensulfid [Nordic expert group for TLV evaluation. 40. Hydrogen sulfide]. Arbeta och hdlsa 31:1-27.


No information.


Current.

http://www.who.dk/air/Activities/20020620_1


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The 24-hour TWA guideline was based on conclusions identified by the Nordic Expert Group in 1982 during their development of occupational exposure limits. The Nordic Expert Group concluded that a threshold of 14 mg/m3 (10 ppm) for eye irritation should be taken into consideration in the establishment of an occupational limit. The threshold limit was based on Savolainen (1982) in which a Lowest-Observed-Adverse-Effect Level (LOAEL) of 15 mg/m3, was identified for eye irritation (WHO, 2000). The TWA was derived by applying a safety factor of 100. This safety factor was applied to address the steep rise in the dose-effect curve, as implied by reports of serious eye damage at 70 mg/m3 (WHO, 2000).

The 7 µg/m3 30-minute average was based on the odour level at which substantial complaints are likely to occur among the persons exposed (WHO, 2000).


The WHO guidelines are not intended to be standards. The WHO recommends that in moving from guidelines to standards, prevailing exposure levels and environmental, social, economic and cultural conditions in a nation or region should be taken into account.


No information.


In development of these guidelines, the size of uncertainty factors applied to published data in deriving a guideline was considered to be a matter for expert judgement, rather than prescription. Where the database was strong, smaller uncertainty factors were used than where the database was weak. Database strength depends upon the availability of published studies relevant to the circumstances of a country for which the guidelines are intended. In moving from guidelines to country-specific standards, the size of the uncertainty factors may require revision.


104

11.0 Appendix B: Acronyms, Abbreviation, and Definitions

AAL Allowable Ambient Level (Massachusetts)

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

ACGIH American Conference of Governmental Industrial Hygienists - a non-governmental organization that 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 U.S. Department of Health and Human Services

BCF Bioconcentration Factor

Blepharospasm Tonic spasm of the orbicularis oculi muscle, producing more or less complete closure of the eyelids

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

CEPA Canadian Environmental Protection Act

CNS Central Nervous System

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

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

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


105

DMS Dimethyl Sulphide

DMDS Dimethyl Disulphide

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

HEAST Health Effects Assessment Summary Tables - prepared by U.S. 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

IRIS Integrated Risk Information System - a database published by the U.S. 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 Interim Threshold Screening Level - similar to the IRSL, however, derived for 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

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

LOEL Lowest-Observed-Effect Level

MAC Maximum Acceptable Concentration

MACT Maximum Achievable Control Technology

MADEP Massachusetts Department of Environmental Protection

MDI Methane diphenyl diisocyanate (CAS# 101-68-8)

ME Manitoba Environment


106

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

NIEHS National Institute of Environmental Health Sciences (USA)

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

NOAEL No-Observed-Adverse-Effect Level

NOEL No-Observed-Effect Level

NPRI National Pollutant Release Inventory

NRCC Natural Resource Conservation Commission - agency in state of Texas

OEHHA Office of Environmental Health Hazard Assessment (California EPA)

OEL Occupational Exposure Level

OSHA Occupational Safety and Health Association - a branch of the U.S. Department of Labour

PEL Permissible Exposure Limit (OSHA air standard)

Photophobia Abnormal visual intolerance of light

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

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


107

SGC Short-term Guideline Concentration (New York State)

STEL Short-term Exposure Limit

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)

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

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

TRS Total Reduced Sulphur

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

U.S. EPA United States Environmental Protection Agency

WHO World Health Organization

mg/L milligram per litre

m/s metre per second

ppm parts per million

ppb parts per billion

mg a milligram, one thousandth of a gram

µg a microgram, one millionth of a gram

ng a nanogram, one billionth of a gram


12.0 Appendix C: Summary of Toxicity Data

12.1 Toxicity Data for Total Reduced Sulphur (TRS)

Table C. 1: Summary of Subchronic/Chronic Toxicity Data for TRS

SUB-CHRONIC/CHRONIC STUDIES Species, Strain,

Sex, Number Route, Dose, Duration Observed Effect(s) NOEL, LOEL and Critical Effect(s) Comments Reference

human, male Finnish sulphate mill workers (n = 4,179)

• employed at the sulphate mill plant for at least 1 year between 1945 and 1961

• exposure to TRS; H2S levels between 0 and 28 mg/m3, methyl mercaptan concentrations varied from 0 to 29 mg/m3, and the highest DMS and DMDS levels were 31 mg/m3 and 6 mg/m3, respectively

• excess mortality from cardiovascular disease and coronary heart disease

Kangas et al., 1984; Jappinen and Tola, 1990

108


SUB-CHRONIC/CHRONIC STUDIES Species, Strain, NOEL, LOEL and Route, Dose, Duration Observed Effect(s) Comments Reference Sex, Number Critical Effect(s)

children, 3 Finnish communities in south eastern Finland (n = 134)

• two communities were in close proximity to pulp mills (n=42 in severely polluted, n=62 in moderately polluted)

• one community is unimpacted by pulp mill activity (n=30)

• annual mean concentrations for H2S and methyl mercaptan were reported as 0.001 to 0.008 mg/m3, and <0.001 to 0.005 mg/m3, respectively

• distributed self-administered questionnaires focussing on eye and respiratory symptoms, and headache or migraine on the previous 4 weeks and 12 months

• higher occurrence, but not statistically significant increase, of eye and nasal symptoms, cough and headache among children for both 4-week and 12-month interval

• the authors concluded that the long-term exposure to malodorous sulphur compounds may increase eye irritation and respiratory symptoms in children

Marttila et al., 1994

109



humans, adults, Finnish community in south eastern Finland (n = 81)

• one community in close proximity to pulp production

• daily mean TRS concentrations varied from 0 to 0.082 mg/m3, and monthly mean varied from 0.003 to 0.019 mg/m3

• involved six questionnaires completed, immediately after a day(s) of exposure

• exposure day(s) were classified into: reference exposure (<0.01 mg/m3 daily mean TRS), medium exposure (0.01 to 0.03 mg/m3) and high (>0.03 mg/m3 daily mean TRS)

• questionnaire focused on eye and respiratory symptoms, headaches and nausea

• dose-related increase in the intensity of eye and respiratory symptoms, and headaches for medium and high exposures to TRS

Marttila et al., 1995

110



humans, adults, 2 Finnish communities in central Finland (n = 336)

• one exposed community in close proximity to pulp and paper mill

• one unexposed community

• air monitoring data collected during March and December 1992

• mean annual TRS levels in the exposed community were 0.002 to 0.003 mg/m3, the 24-hour average TRS concentrations. varied between 0 to 0.056 mg/m3, and the maximum 1-hour concentration was 0.155 mg/m3

• questionnaires focused on eye and respiratory symptoms, headache or migraine during the previous 4 weeks and 12 months

• increased occurrence of cough, respiratory infections and headaches for both the 4-week and the 12-month intervals in the exposed community

• strong association observed between exposure to low-level TRS and higher occurrence of headaches in exposed population for the preceding 4-week and the 12-month intervals

• strong association observed between low-level TRS exposure and higher occurrence of coughs in the exposed population for the preceding 12-month interval

Partti-Pellenin et al., 1996

111


12.2 Toxicity Data for Hydrogen Sulphide (H2S)

Table C. 2: Summary of Acute Toxicity Data for Hydrogen Sulphide (H2S)

ACUTE TOXICITY

Species, Strain, Sex

Route, Dose, Duration Effect Levels/Observations LD50/LC50 Comments Reference

human (gender & age: NS)

