Report 2 Analysis of Coal Composition Ecotoxicity and ... · Analysis of Coal Composition, ... advantages and disadvantages. ... Compared to lignite and sub-bituminous coal, ...

Coal Classification Industry approach to hazard classification under the revised MARPOL Convention and the IMSBC Code

REPORT 2. ANALYSIS OF COAL COMPOSITION, ECOTOXICITY AND HUMAN HEALTH HAZARDS

ARCHE

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www.arche-consulting.be [email protected]

World Coal Association

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World Coal Association

The World Coal Association (WCA) is a global industry association formed of major international coal producers and stakeholders. The WCA works to demonstrate and gain acceptance for the fundamental role coal plays in achieving a sustainable and lower carbon energy future.

Membership is open to companies and not-for-profit organisations with a stake in the future of coal from anywhere in the world, with member companies represented at Chief Executive level.

The publication “Coal Classification - Industry approach to hazard classification under the revised MARPOL Convention and the IMSBC Code” was written by ARCHE, a Belgium-based consultancy specialising in environmental toxicology, under the oversight of the WCA Technical Working Group on Coal Classification and chaired by Dr. Sue Hubbard, Principal Adviser, HSEC Product Regulation & Information Support at Rio Tinto.

ARCHE

ARCHE is a Belgium-based consultancy founded in 2009 by experts with more than 15 years of experience in the field of environmental toxicology, exposure modelling and the preparation of risk assessment dossiers. The company is also recognised as a spin-off of Ghent University.

The experts working at ARCHE have built up in-depth knowledge on the preparation of Chemical Safety Assessments in the framework of the REACH regulation and chemical risk assessments under the predecessor of the REACH regulations (EU regulation 67/1488 on new and existing substances).

One of the key areas of expertise is the preparation of risk assessments for inorganic substances such as metals, alloys, slags etc. ARCHE experts have been involved in the preparation of many guidance documents on these topics - for example Metal Risk Assessment Guidance (MERAG) and a widely used tool for metals classification - MECLAS. The scientific services of ARCHE have also been frequently consulted in the framework of the risk assessment of flame retardants and other organic chemicals.

Any queries related to the publications which are part of this package should be addressed to the WCA Team at [email protected]

Published by the World Coal Association, London, UK Copyright © World Coal Association 2014. All rights reserved. No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, without the prior written permission of the copyright holder.

Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 1

Coal Classification – Industry Approach to Hazard Classification

under the Revised MARPOL Convention and the IMSBC

Report 2. Analysis of Coal Composition, Ecotoxicity and Human

Health Hazards

BACKGROUND

This report forms part of a package of reports - “Coal Classification - Industry approach to hazard

classification under the revised MARPOL Convention and the IMSBC Code”.

The aim of this publication is to help coal producers comply with the new coal classification

requirements introduced by the International Maritime Organisation (IMO) under the International

Convention for the Prevention of Pollution from Ships (MARPOL) and the International Maritime

Solid Bulk Cargoes Code (IMSBC).

The other two reports appearing in this series are:

• Report 1. New Compliance Requirements of the MARPOL Convention and the IMSBC

Code

• Report 3: Coal Classification Guidance

The reports were written by ARCHE, a specialist environmental toxicology consultancy, under the

oversight of the World Coal Association Technical Working Group on Coal Classification, chaired by

Dr. Sue Hubbard, Principal Adviser, HSEC Product Regulation & Information Support at Rio Tinto.

This publication is available free of charge for all WCA Members.

2 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards

TABLE OF CONTENTS

1. CHEM ICAL COM POSITION OF DIFFERENT TYPES OF COAL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

1.1. Coal – general information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

1.2. Inorganic trace elem ents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

1.2.1. Mode of occurrence of trace elements .................................................................................................... 7

1.2.2. Concentrations of trace elements in coal – data in the public domain ........................................ 9

1.2.3. Concentration of trace elements in coal – company-specific data ............................................ 19

1.3. Polycyclic aromatic hydrocarbons in coal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

1.4. Environmental hazard assessment of coal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

1.4.1. Hazard assessment of trace elements in coal .................................................................................... 29

1.4.2. Environmental hazard assessment of PAHs in coal ......................................................................... 34

1.4.3. Data provided by WCA members ............................................................................................................ 35

2. RESULTS OF ECOTOXICOLOGICAL EXPERIM ENTS W ITH COAL SAM PLES . . . . . . . . 40

3. HUM AN HEALTH EFFECTS OF COAL AND COAL TRANSPORT: REVIEW OF

LITERATURE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

3.1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

3.1.1. Relevance of existing literature .............................................................................................................. 43

3.1.2. UN GHS criteria for classification .......................................................................................................... 44

3.1.2.1. Germ cell mutagenicity ........................................................................................................................ 44

3.1.2.2. Carcinogenicity ....................................................................................................................................... 46

3.1.2.3. Reproductive toxicity .......................................................................................................................... 48

3.1.2.4. Specific target organ toxicity – repeated exposure ................................................................ 50

3.2. Literature review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51


3.2.1. Route of exposure ........................................................................................................................................ 52

3.2.2. Human health effects of inhalation exposure to coal ..................................................................... 53

3.2.2.1. Germ cell mutagenicity ........................................................................................................................ 53

3.2.2.2. Carcinogenicity ....................................................................................................................................... 59

3.2.2.3. Reproductive toxicity .......................................................................................................................... 69

3.2.2.4. Specific target organ toxicity – repeated exposure ................................................................ 71

3.3. Sum m ary and conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76

4. REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

5. ANNEXES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99

5.1. Annex I : Summary of the ASTM coal classification system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99

5.2. Annex II : M ode of occurrence of m etals in coal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100

5.3. Annex III : Summary of Transformation/Dissolution Protocol (T/DP)

test data for coal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

5.4. Annex IV: Human health hazards of crystall ine sil ica (fine fraction) . . . . . . . . . . . . . 107


GLOSSARY

ACARP: Australian Coal Association Research Program

ACIRL: Australian Coal Industries Research Laboratories

AM : alveolar macrophages

ASTM : American Society for Testing and Materials

Btu/lb: British thermal unit/pound

CCD: Coal Criteria Document

CLP: classification, labelling and packaging

COPD: chronic obstructive pulmonary disease

CW P: coal workers’ pneumoconiosis

DSD: Dangerous Substances Directive

EPA: Environmental Protection Agency

ERV: Ecotoxicity Reference Value

GHS: Globally Harmonized System of Classification and Labelling of Chemicals

IARC: International Agency for Research on Cancer

IM DG: International Maritime Dangerous Goods

IM SBC: International Maritime Solid Bulk Cargoes

ISO: International Organization for Standardization

M ARPOL: International Convention for the Prevention of Pollution from Ships

M eClas tool: Metals Classification tool

M HB: materials hazardous only in bulk

NIOSH: National Institute for Occupational Safety and Health

PAH: polycyclic aromatic hydrocarbon

PM F: progressive massive fibrosis

HM E: harmful to the marine environment

STOT-RE: Specific Target Organ Toxicity – Repeated Exposure

T/DP: Transformation/Dissolution Protocol

W CA: World Coal Association

W HO: World Health Organization


1. CHEMICAL COMPOSITION OF DIFFERENT TYPES OF COAL

1.1. COAL – GENERAL INFORMATION

Coal originates from a mixture of vegetation that accumulates at the bottom of swamps where no

oxidation occurs, and where the degradation of the organic material is determined by anaerobic

bacterial populations. These swamps are also located in areas with very low erosion and runoff.

This process takes place over millions of years until environmental conditions change; the layer of

former plant material starts to lose part of its water content, gets covered by layers of sediment

and a significant reduction of the layer thickness can be observed (80% reduction).

Minerals in this material have different sources:

• present in the plant material

• associated to mineral particles that have undergone sedimentation during the

formation process

• floods that occurred after the formation period ended (and which added, in general,

multiple layers on top of this material).

Several ranking systems for coal have been developed, each with their own specific parameters

and criteria, advantages and disadvantages. In that respect, both the International Organization for

Standardization (ISO) and American Society for Testing and Materials (ASTM) classification

scheme (ASTM Standard D388-98a, ISO 11760) are commonly used for ranking different types of

coals. The rank of a deposit of coal more or less depends on the pressure and heat acting on the

plant debris as it sinks deeper over a period of millions of years, with each category having its

typical chemical composition, its energy content and, ultimately, its end use.

Lignite and sub-bituminous coals are typically softer, friable substances that have a dull, earthy

appearance. Overall, they are characterized by high moisture levels and lower carbon content (and

consequently a lower energy content).

• Lignite (‘brown coal’) represents an early phase in the transformation process from plant to

coal and is the least mature coal rank. It contains less carbon (40–60% fixed carbon) and


heating value (approx. 5500–8300 Btu/lb) when compared to other types of coal. It also

contains long-chain hydrocarbons (aliphatic structures) with many hydroxic/carboxylic

functional groups. Lignite is used for power generation (e.g. power stations constructed

close to the mine). At this stage of the coal formation, the reduction of the layer thickness

of former plant material is still limited, and therefore layers of lignite can have thicknesses

of up to several hundred metres. Due to the limited reduction of the layer, trace metals are

less concentrated when compared to later stages of the coal-formation process.

• When lignite is subjected to longer and deeper burial, it will be converted into the

harder and darker sub-bituminous coal due to the rearrangement of the long-chain

hydrocarbons into ring-structured aromatics. This more compact structure reduces the

overall porosity of coal and, hence, its potential to leach some of its compounds. The

fixed carbon content of sub-bituminous coal ranges between 46% and 60% and has a

heating value of 8300–13,000 Btu/lb. Typically, sub-bituminous coal contains less

sulfur, resulting in ‘cleaner’ burning.

Higher-ranked coals (bituminous coal, anthracite) are generally harder and stronger, and often

have a black vitreous lustre. Compared to lignite and sub-bituminous coal, these coals have a

higher aromaticity, fixed carbon content, a higher heating value and lower moisture content. In

addition, as the aliphatic compounds are the most volatile fraction of coal, the percentage of

volatile substances is low for higher-ranked coals (e.g. for anthracitic coals below 8%, up to 1% in

extreme cases).

• Bituminous coal (or black coal) is the main fuel source in steam turbine-powered electric

generating plants, and some of it has properties that make it suitable for conversion to coal

used in steelmaking. Bituminous coal has a 46–86% fixed carbon content, and a heating

value of 11,500–15,000 Btu/lb. Due to its compaction of both plant material and mineral

matter, it is considered to be a sedimentary rock.

• Anthracite (also called blue coal, hard coal, stone coal) is a hard black coal with a fixed

carbon content of 86–98%, and a heating value of 13,500–15,600 Btu/lb. It is a product of

metamorphism (associated with metamorphic rock) and could be considered as a transition

stage between bituminous coal and graphite.