• inhalation of 1,112 mg/m3 (800 ppm)

(duration: NS)

Death Verschueren, 1983

human (gender & age: NS)

• inhalation of 834 mg/m3

(600 ppm) for 30 minutes

Death Verschueren, 1983

dogs (gender & breed: NS)

• inhalation of 1,390 to 4,170 mg/m3 (1,000 to 3,000 ppm) for 15 to 20 minutes

Death ACGIH, 1991

rat (strain & gender: NS)

• inhalation of 2,300 mg/m3 (1655 ppm) for 5 minutes

pulmonary edema and death in animals Lopez et al., 1988

monkey, rhesus (gender: NS)


(503 ppm) for 35 minutes

LC50 Lund and Wieland, 1966

mouse (strain & gender: NS)

• inhalation of 1,500 mg/m3 (1,071 ppm) for 18 minutes

LC50 Verschueren, 1983



(273 ppm) for 6.8 hours LC50 Verschueren,

1983

112


ACUTE TOXICITY

Species, Strain, Route, Dose, Duration Effect Levels/Observations LD50/LC50 Comments Reference Sex



(69 ppm) for 13.4 hours LC50 Verschueren,

1983



(17 ppm) for >16 hours LC50 Verschueren,

1983


• inhalation of 1,500 mg/m3 (1079 ppm) for 14 minutes



• inhalation of > 695 mg/m3 (> 500 ppm) for 4 hours

pulmonary edema noted LC50 Khan et al., 1990



(501 ppm) for 4 hours LC50 • all rats

that died had pulmonary edema

Prior et al., 1988



(444 ppm) for 4 hours LC50 • all rats

that died had pulmonary edema

Tansy et al., 1981



(335 ppm) for 6 hours

LC50 • pulmonary edema

Prior et al., 1981

113


ACUTE TOXICITY




(273 ppm) for > 16 hours


rat, Fischer 344, male

• inhalation of 0, 14, 140, 280, or 560 mg/m3 (or 0, 10, 100, 200 or 400 ppm)

• 4-hour exposure • histological

examination of four levels of the nasal cavity at 1, 18 and 44 hours after exposure

• NOAEL = 280 mg/m3 (200 ppm), 4-hours • LOAEL = 560 mg/m3 (400 ppm), 4-hours • no nasal lesions observed in controls nor

in the two lower exposure groups • lesions observed in the respiratory

epithelium involved necrosis, degeneration and exfoliation at 1 and 18 hours post-exposure and regenerative cell growth at 44 hours post-exposure

• lesions observed in olfactory epithelium, degeneration and necrosis continued throughout the 44 hours post-exposure

• study concluded that progression of lesions on inhalation of H2S progresses minimally between acute and subchronic durations in rats

CIIT, 1983b

114


ACUTE TOXICITY


rat, Fischer 344, male,

4 rats/dose/time

• inhalation of 0, 14, 279, or 557 mg/m3 ( 0, 10, 200 or 400 ppm)

• 4-hour exposure • histological

examination of bronchoalveoli and nasal cavity at 1, 20 and 44 hours after exposure

• 557 mg/m3 (400 ppm) - increased number of cells in nasal lavage and increased protein and lactate dehydrogenase in both bronchoalveolar and nasal lavage fluids

Lopez et al., 1987


4 rats/dose/time

• inhalation of 0, 116, or 615 mg/m3 (0, 83, or 442 ppm)

• 4-hour exposure

• 116 mg/m3 (83 ppm) - mild perivascular edema observed

• 615 mg/m3 (439 ppm) - marked perivascular and alveolar edema; bronchioles contained PMN, proteinaceous fluid, fibrin, and exfoliated cells; necrosis of bronchiolar ciliated cells; and hyperplasia of alveolar type II cells

Lopez et al., 1987



(439 ppm) for 4 hours • transient necrosis and exfoliation of nasal

respiratory and olfactory mucosal cells in rat

• reversible pulmonary edema

Lopez et al., 1988

115


ACUTE TOXICITY


rat, CD, male • inhalation of 560 mg/m3

(400 ppm) for 3 hours and necropsied 24 hours later

• six with an occluded right nostril and six with patent nostrils per concentration were exposed nose-only to either HEPA-filtered air or H2S vapours

• consistent olfactory mucosal necrosis that occurred only on the side of the nose with the patent nostril

• demonstrated that systemic delivery did not play a role in the olfactory toxicity of H2S

Dorman et al., 2002



(400 ppm) for 4 hours • transient increase in protein

concentration and activity of lactate dehydrogenase in nasal lavage fluids of rats

Lopez et al., 1987


• inhalation of 278 to 560 mg/m3 (200 to 400 ppm) for 4 hours

• particle-induced oxygen consumption reduced in pulmonary alveolar macrophages in rats

NOEL = 70 mg/m3 (50 ppm)

Khan et al., 1991



(300 ppm) for 4 hours • marked abnormality in surfactant activity

in lavage fluids from rat lungs Green et al.,

1991



(200 ppm ) for 4 hours • detectable histologic lesions in nasal

epithelium of rats Lopez et al.,

1988



(200 ppm) for 4 hours • increase in protein and lactate

dehydrogenase in lavage fluids from rat lung

Green et al., 1991

116


ACUTE TOXICITY



• inhalation of 70 mg/m3 ( >= 50 ppm) H2S for 4 hours

• inhibition of cytochrome oxidase in rat lung cells

NOEL = 14 mg/m3 (10 ppm)

Khan et al., 1990

rat, CD, 10-week old males

• inhalation of 0, 42, 112, 278, or 556 mg/m3 (0, 30, 80, 200 or 400 ppm) H2S for 3 hours/day, for 1 or 5 consecutive days

• examined the noses 24 hours after the end of the inhalation exposure

• extensive loss of olfactory neurons and basal cell hyperplasia (same result as in the subchronic study)

• single exposures at 112 mg/m3 (80 ppm) or higher resulted in localized lesions in the olfactory mucosa

• repeated (5-day) exposures to 112 mg/m3 (80 ppm) or higher resulted in nasal lesions that involved 70 % of the olfactory mucosa

• regeneration of the damaged olfactory mucosa following cessation of the H2S exposure

• olfactory epithelial regeneration was partially complete by 2 weeks after termination of exposure and was nearly complete 4 weeks later

Dorman et al., 2002

117


ACUTE TOXICITY


rat, CD, adult males

• inhalation of 14, 42, 112, 278, or 556 mg/m3 (10, 30, 80, 200 or 400 ppm) H2S for 3 hours

• examined cytochrome oxidase activity and sulphide concentrations

• 112 mg/m3 (80 ppm) or higher - elevated lung sulphide concentrations after 3-hour exposure

• 556 mg/m3 (400 ppm) - sulphide concentrations in the olfactory epithelium were significantly increased but not in respiratory epithelium

• 42 mg/m3 (30 ppm) or higher - decreased cytochrome oxidase activity in lung, and olfactory and respiratory nasal epithelium

• observed inhibition of cytochrome oxidase activity in the absence of elevated tissue sulphide concentration

• authors noted that data suggested cytochrome oxidase inhibition is a more sensitive biomarker of H2S exposure than is tissue sulphide concentration

Dorman et al., 2002

118


ACUTE TOXICITY


human, male (27-year old construction worker)

• inhalation of unknown concentration of H2S during the construction of a sewer system in a 27-foot-deep pit

• subject became unconscious and fell into the pit (no evidence of head trauma)

• police officer trying to rescue the subject was also overcome by fumes and died at the scene