Other important determinants of coal quality relate to its mineral content (sulfur, chlorine,

phosphorus, trace metals). These chemical properties not only affect the behavior of a specific

type of coal in its intended use, but also significantly determine its behavior in the environment.

Based on the overall composition of coal, it can be concluded that the most critical fractions of

coal that may be of concern for the aquatic environment are inorganic trace elements and organic

aromatic compounds such as polycyclic aromatic hydrocarbons (PAHs). Both groups of substances

are further discussed in more detail.

1.2. INORGANIC TRACE ELEMENTS

1.2.1. M ODE OF OCCURRENCE OF TRACE ELEM ENTS

Substantial information on the trace elements content of different types of coal is available. Each

element is associated with one or more typical components in coal such as typical minerals, pyrite,

clay material, carbonates, etc. Consequently, the relevance of each element in a specific type of

coal is related to the presence and abundance of those compounds for that specific coal sample.

Trace element levels are the sum of the fraction that is associated with organic matter and the

fraction that is present in the mineral fraction. Depending on the type of coal, the total fraction of

a specific element will be higher (enrichment) or lower (depletion) than the typical concentration in

the Earth’s crust. Enrichment suggests that the trace element is associated primarily with the

organic matter, while depletion arises simple by the dilution effect of the mineral matter in the

coal. Elements that enrich during coal formation are shown in Table 1. The most significant

enrichment can be found for selenium. Elements depleted in coal are chromium, cobalt, fluorine,

manganese, nickel, thorium, uranium, vanadium and zinc.

Decaying plant material contains many (essential) trace elements that have an affinity to form

chemical bonds with organic matter; these elements are found at elevated levels in coal (compared

to the Earth’s crust). In addition, some elements are enriched due to the co-crystallization with

secondary minerals. The insoluble pyrite (FeS2) can be formed in the anoxic environment of a coal-

forming swamp, and some trace elements are associated with this secondary mineral.


Table 1 Enrichment factors for trace elements in coal relative to the Earth’s crust (1)

Element Limited

enrichment

M oderate

enrichment

Significant

enrichment

Antimony 6

Arsenic 6

Boron 5

Cadmium 7

Lead 1.3

Mercury 2.3

Molybdenum 2.0

Selenium 82 (1) From US National Committee for Geochemistry, 1980 (Dale, 2009).

Several authors reported on the likely mode of occurrence of trace elements in coal (data shown in

Annex), This information has led to a summary overview where the most probable mode of

occurrence is outlined, together with a confidence level (CL) for each specific element:

• antimony (CL: low): possibly associated with sulfides and organic

• arsenic (CL: medium): associated with sulfide, with minor organic and clay

• beryllium (CL: high): associated with clays

• boron (CL: high): associated with organics

• cadmium (CL: low): probably associated with sulfides

• chromium (CL: medium): associated with clays and minor organic association

• cobalt (CL: low): possibly associated with organic, clay, sulfide, carbonate

• copper (CL: medium): associated with sulfide and clay

• lead (CL: high): associated with sulfide

• manganese (CL: high): associated with carbonate

• mercury (CL: high): associated with sulfide, and possibly organic

• molybdenum (CL: high): associated with organic and sulfide

• nickel (CL: low): possibly associated with sulfide, carbonate, organic

• selenium (CL: high): associated with organic and sulfide

• thorium (CL: high): predominantly in clays

• uranium (CL: high): associated with clays, acid resistant minerals and organic


• vanadium (CL: high): associated with clays and organic

• zinc (CL: high): associated with sulfide.

This enumeration can be used for the identification of the most relevant trace elements for

specific coal types.

Identification of the modes of occurrence has been conducted in several ways:

• Column separation or heavy liquid separation has been used to separate the coaly matter

from the mineral matter. The method also allows the separation of mineral phases with

different density. Trace metal content is then determined for each phase.

• Sequential leaching procedures where each step releases the trace elements that are

associated to a different mineral/organic fraction: loosely bound ions on clays and organic

matter, bound to carbonates and monosulfides, bound onto disulfides (e.g. pyrite), bound to

silicates, etc.

1 .2.2. CONCENTRATIONS OF TRACE ELEM ENTS IN COAL – DATA IN THE PUBLIC

DOM AIN

The objective of this (and the following) section is to define representative ranges of different

trace elements in various types of coal (where possible). Readily available information was brought

together from different review reports. It should be noted that there are limitations to the global

coverage of these ranges as not every region or type of coal is equally represented in the database.

It should be stressed, however, that the main objective at this stage of the evaluation was not to

determine exact ranges for each coal type but to get a good approximation of the order of

magnitude (percent-wise) that an element may occur in one or more types of coal. In a next phase,

the maximum values for each element are used to prioritize the most critical trace elements using

an existing metal classification tool (MeClas tool, see further). Guidance on how to demonstrate

that a coal sample should not be considered as a substance harmful to the marine environment

(HME) will be based on the outcome of this prioritization process.

Review data on coal trace element composition were collected from the Australian Coal

Association Research Program (ACARP) report (Riley, 2005), Dale (2009) and Ahrens and Morrisey


(2005). The ACARP report (Riley, 2005) gives an overview of trace element concentrations in three

types of coal:

• Australian export coal (predominantly bituminous coal with high calorific value)

• a limited selection of non-Australian internationally traded coals

• Australian domestic coals (bituminous coal that is used in Australian power plants).

Samples were analysed by the Commonwealth Scientific and Industrial Research

Organisation (CSIRO) using standard methods accredited by Standards Australia (SA), the

ASTM and the ISO. Many of the methods used were developed in work undertaken within

ACARP. The analysis scheme used was according to AS 1038.10.0 – Coal and coke – analysis

and testing, Part 10.0: Determination of trace elements – Guide to the determination of trace

elements (2002). The methods are based on modern instrumental techniques, including

inductively coupled plasma mass spectrometry, inductively coupled plasma atomic emission

spectrometry, hydride generation and cold vapour atomic fluorescence spectrometry, X-ray

fluorescence spectrometry and proton-induced gamma emission. All are capable of

accurately determining the concentrations of the trace elements at the levels normally

present in thermal coal products. Average concentrations (plus range in parentheses) for

each type of coal is provided in Table 2. The ACARP reports, however, did not specify

whether the moisture content was taken into account when reporting concentration levels. It

is assumed that values are expressed on a dry matter basis. One should be aware that the

elemental ranges for non-Australian traded coals in Table 2 only represent a very limited

number of selected coal samples (approx. 60), and the relevance with regard to global non-

Australian export coals is uncertain. Table 3 compares the average of trace elements in

Australian export coals with concentrations (averages, minimum/maximum ranges) that were

reported for other coal samples.

The information on coal composition that is provided in Table 2 and Table 3 is predominantly

relevant for coal that has been mined in Australia. The composition of coal, however, can vary

significantly among different geographic areas. Several papers have compared the composition of

coal samples that originate from other areas in the world. Dale (2009) has presented the composition

of selected coal that was mined in China, Colombia, Indonesia, Poland, Russia, South Africa, Ukraine,


United States and Venezuela (Table 4). For most elements the reported min-max ranges are

comparable, though it can be seen that sometimes the concentration of an element is somewhat

higher for a specific country (e.g. Sb in Poland, B in Indonesia/Colombia, Cu in Poland/USA). However,

as the amount of coals that are represented in each country-specific range is limited, no conclusions

on regional differences should be drawn from these data sets. A second set of region-specific

compositions of coal samples was identified in Ahrens and Morrisey (2005) (Table 5).

Table 2 Trace element concentration in different types of coal (average and min-

max range) (Riley, 2005) – the ACARP report does not specify whether reported

concentrations levels take the m oisture content of the sam ples into account

Element Australian export

coals

Australian domestic

coals

Limited selection of

non-Australian traded

coals

Approx. 100 samples, not specified

per category (1)

Approx. 60 samples (1)

mg/kg

Antimony 0.39

(0.05–1.0)

0.55

(0.06–1.0)

0.33

(0.02–1.4)

Arsenic 1.05

(0.2–2.2)

1.6

(0.4–7.0)

3.6

(0.3–13.0)

Barium 180

(16–1010)

115

(15–250)

500

Beryllium 0.9

(0.2–3.2)

1.2

(0.4–2.5)

0.9

(0.1–3.2)

Boron 19

(5–70)

32

(7–141)

72

(11–430)

Cadmium 0.11

(0.01–0.31)

0.15

(0.03–0.38)

0.08

(0.01–0.31)

Chromium 10

(2–25)

10

(2–23)

16

(1–35)

Cobalt 4

(1–14)

4

(1–12)

4

(>1–13)

Copper 15

(6–27)

4

(1–12)

9

(<1–23)

Lead 3

(2–14)

10

(3–18)

6

(<1–22)

Manganese 125

(5–700)

160

(19–430)

40

(7–117)

Mercury 0.04

(0.01–0.11)

0.04

(0.02–0.13)

0.09

(0.02–0.19)


Molybdenum 0.8

(0.1–2.6)

0.9

(<0.1–1.9)

1.2

(0.1–4.0)

Nickel 6

(4–23)

6

(2–18)

10

(2–22)

Selenium 0.5

(0.1–1.0)

0.6

(0.3–1.1)

1.5

(0.1–5.0)

Thorium 2.8

(0.1–7.3)

2.9

(1.2–5.5)

3.8

(0.3–12.0)

Uranium 1.1

(0.3–4.1)

0.9

(0.5–2.1)

1.3

(<0.1–3.8)

Vanadium 28

(7–75)

No sufficient data 19

(1–50)

Zinc 18

(3–26)

0.03

(<0.01–0.14)

11

(4–23) (1) Amount of samples not specified for each element. Source: Riley, 2005.


Table 3 Trace element concentration on different types of coal – no specification whether reported concentrations levels are

based on wet weight or dry weight (a ssumption: mg/kg DW)

Element Australian

export coals

(2005)

ACIRL database

(both export

and domestic

coals)

Valcovic. 1983

(mg/kg)v

Dale, 2009

(compilation of

Clark and

Swaine, 1962;

Swaine 1977,

1979)

Coals in New

South W ales

and Queensland

power stations

Australian

export coals

(2009)

(typical value)

mg/kg

Antimony 0.39 (0.05–1.0) 0.33 (max: 1.69) 3 0.84 (<0.1–2) 0.56 (0.05–1) 0.40 (0.05–1.2)

Arsenic 1.05 (0.2–2.2) 0.62 (max: 3.2) 5 2.7 (<0.1–55) 1.6 (0.2–7) 0.86 (0.1–2.7)

Barium 180 (16–1010)

Beryllium 0.9 (0.2–3.2) 3 1.5 (<0.4–8) 0.9 (0.2–2.2) 0.6 (0.2–2.1)

Boron 19 (5–70) 18.6 (max: 70) 75 60 (2– 300) 16 (<5–45) 17 (4–36)