• examined long-term neurological effects following acute exposure

• 16 days after hospital admission, subject found to have slowed speech, impaired attention span, retrograde amnesia, decreased insight and ability to communicate, flat affect and impaired visual memory with poor acquisition, retention and recall of new information

• over four years after the accident, the subject is noted by family and health professionals to have continued problems with short-term memory, sequential thinking, decreased attention and lack of initiative

Schneider et al., 1998

human, male (n=16)

• oral inhalation of 0, 0.7, 2.8 and 7 mg/m3 (0, 0.5, 2 and 5 ppm) H2S for an average of 20 minutes

• ventilation at 5 ppm

• no changes in cardiovascular and metabolic variables

• significant increase in blood lactate at 5 ppm compared to control exposure

• inverse relationship between VO2max and blood lactate concentration at 5 ppm

Bhambani, 1999

119


ACUTE TOXICITY


human, male (n=13) & female (n=12)

• oral inhalation of 7 mg/m3 (5 ppm) for 30 minutes

• no significant changes in arterial blood gases, hemoglobin saturation, cardiovascular and metabolic variables in both genders

• no significant change in blood and lactate concentration in both genders

Bhambani, 1999


• oral inhalation of 7 mg/m3 (5 ppm) for 30 minutes

• no significant change in muscle lactate concentration in both genders

• significant decrease in citrate synthase activity in men

• no significant change in lactate dehydrogenase and cytochrome oxidase activity in both genders

Bhambani, 1999;

Bhambani et al., 1996a

120


ACUTE TOXICITY



• two 30-minute exercise sessions, the subjects inhaled either medical air or air containing 14 mg/m3 (10 ppm) H2S while performing at 50% of their VO2max

• monitored a number of physiological parameters including blood pressure and expiratory gasses

• Muscle biopsies, blood analyses, and tissue analyses were performed

• significantly reduced the oxygen uptake (VO2)in both genders

• neither heart rate nor blood pressure was affected

• muscle lactate increased, although not significantly in exposed men and women

• the activities of lactate dehydrogenase (LDH), citrate synthase (CS), and cytochrome oxidase were not significantly altered by H2S exposure

• LDH and CS activities each decreased by about 7% after H2S inhalation

• cytochrome oxidase activity decreased by 16% in men and increased by 11% in women

Bhambani, 1999; Bhambani et al., 1997

Notes: NS = Not Specified

121


Table C. 3: Summary of Short-Term Toxicity Data for Hydrogen Sulphide (H2S)

SHORT-TERM STUDIES Species, Strain, Sex, Number

Route, Dose, Duration Observed Effect(s) NOEL, LOEL and Critical Effect(s)

Comments Reference

rat, CD, male two test groups (10/dose/group)

• 1st Group: nose-only inhalation of 0, 14, 42 or 112 mg/m3 H2S (0, 10, 30 or 80 ppm), for 3 hours per day, for 5 days per week

• 2nd Group: whole-body inhalation of 0, 14, 42 or 112 mg/m3 H2S (0, 10, 30 or 80 ppm), for 3 hours per day, for 5 days per week

• 1st Group: tested immediately following exposure for spatial learning and body temperature monitoring

• 2nd Group: tested for spontaneous motor activity immediately following fifth exposure

• noted significant reduction in motor activity, water maze performance, and body temperature following exposure to 112 mg/m3 (80 ppm) of H2S

• no effect on regional brain catecholamine concentrations

Struve et al., 2001

guinea pig (gender: NS)

• inhalation of 101 mg/m3 (72 ppm) for 1.5 hours per day, for several days

• various cardiac arrhythmias including ventricular extrasystoles

Kosmider et al., 1967

122


SHORT-TERM STUDIES Species, Strain, Sex, Number


Comments Reference


• inhalation of 140 mg/m3 (100 ppm) for 2 hours per day, 4-day intervals, 4 times

• increasing inhibition of cerebral cytochrome oxidase activity and decreased protein synthesis in brain

Savolainen, 1982; Savolainen et al., 1980


• inhalation of 140 mg/m3 (100 ppm) for 3 hours per day, for 5 days

• increased level of L-glutamate in hippocampus

Nicholson et al., 1998

Notes:

NS = Not Specified

123


Table C. 4: Summary of Sub-Chronic/Chronic (Non-Cancer) Toxicity Data for H2S

SUB-CHRONIC/CHRONIC STUDIES

Species, Strain, Sex, Number


Comments Reference


• inhalation of 1.4, 14, and 140 mg/m3 (1, 10, and 100 ppm), 8-hours per day, for 5 weeks

• no effects on baseline measurements of airway resistance, dynamic lung compliance, tidal volume, minute volume or heart rate

• maximal changes in airway resistance and dynamic lung compliance with a methacholine challenge were comparable in all exposed groups

• significant increase in bronchial responsiveness as a result of exposure

Reiffenstein et al., 1992

124



Species, Strain, Sex, Route, Dose, Duration Observed Effect(s) NOEL, LOEL and Comments Reference Number Critical Effect(s)


• inhalation of 0, 1.4, 14, and 140 mg/m3

(0, 1, 10, and 100 ppm), 8-hours per day, 5 days per week, for 5 weeks (35 days)

• analyses of biochemical activities in lung, brain, and liver mitochondria for cytochrome oxidase, and in erythrocytes for superoxide dismutase and glutathione peroxidase

• no significant change in biochemical activities in rats exposed to 1.4 mg/m3 (1 ppm)

• at 14 mg/m3 (10 ppm) and 139 mg/m3 (100 ppm), significant reduction in cytochrome oxidase activity in lung mitochondria and reduced activity in brain as compared to control groups

• no significant change in cytochrome oxidase activity in liver mitochondria

Khan et al., 1998

125




rat, CD, male (n=12/group)

• inhalation of 0, 14, 42, 112 mg/m3 H2S ( 0, 10, 30 or 80 ppm) for 6 hours/day, for 70 days

• dose-related nasal lesions in the olfactory mucosa characterized by extensive loss of olfactory neurons and hyperplasia of the basal cells

• NOAEL = 14 mg/m3 (10 ppm) for nasal olfactory lesions

• LOAEL = 42 mg/m3 (30 ppm)

• olfactory lesions seen with H2S exposure are similar to those observed following inhalation exposure to other irritant gases

Brenneman et al., 2000; Dorman et al., 2002

126




mouse, B6C3F1, male and female, 10 males & 12 females per dose per group

• inhalation of 0, 14.1, 42.5, and 110 mg/m3

(0, 10.1, 30.5 and 80 ppm) or clean air (control)

• 6-hour exposures, 5 days per week, for 90 days

• animals were examined using neurological function tests of posture, gait, facial muscle tone, and reflexes; ophthalmological examination using a slit-lamp scope; hematological parameters; and detailed necropsy, including brain, spinal cord, peripheral nerves, eyes, heart, lungs, nasal turbinates, and other organs

• 110 mg/m3 (80 ppm) - inflammation of the nasal mucosa in the anterior segments of the nose in 8/9 males and 7/9 females

• lesion was also present in two high-dose mice that died during the course of the study

• lesion was generally minimal to mild in severity

• lesion not present in other exposure groups

• LOAEL= 110 mg/m3 (80 ppm)

• NOAEL = 42.5 mg/m3 (30.5 ppm)

CIIT, 1983a

127




rat, Sprague-Dawley, male and female, 15/sex/dose

rat, Fischer 344, male and female, 15/sex/dose

• inhalation of 0, 14.1, 42.5, and 110mg/m3( 0, 10.1, 30.5 and 80 ppm) or clean air (control), 6-hour per day, 5 days per week, for 90 days