Cadmium 0.11 (0.01–0.31) 0.04 (max: 0.14) 1.3 0.07 (0.05 –0.2) 0.11 (0.03–0.16) 0.07 (0.01–0.28)

Chromium 10 (2–25) 14.9 (max: 49) 10 9 (<2–56) 12 (3–25) 7 (2.9–24)

Cobalt 4 (1–14) 4.3 (max: 14.2) 5 5 (<0.6–30) 5 (1–14) 3.0 (1.2–12)

Copper 15 (6–27) 20.1 (max: 49) 15 15 (3–40) 21 (7–35) 13 (6.2–32)

Lead 3 (2–14) 6.93 (max: 21.6) 25 10 (1.5–60) 8 (3–14) 5.6 (2.2–14)

Manganese 125 (5–700) 50 135 (3–900) 155 (1–570) 42 (4–700)

Mercury 0.04 (0.01–0.11) 0.07 (max: 0.241) 0.12 0.1 (0.026–0.4) 0.052 (0.006–

0.11)

0.021 (0.006–

0.08)

Molybdenum 0.8 (0.1–2.6) 0.87 (max: 2.6) 5 1.5 (<0.3–6) 1 (0.06–2.5) 0.66 (0.1–2.7)

Nickel 6 (4–23) 7.81 (max: 26.1) 15 15 (1–70) 12 (4–23) 7.5 (1.4–31)

Sulfur (%) 0.42% (0.1–0.73) 0.47% (0.21–0.95)

Selenium 0.5 (0.1–1.0) 0.77 (max: 2.94) 3 0.8 (0.18–2.6) 0.69 (0.21–0.9) 0.42 (0.12–1.1)

Thorium 2.8 (0.1–7.3) 2 4.2 (<0.2–8) 3.5 (0.7–7.3) 2.4 (0.5–6.9)


Uranium 1.1 (0.3–4.1) 1 1.7 (0.28–5) 2.9 (0.52–4.1) 0.82 (0.27–2.5)

Vanadium 28 (7–75) 25.1 (max: 61) 25 26 (4–90) 32 (7–75) 22 (7–62)

Zinc 18 (3–26) 16.12 (max: 65) 50 100 (6–500) 21 (3–125) 11 (4–51)


Table 4 M ean and maximum values for trace elements in a selected number of thermal coals from individual countries –

no specification whether reported concentrations levels are based on wet weight or dry weight (assumption: mg/kg DW)

Element South

Africa

n = 21

China

n = 12

Poland

n = 6

Indonesia

n = 38

Colombia

n = 18

Russia

n = 5

Ukraine

n = 3

USA

n = 6

Venezuela

n = 2

mg/kg

Antimony 0.29–0.8 0.34–0.67 1.3–1.4 0.12–0.36 0.57–1.5 0.31–0.34 0.44–0.67 0.73–1.4 0.56–0.57

Arsenic 2.7–9.4 1.3–4.1 3.1–4.7 2.8–9.7 3.0–10 3.0–3.9 5.9–9.9 12–26 1.3–1.8

Beryllium 2.1–4.0 1.3–2.1 1.5–1.8 0.46–1.8 0.42–0.59 0.52–0.60 1.1–1.5 2.3–3.2 0.7

Boron 37–96 53–95 26–33 88–146 55–175 63–78 59–75 33–61 47

Cadmium 0.1–0.19 0.07–0.18 0.14–0.23 0.046–1.9 1.8–0.38 0.09–0.13 0.084–

0.096

0.11–0.14 0.11

Chromium 26–34 8–21 21–24 6.7–22 16–28 12–19 14 13–22 19–26

Cobalt 7–14 5–13 8–10 3.3–9 2.3–5 3.0–3.6 5.5–6 7–11 1.9–2.0

Copper 12–20 9–12 21–24 6.1–19 6–10 8–9 10 15–28 5–6

Lead 8–14 12–22 15–19 3.3–6 2.7–4.8 5.4–6.9 7.8–8.9 9.6–14 4.8–6.0

Manganese 92–255 63–123 80–124 26–55 47–68 39–52 97–152 38–100 30–39

Mercury 0.09–0.13 0.068–0.19 0.09–0.1 0.043–0.18 0.040–0.1 0.037–

0.058

0.078–0.11 0.1–0.14 0.1–0.11

Molybdenum 2.3–6.9 1.1–2.3 1.4–2.0 0.51–1.7 1.7–5.0 2.3–1.5 1.0–1.2 2.3–4.2 0.85–1.1

Nickel 14–29 7–14 19–22 7.0–21 9.2–14 9–10 10 14–21 12

Sulfur (%) 0.59–0.94 0.54–0.95 0.63–0.71 0.52–1.1 0.72–1.0 0.35–0.47 0.72–1.0 1.49–3 0.59–0.64

Selenium 0.70–1.3 1.9–4.4 0.77–0.90 0.41–3.8 4.2–5.7 0.32–0.51 1.26–2.01 4.3–5.3 5.3–5.5

Thorium 8.1–21 5.5–8.6 2.8–3.6 1.2–9 1.3–5.0 2.3–2.0 1.8–2.0 3.4–6.9 1.6–1.8

Uranium 2.8–6.8 2.2–5.5 1.9–2.3 0.55–9 0.62–0.9 1.0–1.2 1.10–1.2 1.40–2.8 0.56–0.64


Vanadium 47–128 14–23 35–40 15–60 26–35 15–19 20–24 32–51 29–32

Zinc 13–29 14–55 24–41 10–23 18–23 15–18 18–20 13–21 14–16 Source: Dale, 2009


Table 5 Inorganic chemical properties of particulate coal; concentrations by dry weight

Element UK Germany Canada Spain USA Australia New

Zealand

Rank(1) B L, B B SB, B B, SB SB, B SB, B

mg/kg

Silver 0.01–

0.08

<0.2–1 0.003–

0.19

Arsenic 1–73 1.5–50 0.2–240 56.3–

35.7

0.34–120 <1–55 <1.5–27.5

Boron 0.5–60 2–236 9–360 141–436 5–230 1.5–300 10–708

Barium <6–500 45–350 10–1000 36–91 5.0–1600 <40–1000 8.3–148

Cadmium 0.02–5 0.02–21 0.26–

0.33

0.10–65 0.05–0.2 <0.3–1.7

Cobalt 0.4–60 7–30 0.2–21 4–12.5 0.6–34 <0.06–30 <0.1–14.0

Chromium 1–45 4–80 2.1–95 11–38 2.4–90 <1.5–30 0.4–20.9

Copper 5–240 10–60 0.2–52 7–16 3.1–44 2.5–40 0.95–13.6

Fluor 5–500 20–370 31–890 19–150 15–500

Iron 104–

33,265

1780–

14,900

Gallium 3–10 5–10 0.8–11 1–20 0.14–5.8

Germanium 2–80 1.2–2 0.1–43 <0.3–30 0.05–7.8

Mercury 0.03–2.0 0.1–1.4 0.02–1.3 0.05–6.3 0.026–29 0.12–0.56

Manganese 1–1600 55–68 2–600 40–86 1.4–220 2.5–900 1.3–63

Molybdenu

m

0.1–20 6–30 0.4–13 0.6–32 0.10–30 <0.23–6 <0.02–

0.76

Nickel 3–60 15–95 2–38 8–33 1.5–68 0.8–70 0.6–27.5

Phosphorus <10–

1000

40–1240 45–5200 68–275 10–1500 30–4000 <1.6–29.3

Lead 1–900 0.1–390 1.8–53 5–21 0.7–220 1.5–60 0.3–18.0

Antimony 1–10 0.14–5.0 0.1–16 0.7–3.2 <0.04–3.7

Selenium 0.3–5.1 0.6–5.5 <0.1–8.0 0.5–1.6 0.4–8.1 0.21–2.5

Tin 0.3–75 3.6–3.9 2–15 0.9–2.3 0.1–51 <0.9–15 0.14–17.5

Thorium 0.7–6.7 1.6–4.4 0.1–9 2–6

Thallium 0.6–1.7 0.01–0.72 0.20–

0.39

0.62–51 <0.2–8 <0.004–

6.7

Uranium 1.1–3.0 0.3–2.2 0.4–12 0.9–26 0.30–4.6 0.4–5

Vanadium 3–150 31–179 3.4–200 14–76 4.8–90 4–90 0.68–18.5

Zinc 3–7000 14–1742 2.0–62 35–95 0.3–5300 12–73 0.7–55.5 (1) L = lignite; SB = sub-bituminous; B = bituminous.

Source: Ahrens and Morrissey, 2005 (data taken from: Francis, 1961; Swaine and Goodarzi, 1995; Querol et

al., 1996; Gluskoter et al., 1977; Ward, 1984; Fendinger et al., 1989; Davis and Boegly, 1981; Swaine, 1977;

Solid Energy New Zealand Ltd, 2002; Soong and Berrow, 1979; Sim, 1977; ANZECC, 2000)


The observed worst-case concentration for each element (i.e. highest reported concentration in

Table 2 to Table 5) is summarized in Table 6. This table also provides the total amount of trace

elements in 100 mg and 1 mg of coal as these amounts are relevant when implementing a

bioavailability correction on the classification. Such correction is based on the outcome of

Transformation/Dissolution Protocol (T/DP) tests (see further).

Table 6 W orst-case concentration levels (mg/kg; % ) of trace metals in coal;

worst-case amount to be released at loadings 100 mg and 1 mg coal/L – data

assumed to be on a dry weight basis

Element W orst-case

concentration

(mg/kg coal)

% in coal Amount in 100

mg coal

(= max release in

a T/DP at this

loading)

(µg)

Amount in 1 mg

coal

(= max release in a

T/DP at this

loading)

(µg)

Silver 0.19 0.000019 0.019 0.00019

Antimony 16 0.0016 1.6 0.016

Arsenic 240 0.0240 24.0 0.240

Barium 1600 0.160 160 1.6

Beryllium 8 0.0008 0.8 0.008

Boron 708 0.0708 70.8 0.71

Cadmium 65 0.0065 6.5 0.065

Chromium 95 0.0095 9.5 0.095

Cobalt 60 0.006 6 0.06

Copper 240 0.024 24.0 0.24

Iron 33,265 3.327 3326.5 33.27

Gallium 20 0.002 2 0.02

Germanium 80 0.008 8 0.08

Lead 900 0.09 90 0.90

Manganese 1600 0.16 160 1.6

Mercury 29 0.0029 2.9 0.029

Molybdenum 32 0.0032 3.2 0.032

Nickel 95 0.0095 9.5 0.095

Selenium 8.0 0.0008 0.8 0.008

Tin 75 0.0075 7.5 0.075

Thorium 21 0.0021 2.1 0.021

Thallium 51 0.0051 5.1 0.051

Uranium 26 0.0026 2.6 0.026

Vanadium 200 0.020 20.0 0.20

Zinc 7000 0.70 700 7.0


1.2.3. CONCENTRATION OF TRACE ELEM ENTS IN COAL – COM PANY-SPECIFIC

DATA

Information on typical compositions of coal was requested from the members of the World Coal

Association (WCA), and reports on several coal composition analyses were provided to ARCHE. It

should be noted that agreement on a standardized method of analysis is essential when setting a

global classification system for coal that is based on its composition. Huggins (2002), for instance,

published a summary of analytical procedures for the analysis of coal for inorganic constituents.