• animals were examined using neurological function tests of posture, gait, facial muscle tone, and reflexes; ophthalmological examination using a slit-lamp scope; hematological parameters; and detailed necropsy, including brain, spinal cord, peripheral nerves, eyes, heart, lungs, nasal turbinates, and other organs

• significant reduction in body weight gain observed in all animals exposed to 110 mg/m3 (80 ppm)

• significant brain weight reduction in male Sprague-Dawley rats exposed to 110 mg/m3 (80 ppm)

• LOAEL= 110 mg/m3 (80 ppm)

• NOAEL = 42.5 mg/m3 (30.5 ppm)

CIIT, 1983b and 1983c

128




human, Caucasian males (n=123)

• employed at a viscose rayon plant >= 1 year

• exposure to H2S and carbon disulphide (CS2) simultaneously as part of work activities

• H2S concentrations ranged from 0.2 to 8.9 mg/m3

• CS2 concentrations ranged from 4 to 112 mg/m3

• exposed subjects had significantly higher incidence of eye pain, burning, and photophobia

• authors commented that it was not possible to conclusively state which of CS2 or H2S was responsible for ocular effects

• worker exposures were monitored using personal monitoring pumps

Vanhoorne et al., 1995

129




human (gender: NS) (n=81)

• exposed to H2S concentrations of less than 30 mg/m3 (20 ppm) and to methyl mercaptan concentrations of less than 29.6 mg/m3 (15 ppm)

• loss of concentration capacity and chronic or recurrent headache more frequently than a non-exposed control group

• increased incidence of restlessness, lack of vigour and more frequent sick leave among the exposed group

• study of Finnish pulp mill workers

Kangas et al., 1984

130


Table C. 5: Summary of Reproductive and Developmental Toxicity Data for H2S

REPRODUCTIVE AND DEVELOPMENTAL TOXICITY


Route, Dose, Duration Critical Effect(s) NOEL, LOEL and Critical Effect(s)

Comments Reference

rat, female, 7 to 9/dose (strain: NS)

• inhalation of 0, 69.7, 139 or 209 mg/m3 (0, 50, 100 or 150 ppm) , 6-hours per day on gestational days 6 through 20

• slight reduction in fetal body weight in all exposed groups

• 209 mg/m3 (150 ppm) - reduced maternal body weight gain; and in dams, observed reduced absolute weight gain, increased implantations and live fetuses

• 139 mg/m3 (100 ppm) - in dams, observed reduced absolute weight gain, increased implantations and live fetuses

• LOAEL = 69.7 mg/m3 (50 ppm) for maternal weight gain

• NOAEL = 139 mg/m3 (100 ppm) for maternal effects and developmental effects

Saillenfait et al., 1989

rat, female, 20/dose (strain: NS)

• inhalation of 209 mg/m3 (100 ppm), 6-hours per day on gestational days 6 through 20

• observed fetal weights, number of live and dead fetuses, number of implantation sites and resorptions, and external malformations

• no maternal, embryonic or fetal toxicity observed


131



Species, Strain, Sex, Route, Dose, Duration Critical Effect(s) NOEL, LOEL and Comments Reference Number Critical Effect(s)

rat, Wistar, female, 10/dose

• inhalation of 307 mg/m3 (220 ppm) for 3 hours/day for 1 week, then mated over a 10-week period

• no exposure-related effects on fertility, corpora lutea, implants or resorptions

Andrew et al., 1980

rat, Wistar, female • inhalation of 307 mg/m3 (220 ppm) for 3 hours/day, 5 days/week on gestation days 1 to 18, 7 to 11, or 12 to 16

• no maternal toxicity, fertility, prenatal mortality, or litter weight effects were observed

• increase in minor skeletal anomalies observed

Andrew et al., 1980

rat, Sprague-Dawley, female, adults & pups

• inhalation of 27.9, 69.7, or 105 mg/m3 (20, 50, or 75 ppm), 7-hours/day on gestational day 1 through postpartum day 21

• collection and analysis of blood samples for glucose, triglycerides, cholesterol, alkaline phosphatase, lactate dehydrogenase, SGOT, and protein on postpartum days 7, 14 and 21 in pups, and on day 21 in the parents

• maternal blood glucose was significantly elevated in all exposed groups at day 21 postpartum

Hayden et al., 1990a

132




rat, pups (strain & gender: NS)

• inhalation of 105 mg/m3 (75 ppm) for 7 hours/day from gestational day 5 to postnatal day 21

• observed several amino acids on postnatal days 7, 14, and 21 in rat pup cerebrum and cerebellum

• changes in aspartate, glutamate and taurine levels

• the adversity of these changes in brain levels of neurotransmitter is unclear

• in a follow-up study of similar experimental design, exposure to 50 ppm H2S resulted in significantly increased maternal blood taurine levels on the day of parturition and on postpartum day 21

Hannah et al., 1989

133




rat, Sprague-Dawley, female

• inhalation of 27.9, 69.7, or 105 mg/m3 (20, 50, or 75 ppm) on gestational day 6 through postpartum day 21

• observed reproductive and physical developmental endpoints

• no effects in gestation length, litter size, viability, pup body and organ weights, maternal weights, or liver or brain content of protein, DNA or cholesterol were observed

Hayden et al., 1990b

rat, Sprague-Dawley, female, 10/dose

• inhalation of 0, 27.9, or 69.7 mg/m3 (0, 20, or 50 ppm), for 7 hours/day on gestational day 6 through postpartum day 21

• observed neuronal development of cerebellar Purkinje cells

• significant effects were seen at both concentrations or measurements reflecting the number, symmetry, and length of branches

• LOAEL (HEC) = 27.9 mg/m3 (20 ppm)

• the LOAEL(HEC) for developmental neuronal effects is considerably higher than the LOAEL for respiratory system effects

Hannah and Roth, 1991

134




rat, CD, male & female (n=12/sex/dose)

• inhalation of 0, 14, 42 or 111 mg/m3 (0, 10, 30 or 80 ppm), for 6 hours/day, 7 days/week

• 10-week old parental rats were exposed to H2S vapours for a 2-week prebreed exposure period followed by a 2-week mating period

• pregnant female rats were exposed to H2S vapours from gestational day 0 through 19

• dams & pups were concurrently exposed to H2S vapours on postnatal day 5 through 18

• male rats were exposed for 70 consecutive days

• no deaths and no adverse physical signs observed in adult male and female rats

• statistically significant decrease in feed consumption observed in adult male rats from the 111 mg/m3 (80 ppm) group during the first week of exposure

• no statistically significant effects on the reproductive performance of the adult rats as evidenced by the number of females with live pups, litter size, average length of gestation , and the average number of implants per pregnant female

• no effects on pup growth, development or performance on any of the behavioural tests

• authors concluded that H2S is neither a reproductive toxicant nor a behavioural developmental neurotoxicant in the rat at occupationally relevant exposures (<10 ppm)

Dorman et al., 2000

135


12.3 Toxicity Data for Methyl Mercaptan

Table C. 6: Summary of Acute Toxicity Data for Methyl Mercaptan

ACUTE TOXICITY




inhalation, 4 hours (dosing regimen: NS)

3,261 mg/m3 (1,664 ppm) LC50 Reed, 1983

rat (male & female, strain: NS)


1,323 mg/m3 (675 ppm) LC50 NOAEL = 784 mg/m3 (400 ppm) (100% mortality)

Tansy et al., 1981


inhalation, 15 minutes (dosing regimen: NS)

LOAEL (serious) = 2,744 mg/m3 (1,400 ppm), produced lethargy or coma

NOAEL = 2,352 mg/m3 (1,200 ppm)

Zieve et al., 1984


136


Table C. 7: Summary of Short-Term Toxicity Data for Methyl Mercaptan

SHORT-TERM STUDIES



Comments Reference

human (53-year old black male)

• inhalation and dermal exposure to an unknown level of methyl mercaptan for 1week (dosing regimen: NS)

• exposure occurred while emptying tanks containing methyl mercaptan

• hospitalised in a coma, developed hemolytic anemia and methemoglobinemia, and died 28 days after admission

• increased pulse rate and blood pressure

• minimal movement in response to painful stimuli, hypoactivity of all deep tendon reflexes and seizure activity

cause of death was a massive embolus that occluded both main pulmonary arteries

Shults et al., 1970


137


Table C. 8: Summary Sub-Chronic/Chronic (Non-Cancer) Toxicity Data for Methyl Mercaptan




Comments Reference

2. rat, male (strain & number: NS)

• inhalation of 0 to 112 mg/m3 (0 to 57 ppm), 7-hours per day, 5 days per week, for 3 months

• decreased body weight • no histopathological

changes were observed in lungs, liver, kidneys, heart or small intestine

NOAEL = 112 mg/m3 (57 ppm)

• decreased body weight was not considered an adverse effect

3. Tansy et al., 1981


138


12.4 Toxicity Data for Dimethyl Sulphide (DMS)

Table C. 9: Summary of Acute Toxicity Data for DMS

ACUTE TOXICITY




inhalation (dosing regimen & duration: NS)

103,845 mg/m3 (40,250 ppm) LC50 Tansy et al., 1981


inhalation (dosing regimen & duration: NS)

32 mg/m3 (12.5 ppm) LC50 Unknown, 1972


oral (dosing regimen & duration: NS)

3,300 mg/kg LD50 Behavioural - general anesthetic, changes in motor activity and irritability

Unknown, 1967


oral (dosing regimen & duration: NS)

3,700 mg/kg LD50 Behavioural - changes in motor activity and antipsychotic; nutritional and gross metabolic changes

Unknown, 1979


intraperitoneal (dosing regimen & duration: NS)

8, 000 mg/kg LD50 Unknown, 1961

rabbit (strain & gender: NS)

dermal (dosing regimen & duration: NS)

> 5,000 mg/kg LD50 Unknown , 1979


139


12.5 Toxicity Data for Dimethyl Disulphide (DMDS)

Table C.10: Summary of Acute Toxicity Data for DMDS

ACUTE TOXICITY





16 mg/m3 (4 ppm) LC50 Unknown, 1972



12 mg/m3 (3 ppm) LC50 Unknown, 1972


140


13.0 Appendix D: Relevant Toxicity Data For H2S

[Taken from Appendix B of Massachusetts Department of Environmental Protection (2001)]

Table D. 1: Human Acute Lethality Data

Subjects Exposure Levels (ppm)

Exposure Duration

System /Organ

Affected

NOAEL LOAEL

Less

Serious Serious

References

All data in the Table are

summarized from ATSDR, 1999 and U.S.

EPA, 2000

Osbern and Crapo, 1981

Human (4) 76 (measured a week after the accident, however, concentrations of H2S could be higher due to differences in temperature and manure concentration at exposure

Few minutes Respiratory. A farmer entered an underground manure pit and became unconscious along with three people who came to rescue him Three of the exposed people died and surviving patient had hemodynamic instability, respiratory distress syndrome, and infection

Human (2) 200 (measured 6 days after the accident)

45 minutes Not reported Two workers at an animal tanning company collapsed and died after entering a sewer manhole

NIOSH, 1991

Human (1) 2000 - 4000 15-20 minutes Pulmonary, intracranial, and cerebral edema and cyanosis

The exposed individual was a worker at a poultry processing plant died within 15-20 minutes after exposure

Breysse, 1961

141


Subjects Exposure Exposure System NOAEL LOAEL References Levels (ppm) Duration /Organ

Affected All data in the Table are


EPA, 2000

Less

Serious Serious

Human (10) 429 ( measured 4 hours after the accident)

Death – immediate

Unconsciousness in survivors within 2-20 minutes

Abnormal EEG, BUN, and SGPT in survivors

10 cases of accidental H2S poisoning – five of the victims died at the site of exposure, four lost consciousness within 2-20 minutes and regained consciousness only after extensive hyperbaric oxygen therapy.

Hsu et al., 1987

Human (14) Unknown 1/14 died after few hours

CNS, Ocular and the respiratory system

Fourteen workers were exposed to H2S from toilet facilities at work that were connected to manure pit without a siphon. Workers complained of eye, nose, and throat irritation, nausea, dizziness, vomiting, and dyspnea. One worker died a few hours after hospital admission. Hemorrhagic bronchitis and asphyxia were identified at autopsy. Of the recovering patients, one reported dyspnea, chest tightness, hemoptysis and mild bilateral fibrosis and mild restrictive pulmonary disease was also observed. Five months after, patient demonstrated only residual exertion dyspnea.

Parra et al., 1991

142


Subjects Exposure Exposure System NOAEL LOAEL References Levels (ppm) Duration /Organ

Affected All data in the Table are


EPA, 2000

Less

Serious Serious

Human (37) Unknown 1/37 died but duration not reported

CNS, Ocular and the respiratory system

Workers (37) were accidentally exposed to H2S while drilling a pit to lay a foundation for municipal sewage pumping station. Symptoms reported were, eye and nose irritation headache, dizziness, breathlessness cough, burning, chest tightness, nausea and vomiting. One worker died and one was comatose, but most workers recovered. The comatose patient recovered with permanent neurological effects.

Snyder et al., 1995

143


Table D. 2: Human Non-lethal Toxicity Case reports

Species Exposure Levels (ppm)

Exposure Duration

System/Organ Affected

NOAEL LOAEL

Less Serious Serious

References


summarized from ATSDR,

1999 and U.S. EPA,

2000

20-month male child

>6ppm 1 year CNS The child’s family lived near a coal mine where a burning tip had been emitting hydrogen sulfide for approximately one year. He first presented with intermittent paroxysomal tonic deviation of the eyes, upward to the right. The abnormal eye movements resolved after a few months and were followed by progressive involuntary movements of the entire body. He fell frequently and had ataxia, choreoathetosis and dystonia. A CT scan identified abnormalities in the basal ganglia and in some surrounding white matter. His conditions improved after hospital admission. After 10 weeks the brain scan indicated complete recovery and that ataxia had also resolved.

Gaitonde et al., 1987

144



Exposure Duration


NOAEL LOAEL


References



1999 and U.S. EPA,

2000

Human 0.09 (30 minute down-wind average)

5 hours Respiratory tract, CNS and eyes

Staff of the Texas Natural Resources Conservation Commission (TNRCC) conducting a mobile laboratory sampling in corpus Christ, Texas were exposed to a to 0.09 ppm of H2S that was measured downwind from an oil refinery. Exposure was for about five hours. All six staff members experienced persistent odours, eye and throat irritation, headache and nausea. Symptoms subsided within few hours after leaving the site; although, throat irritation persisted in two staff members through the fol0lwing day. Sulfur dioxide, benzene, methyl t-butyl ether and toluene were also detected. However the measured concentrations of these chemicals would not be expected to cause health effects.

TNRC, 1998

145



Exposure Duration


NOAEL LOAEL


References



1999 and U.S. EPA,

2000

Tvedt et al., 1991a; 1991b

6 patients

Not reported

Not reported

CNS Six patients were examined 5-10 years after accidental exposure to unknown concentrations of H2S. Patients were unconscious 5- 20 minutes. Impaired vision, memory loss, decreased motor function, tremors, ataxia, abnormal learning and retention and slight cerebral atrophy were observed. One patient was severely demented.