Riley et al (2005) developed a standard method (Australian Standard AS 1038.10.0-2002 (R2013);

Coal and coke – analysis and testing – Determination of trace elements – Guide to the

determination of trace elements; standard published by Standards Australia). This standard was

adopted as ISO 203380 Standard (2008, revised 2013): Selection of methods for the

determination of trace elements in coal. The ISO 23380:2013 provides guidance on the selection

of methods used for the determination of environmentally relevant trace elements, including

antimony, arsenic, beryllium, boron, cadmium, chlorine, chromium, cobalt, copper, fluorine, lead,

manganese, mercury, molybdenum, nickel, selenium, thallium, vanadium, and zinc. The standard,

however, does not prescribe the methods used for the determination of individual trace elements.

The ASTM also published two standard test methods with regard to the determination of trace

elements in coal:

• ASTM D3683-11: Standard Test Method for Trace Elements in Coal and Coke by Atomic

Absorption

• ASTM D6357-11: Test Methods for Determination of Trace Elements in Coal, Coke, &

Combustion Residues from Coal Utilization Processes by Inductively Coupled Plasma

Atomic Emission, Inductively Coupled Plasma Mass, & Graphite Furnace Atomic Absorption

Spectrometry.

Four different companies provided trace element compositions for various coal samples. All

reported concentration levels are based on dry weight analysis.1 Companies and references to the

mining sites have been anonymized for confidentiality reasons. In addition, the provided coal

1 Dry weight levels are higher than wet weight levels, and can therefore be considered as worst-case

concentration levels.


sample compositions are grouped according to coal type (lignite, (sub-)bituminous,

(semi-)anthracite, etc.), and not according to region or company, thus further anonymizing the

information. Grouping was based on the ASTM ranking system (see Annex for more detailed

information on this ranking system) as the provided properties of the different coal samples did

not always allow a categorization according to the ISO ranking procedure, for example.

All coal samples were categorized as either bituminous or sub-bituminous, and further distinction

was made based on the reported British thermal unit (Btu) value (classification according to ASTM

D388). Both ranks of coal represent the great majority of seaborne-traded coals. Table 7 compiles

the trace element composition of seven high-volatile C bituminous coal samples (11,500–13,000

Btu/lb). The composition of four sub-bituminous A coals are given in Table 8. The trace element

content of two sub-bituminous C coal samples is shown in Table 9.

Table 10 presents the maximum concentration for each trace element for the different

types of coal, and compares these with the maximum value that was found in the literature.

This comparison demonstrates that the worst-case assumption that is based on literature

data is sufficiently conservative as all maximum concentration levels in the coal samples

that were provided by WCA members were below these maximum levels. Therefore, the

literature-based worst-case values will be used to define the most critical elements that

may drive the environmental classification of coal.


Table 7 Sum m ary of high-volatile C bituminous coal sam ples (fixed carbon < 69% , Btu/lb 11,500–13,000) – reported