Land fill abutters

<2 ->300 Respiratory tract and CNS

In May and June 1964 an H2S emission from industrial landfill in Terre Haute Indiana resulted in odour complaints and nausea, loss of sleep, shortness of breath, and headache. Observation was confounded by concurrent exposure to other malodorous compounds.

U.S. DHEW, 1964

146


Table D. 3: Epidemiological Studies

Study subjects Exposure Levels (ppm)

Exposure Duration

Endpoint Investigated

NOAEL (ppm)

LOAEL (ppm) Less Serious Serious

References All data in the

Table are summarized from ATSDR, 1999 and U.S.

EPA, 2000 Male pulp mill workers (26) <10 Not

reported Respiratory No change

in respiratory parameters tested

Jappinen, 1990

175 oil and gas workers Not available but categorized by symptom

Not available

Respiratory Exposure was determined by questioning the workers about “exposure strong enough to cause symptoms”, “exposure causing unconsciousness (knockdown)” or “no exposure”. 51 reported“exposure strong enough to cause symptoms” while 14 workers reported “knockdown”. 110 reported “no exposure”. Exposures strong enough to cause symptoms were not associated with lower spirometric values. Knockdowns were not associated with lower spirometric values, but were associated with shortness of breath while hurrying on the level or up a slight hill; wheezing with chest tightness, and wheezing attacks.

Hessel et al., 1997

147


Study subjects Exposure Levels (ppm)

Exposure Duration

Endpoint Investigated

NOAEL (ppm)

LOAEL (ppm) References Less Serious Serious All data in the

Table are summarized from ATSDR, 1999 and U.S.

EPA, 2000 21 swine confinement facility owner/operators

Not available

Duration not reported, but tested after a 4-hour work period

Respiratory The forced expiratory flow (FEF) was significantly decreased in workers. The work environment was sampled for particulates and gases and there was suggestive evidence for a dose-response relationship between carbon dioxide and H2S and lung function decrements

Donham et al., 1984

Developmental/reproductive Not reported

Not reported

Significant association between occupational H2S and increased frequency of spontaneous abortion. Exposure duration and concentration not reported

Xu et al., 1998

148


Table D. 4: Human Experimental Studies

Study Subjects

Exposure Levels (ppm)

Exposure Duration

Endpoints Examined

NOAEL (ppm)

LOAEL (ppm)

Less serious Serious

References



EPA, 2000

10 asthmatics (7 women and 3 men)

2 Respiratory 2 ppm A group of 10 asthmatics were exposed to 2 ppm H2S for 30 minutes. The subjects had had bronchial asthma for 1- 13 years and had been using medication. Severe asthmatics were excluded from the study. All asthmatic subjects complained of an unpleasant odour nasal and pharyngeal dryness at the start of exposure. Three of 10 complained of headache after exposure. There were no significant effects on FVC, FEV1, or FEF values due to H2S exposure. Raw was slightly decreased in 2 and increased in eight subjects SGaw was decreased in 6 and increased in 4 subjects. These effects were not significant, but in 2 subjects were greater than 30% in both Raw and SGaw.

Jappinen et al., 1990

16 healthy heavily exercising male volunteers

0, 0.5, 2, and 5

Up to 16 minutes

Cardiac and respiratory performance; aerobic and anaerobic metabolism

5 ppm Sixteen male volunteers were exposed to H2S for up to 16 minutes during graded cycle exercise performed to exhaustion. Increased O2 uptake and decreased CO2 out put were observed at 5 ppm. Blood lactate level was also significantly increased at 5 ppm.

Bhambhani and Singh, 1991

25 (13 men, 12 women) healthy

5 30 minutes

Cardiac and respiratory performance;

5 ppm Male (13) and female (12) volunteers were exposed to 0 or 5 ppm H2S for 30 minutes at 50% of their maximum power output. In men

Bhambhani et al., 1994,

149


Study Exposure Exposure Endpoints NOAEL LOAEL (ppm) References Subjects Levels

(ppm) Duration Examined (ppm)

Less serious Serious All data in the Table are


EPA, 2000

moderately exercising volunteers

aerobic and anaerobic metabolism

muscle citrate synthetase decreased significantly compared to control. There were also slight increase in muscle lactate and lactic acid dehydrogenase in males. These parameters were not altered in females. No other adverse effects were reported

1996a

19 (9 male, 10 female) moderately exercising volunteers

0, 10 15 Respiratory (FVC, FEV1, peak expiratory flow rate, forced expiratory flow rate, maximal ventilation volume

10 ppm,

Bhambhani et al., 1996b

28 (15 male, 13 female) moderately exercising volunteers

0, 10 30 Cardiac and respiratory performance; aerobic and anaerobic metabolism

5 ppm Male (15) and female (13) volunteers were exposed to 0 or 5 ppm H2S for 30 minutes at 50% of their maximum power output. For 30 minutes. Muscle lactic acid increased 33% (non significantly) in men and 16% in women (non significantly) in women. Muscle cytochrome oxidase decreased by 16% in men, whereas it increased by 11% in women. Subjects reported no health effects.

Bhambhani et al., 1996b

150


Table D. 5: Animal Mortality Studies


Exposure Duration

End point

NOAEL (ppm)

LOAEL (ppm)

Less serious Serious

References

All data in the Table

are summarized

from ATSDR,

1999 and U.S. EPA,

2000

Wistar rats (5 male and 5 female)

Varying concentrations

10, 30. or 50 minutes

Mortality 10 minute LC50 = 835

30 minute LC50 =726

50 minute LC50 = 683

Zwart et al., 1990; Arts et al., 1989

Male Sprague-Dawley rats (10)

400, 504. 635 or 800

1 hour Mortality Concentration Mortality

400 0/10 504 0/10 635 1/10 800 9/10

A 1 hour LC50 of 712 ppm was calculated

Gasping was observed during exposure. Rats surviving the 14 day observation period exhibited normal weight gain but mottling of the kidney and liver accompanied by moderate fatty changes in the liver were observed at necropsy.

McEwen and Vernot 1972

Sprague-Dawley rat (5 males, 5

0-600 4 hours Mortality LC50 = 444 ppm Tansy et al., 1981

151


Species Exposure Exposure End NOAEL LOAEL (ppm) References Levels (ppm) Duration point (ppm)

Less serious Serious All data in the Table

are summarized

from ATSDR,

1999 and U.S. EPA,

2000

females)

Long Evans, Sprague_Dawely, and Fischer 344 rats


2,4 or 6 hours Mortality 2 hour LC50 = 587 ppm

4 hour LC50 = 501 ppm

6 hour LC50 = 335 ppm

No strain differences were observed

Prior et al., 1988

Groups of 5 male Sprague-Dawley rats

1655.4 ± 390.9 ppm

3 minutes Mortality All test rats died within 3 minutes. Test animals exhibited dyspnea characterized by exaggerated abnormal, audible respiration and had frothy fluid from the nose and mouth during exposure. Pulmonary edema was observed in exposed rats at necropsy

Lopez et al., 1989

Swiss mice (5 male, 5 female)


10, 30, 50 minutes

Mortality 10 minute LC50 = 1160 ppm

30 minute LC50 = 800 ppm

50 minute LC50 = 676 ppm

Zwart et al., 1990; Atrs et al., 1989

152


Species Exposure Exposure End NOAEL LOAEL (ppm) References Levels (ppm) Duration point (ppm)

Less serious Serious All data in the Table

are summarized

from ATSDR,

1999 and U.S. EPA,

2000

Male CF1 mice (10)

400, 504, 635, 800

1 hour Mortality 1 hour LC50 = 634 ppm

Survivors from 635 and 800 ppm exposure had blocked urethral openings consequently bladders were extended.

McEwen and Vernot 1972

Monkey 500

500

500

22 minutes

35 minutes

25 minutes followed with 17 minute exposure to 500 ppm

Ataxia, anorexia, and parenchymal necrosis in the brain

Conjunctival irritation, sudden loss of consciousness respiratory and cardiac arrest

25 minutes followed with 17 minute exposure to 500 ppm three days later had changes in the brain and liver on necropsy

Lund and Wieland, 1966

153


Table D. 6: Animal Non-Lethal Studies Species Exposure

Levels (ppm)

Exposure Duration

End point NOAEL (ppm)

LOAEL (ppm) Less serious Serious

References All data in the Table

are summarized from ATSDR, 1999 and U.S. EPA, 2000 Lopez et al., 1987; Lopez et al., 1988

Male Fischer 344 rats (groups of 12)

0, 10, 200, or 400

4 hours Respiratory effects

10 No animals died during exposure. The 400 ppm group were lethargic at the end of exposure but rapidly recovered. Transient increase in lactate dehydrogenase activity and protein in nasal passages in the 400 ppm group. Decreased bronchoalveolar cell count, (400 ppm) and significantly increased alkaline phosphatase. lactate dehydrogenase (200 and 400), and lung protein (400 ppm) were observed in lung lavage fluid. Nasal lesions were observed at 400 ppm .

Necrosis and exfoliation of respiratory and olfactory mucosal cells were observed at 400 ppm. Injured respiratory mucosa was in reparative stage at 44 hours but olfactory mucosa continued to exfoliate after 44 hours


0, 200 0r 300

4 hours Pulmonary effects and anaerobic metabolism

Animal in the 200 ppm group had significant increase in protein and lactate dehydrogenase in lung lavage fluid.

Proteinaceous material in the alveoli were observed in animal from the 200 ppm group. In the 300 ppm group, lungs showed focal areas of red atelectasis and patchy alveolar edema also, lung lavage fluid showed significant increase in protein concentration and lactate dehydrogenase activity with abnormality in lung surfactant activity

Green et al., 1991


0, 10, 50, 400, or 500 –700

4 hours Aerobic and anaerobic metabolism

10 Cytochrome c oxidase activity was significantly decreased at 50 ppm 200 ppm, 400 ppm at 1-hour post-exposure, Succinate oxidase was significantly decreased at 200 and 400 ppm exposure at the 1 hour post exposure.

Animals exposed 500-700 ppm died from exposure and had >90% of inhibition of cytochrome c oxidase activity.

Khan et al., 1990


0, 50, 200, 400

4 hours Immune cells 50 Macrophage viability was significantly decreased at 400 ppm. Zymosan induced stimulation of respiratory rates of the

Khan et al., 1991

154

ndards for Total Reduced Sulphur

155


Exposure Duration




are summarized from ATSDR, 1999 and U.S. EPA, 2000

macrophages from animals exposed to 200 and 400 ppm was completely inhibited.

Male Wistar rats

75 ppm 20-60 minutes

Cardiac and pulmonary effects

Heart rate was decreased 10-27% during exposure and 1 hour post-exposure

Slight lung congestion in exposed animals

Kohno et al., 1991

Male Sprague-Dawley rats (groups of 5)

25, 50, 75, 100

3 hr/day for 5 days

CNS effects hippcampal theta activity increased in a cumulative manner in both the dentate gyrus and CA1 regions during exposure to 25, 50, 75 and 100 ppm H2S .The increase was significant on days 3, 4 and 5

Skrajny et al., 1996

Male and female Sprague-Dawely rats groups of 15)

0,10.1, 30.5, 80

6 hrs/day, 5 days/week for 90 days

Round ear tags, crusty noses, eyes and muzzles; red stained fur, swollen ears; lacrimation, and swollen muscles and or eyes. Decreased brain weight and body weight gain were observed at high concentration In both sexes.

Toxigenics, 1983a

CB-20 mice 100 2 hours Brain protein, RNA and lysosmal acid prteinase activity content

Uptake of labelled leucine in brain was significantly lowered in brain homgenate (24 and 48 hours post-exposure and myelin fraction (48-hour post-exposure) along with acid proteinase activity.

Elovaara et al., 1978

Groups of 15 B6C3F1 mice

10.1,30.5 or 80

6 hours /day, 5 days/week for 90 days

Respiratory and neurological effects

Clinical observations included alopecia, missing anterior appendages and loss of use of anterior appendages that resulted in irregular gait. 2 animals not responding to artificial light. At sacrifice 89% of high-concentration males and 78% of high-concentration females had inflammation of the nasal mucosa in the anterior segments of the nose

Toxicogenics, 1983b

Mixed breed rabbits

72 1.5 hours or 0.5 hours/day for 5 days

Cardiac effects

Change in ventricular repolarization and cardiac arrythmia

Kosmider et al., 1966

Pregnant Sprague Dawley rats

0, 50, 100 or 150

6 hours/day days 6-20 of gestation

Body weight change

Slight but significant decrease in fetal body weight in the 100 and150 ppm exposure group. Dams also lost weight.


Ontario Air Sta

ndards for Total Reduced Sulphur

156


Exposure Duration




are summarized from ATSDR, 1999 and U.S. EPA, 2000

(eight/group) Groups of 17-24 Sprague-Dawley rats (and off springs)

0, 20, 50, or 75

7 hours/day from gestation day through postnatal 21.

Maternal blood glucose level was increased 50% on day 21 postpartum in all exposure groups . Serum triglyceride was decreased in both dams and pups on day 21.

Hayden et al., 1990a

Groups of 5 or 6 pregnant Sprague-Dawley rats

0, 20, 50, or 75

7 hours/day from gestation day 6 through postpartum day 21.

Dose-dependent increase in parturition time. Maternal liver cholesterol was significantly increased at the 75 ppm group.

The mean purkinje cell terminal path length was significantly increased in the 20 and 50 ppm groups

Hayden et al., 1990b

Hannah and Roth 1991

Sprague-Dawley rats

0,20, 50 7 hours/day from gestation day 5 through postpartum day 21.

Neurons

Groups of 20 Sprague-Dawley rats

0, 20, 75 7 hours/day from day 5 postcoitus through postpartum day 21.

Brain neuroamines

Alter brain neuroamine levels were observed at 20 and 75 ppm exposure levels.

Skrajny et al., 1996

Guinea pig 20 11 days, 1 hour/d

Brain size and lipids

Decreased cerebral hemisphere and brain stem total lipids and phospholipids, fatigue, somnolence and dizziness

Haider et al., 1980

Ontario Air Sta


14.0 Appendix E: References (Appendicies C & D)

Arts, J. H. E., Zwart, A., Schoen, E. D., et al. 1989. Determination of concentration-time-mortality relationships versus LC50s according to OECD guideline 403. Exp. Pathol. 37: 62-66.

Bhambhani, Y., Burnham, R., Snydmiller, G., et al. 1994. Comparative physiological responses of exercising men and women to 5 ppm hydrogen sulfide exposure. Am. Ind. Hyg. Assoc. J. 55: 1030-1035.

Bhambhani, Y., Burnham, R., Snydmiller, G., et al. 1996a. Effects of 5 ppm hydrogen sulfide inhalation on biochemical properties of skeletal muscle in exercising men and women. Am. Ind. Hyg. Assoc. J. 57: 464-468.

Bhambhani, Y., Burnham, R., Snydmiller, G., et al. 1996b. Effects of 10 ppm hydrogen sulfide inhalation on pulmonary function in healthy men and women. JOEM. 38: 1012-1017.

Bhambhani, Y. and Singh, M. 1991. Physiological effects of hydrogen sulfide inhalation during exercise in healthy men. J. Appl. Physiol. 71: 1872-1877.

Breysse, P. A. 1961. Hydrogen sulfide fatality in a poultry feather fertilizer plant. Am. Ind. Hygiene Assoc. J. 22: 220-222. (Cited in ATSDR, 1997

Donham, K. J., Zavala, D. C., and Merchant, J. 1984. Acute effects of the work environment on pulmonary functions of swine confinement workers. Am. J. Ind. Med. 5: 367-376.

Elovaara, E., Tossavainen, A., Savolainen, H. 1978. Effects of subclinical hydrogen sulfide intoxication on mouse brain protein metabolism. Exp. Neurol. 62: 93-98.

Gaitonde, U. B., Sellar, R. J., O’Hare, A. E. 1987. Long term exposure to hydrogen sulfide producing subacute encephalopathy in a child. Br. Med. J. 294: 614.

Green, F. H. Y., Schurch, S., DeSanctis, G. T., et al. 1991. Effects of hydrogen sulfide exposure on surface properties of lung surfactant. J. Appl. Physiol. 70: 1943-1949.

Haider, S.S., Hasan, M., Islam, F. (1980). Effect of air pollutant hydrogen sulfide on the level of total lipids, phospholipids and Cholesterol in different regions of guinea pig brain. Indian J Exp. Biol. 18:418-420.

157


Hannah, R.S., and Roth, S.H., 1991. Chronic exposure to low concentrations of hydrogen sulfide produces abnormal growth in developing cerebellar Purkinje cells. Neurosci. Lett. 122: 225-228.

Hayden, L. J., Goeden, H., Roth, S. H. 1990a. Exposure to low levels of hydrogen sulfide elevates circulating glucose in maternal rats. J. Toxicol. Environ. Health. 31: 45-52.

Hayden, L. J., Goeden, H., Roth, S. H. 1990b. Growth and development in the rat during sub-chronic exposure to low levels of hydrogen sulfide. Toxicol. Ind. Health. 6: 389-401.

Hessel, P. A., Herbert, F. A., Melenka, L. S., et al. 1997. Lung health in relation to hydrogen sulfide exposure in oil and gas workers in Alberta, Canada. Am. J. Ind. Med. 31: 554-557.

Hsu, P., Li, H. W., Lin, Y. T. 1987. Acute hydrogen sulfide poisoning treated with hyperbaric oxygen. J. Hyperbaric Med. 2: 215-221.

Jappinen, P., Vilkka, V., Marttila, O., et al. 1990. Exposure to hydrogen sulfide and respiratory function. Br. J. Ind. Med. 47: 824-828.

Khan, A. A., Schuler, M. M., Prior, M. G., et al. 1990. Effects of hydrogen sulfide exposure on lung mitochondrial respiratory chain enzymes in rats. Toxicol. Appl. Pharmacol. 103: 482-490.

Khan, A. A., Yong, S., Prior, M. G., et al. 1991. Cytotoxic effects of hydrogen sulfide on pulmonary alveolar macrophages in rats. J. Toxicol. Env. Health. 33: 57-64.

Kohno, M., Tanaka, E., Nakamura, T., et al. 1991. Influence of the short-term inhalation of hydrogen sulfide in rats. Eisei Kagaku. 37: 103-106.

Kosmider, S., Rogala, E., Pacholek, A. 1966. Untersuchungen uber den toxischen Wirkungsmechanismus des Schwefelwasserstoffs. Int. Archiv. Gewerbepathologie und Gewerbehygiene. 22: 60-76.

Lopez, A., Prior, M., Reiffenstein, R. J., et al. 1989. Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. Fund. Appl. Toxicol. 12: 367-373.

Lopez, A., Prior, M., Yong, S., et al. 1987. Biochemical and cytologic alterations in the respiratory tract of rats exposed for 4 hours to hydrogen sulfide. Fund. Appl. Toxicol. 9: 753-762.

158


Lopez, A., Prior, M., Yong, S., et al. 1988. Nasal lesions in rats exposed to hydrogen sulfide for 4 hours. Am. J. Vet. Res. 49: 1107-1111.

Lund, O. E. and Wieland, H. 1966. Pathologisch-anatomische befunde bei experimenteller schwefelwasserstoff-vergiftung. Int. Archiv. Gewerbepathologie und Gewerbehygiene. 22: 46-54.

MacEwen, J. D. And Vernot, E. H. 1972. Toxic Hazards Research Unit Annual Report. Aerospace Medical Research Laboratory, Air Force Systems Command, Wright-Patterson Air Force Base, Ohio. Report No. ARML-TR-72-62. Pp. 66-69.

NIOSH (National Institute of Occupational Safety and Health). 1991. Fatal accident circumstances and epidemiology (FACE) report: two maintenance workers die after inhaling hydrogen sulfide in manhole, January 31, 1989. Morgantown WV. (Cited in ATSDR, 1997)

Osbern, L. N. and Crapo, R. O. 1981. Dung lung: a report of toxic exposure to liquid manure. Ann. Intern. Med. 95: 312-314.

Parra, O., Monso, E., Gallego, M., et al. 1991. Inhalation of hydrogen sulfide a case of subacute manifestations and long term sequelae. Br. J. Ind. Med. 48: 286-287.

Prior, M. G., Sharma, A. K., Yong, S., et al. 1988. Concentration-time interactions in hydrogen sulfide toxicity in rats. Can. J. Vet. Res. 52: 375-379.

Saillenfait, A. M., Bonnet, P., de Ceaurriz, J. 1989. Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats. Toxicol. Lett. 48: 57-66.

Skrajny, B., Reiffenstein, R. J., Sainsbury, R. S., et al. 1996. Effects of repeated exposures of hydrogen sulfide on rat hippocampal EEG. Toxicol. Lett. 84: 43-53.

Snyder, J. W., Safir, E. F., Summerville, G. P., et al. 1995. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sulfide. Am. J. Emer. Med. 13: 199-203.

Tansy, M.F., Kendall, F. M., Fantasia, J., et al. 1981. Acute and subchronic toxicity studies of rats exposed to vapors of methyl mercaptan and other reduced-sulfur compounds. J. Toxicol. Environ. Health. 8: 71-88.

Ten Berge, W.F., Zwart, A., Appelman, L.M. 1986. Concentration-time mortality response relationship of irritant and systemically acting vapors and gases. J. Hazard. Mater.13:301-309.

159


TNRCC (Texas Natural Resources Conservation Commission) 1998. Memo from Tim Doty to JoAnn Wiersma. Corpus Christi Mobile Laboratory Trip, January 31- February 6, 1998; Real-Time Gas Chromatography and Composite Sampling, Sulfur Dioxide, Hydrogen Sulfide, and Impinger Sampling. April 20, 1998.

Toxigenics. 1983a. 90-Day Vapor Inhalation Toxicity Study of Hydrogen Sulfide in Sprague-Dawley Rats. Study 420-0710B. February 25, 1983.

Toxigenics. 1983b. 90-Day Vapor Inhalation Toxicity Study of Hydrogen Sulfide in B6C3F1 Mice. Study 420-0710C. February 25, 1983.

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