concentrations on a dry weight basis

Element Sam ple #1

Sam ple #2

Sam ple #3

Sam ple #4

Sam ple #5

Sam ple #6

Sam ple #7

M ax value

mg/kg DW

Antimony <1 0.41 0.9 0.6 0.2 0.7 0.9

Silver <0.2 0.03 0.05 0.03 0.05 0.05

Arsenic 13 6 8.5 12.4 3.2 1.3 2.8 12.4

Boron 80 21 25.3 80

Barium 70 46 64.3 138.3 97.0 340.0 93.2 340.0

Beryllium 1 2.3 0.9 2.1 2.7 0.3 3.1 3.1

Cadmium 2 <0.2 0.08 0.01 0.06 0.07 0.07 2

Cobalt 6 8 3.6 7.7 9.3 1.3 8.8 9.3

Chromium 4 12 17.0 26.7 22.5 4.0 27.8 27.8

Copper 5 19 7.5 22.7 14.3 6.0 17.0 22.7

Iron 1900 1900

Mercury <0.05 0.06 0.1 0.1 0.05 0.03 0.05 0.14

Manganese 11 8 18.4 14.6 13.8 14.0 8.5 18.4

Molybdenum 2 2 1.1 2.1 1.8 0.6 2.0 2.1

Nickel 7 16 11.9 18.0 16.0 2.3 16.5 18.0

Lead 15 7 4.4 8.4 7.5 3.9 9.5 15

Selenium <3 3 1.0 3.9 5.0 0.8 5.8 5.8

Tin <3 <1 0.6 0.9 0.9 0.4 0.9 0.9

Strontium 69 57 90.0 61.0 175.3 54.5 175.3

Titanium 350 350


Thorium <1 1.5 0.4 0.3 0.15 0.3 1.52

Thallium <1 0.5 0.52

Uranium 0.7 1.0 0.7 1.5 1.5

Vanadium 14 25 31.1 36.1 32.00 11.0 42.0 42.0

Zinc 23 14 13.2 16.0 13.3 6.3 15.3 23.0

Zirconium 16 24.4 26.0 15.9 31.8 31.8


Table 8 Summary of sub-bituminous A coal samples (fixed carbon < 69% ,

Btu/lb 10,500–11,500) – reported concentrations on a dry weight basis

Element Sam ple #1

Sam ple #2

Sam ple #3

M ax value

mg/kg DW

Antimony <2 0,3 1.0

Silver <1 <0.2 0.04 0.04

Arsenic 10 1 1.6 10

Boron 62 136 233 233

Barium 24 340 30 340

Beryllium 3 0.6 1.0 3

Cadmium <0.3 <0.3 0.2 0.2

Cobalt 3 1 3 6.1

Chromium 3 5 22 22

Copper 6 6 8 13.0

Iron 2700 2700

Mercury 0.05 0.03 0.06 6

Manganese 29 9 24 24

Molybdenum 2 <3 7 29

Nickel 9 3 13 13

Lead 10 6 5 10

Selenium <3 <1 2.2 6

Tin <3 1 0.5 0.5

Strontium 10 190 21 21

Titanium 480 480

Thorium 1.5

Thallium <1 <1 0.6 0.4

Uranium 3.0 1.1

Vanadium 12 9 32 32

Zinc 16 6 41 41

Zirconium 40 15 40


Table 9 Summary of sub-bituminous C coal sam ples (fixed carbon < 69% , Btu/lb

8300–9500), a high-volatile B bitum inous coal sample (Btu/lb 13,000–14,000)

and a medium-volatile bituminous coal sam ple (Btu/lb > 14,000) – reported

concentrations on a dry weight basis

Element Sam ple #1

Sam ple #2

Sam ple #3

M ax value

Sub-bituminous C High-volatile B

bituminous

mg/kg DW

Antimony <1 0.1 1.0 0.1

Silver <0.2 0.03 0.03

Arsenic <1 1.2 7.7 1.2

Boron 29 35 35

Barium 345 340.8 126.2 345

Beryllium 0.2 0.2 1.0 0.2

Cadmium <0.2 0.08 0.04 0.08

Cobalt 2 1.5 6.1 2.0

Chromium 4 4.0 10.5 4.0

Copper 11 9.0 13.0 11.0

Iron

Mercury 0.1 0.07 0.09 0.1

Manganese 7 14.8 27.6 14.8

Molybdenum <2 0.6 2.9 0.6

Nickel 3 3.3 11.8 3.3

Lead <2 2.3 5.1 2.3

Selenium <1 0.6 2.3 0.6

Tin <1 0.3 0.3 0.3

Strontium 160 158.0 160

Thallium <1 0.08 0.4 0.08

Uranium 10 0.4 1.1 10

Vanadium 13.5 20.5 13.5

Zinc 7 8.8 12.6 8.8

Zirconium 14 12.3 14


Table 10 M aximum trace element concentration in different coal types (data

provided by W CA members and l iterature data) – reported concentrations on a

dry weight basis

Element High-

volatile B

bituminous

High-

volatile C

bituminous

Sub-

bituminous A

Sub-

bituminous C

Literature

worst-case

mg/kg DW

Antimony 1.0 0.9 1.0 0.1 16

Silver 0.05 0.04 0.03 0.19

Arsenic 7.7 12.4 10 1.2 240

Boron 80 233 35 708

Barium 126.2 340.0 340 345 1600

Beryllium 1.0 3.1 3 0.2 8

Cadmium 0.04 2 0.2 0.08 65

Cobalt 6.1 9.3 6.1 2.0 60

Chromium 10.5 27.8 22 4.0 95

Copper 13.0 22.7 13.0 11.0 240

Iron 1900 2700 33265

Mercury 0.09 0.14 6 0.1 29

Manganese 27.6 18.4 24 14.8 1600

Molybdenum 2.9 2.1 29 0.6 32

Nickel 11.8 18.0 13 3.3 95

Lead 5.1 15 10 2.3 90

Selenium 2.3 5.8 6 0.6 8.0

Tin 0.3 0.9 0.5 0.3 75

Strontium 175.3 21 160

Titanium 350 480

Thorium 1.5 1.52 1.5 21

Thallium 0.4 0.52 0.4 0.08 51

Uranium 1.1 1.5 1.1 10 26

Vanadium 20.5 42.0 32 13.5 200

Zinc 12.6 23.0 41 8.8 7000

Zirconium 1.0 31.8 40 14

1.3. POLYCYCLIC AROMATIC HYDROCARBONS IN COAL

Polycyclic aromatic hydrocarbons (PAHs) are composed of many carcinogenic substances that are

ubiquitous in the environment. In addition to sorbed PAHs, once being exposed to the environment,

original hard (unburnt) coal from the seam can contain PAHs up to hundreds and, in exceptional

cases, thousands of mg/kg (Willsch and Radke, 1995; Stout and Emsbo-Mattingly, 2008).


Formation of PAHs is the result of the transformation of resistant plant biopolymers (e.g. lignin)

into a highly aromatic, three-dimensional, network matrix under the influence of temperature and

pressure (Taylor et al., 1998). In coals of low rank (e.g. lignite, sub-bituminous coal, brown coal),

significantly lower PAH concentrations are detected (e.g. Püttmann, 1988). In theory, the native

PAH content could pose a risk to the environment (and more specific soil and sediment); yet, no

studies have clearly showed such a risk (Achten and Hofmann, 2009). Risks towards the water

column are less likely to occur due to the hydrophobic properties of PAHs. Several authors

demonstrated that non-native PAHs were effectively sorbed to simultaneously present coal

particles, and this sorption was related to high sorption affinity and slow desorption kinetics

(Kleineidam et al., 2002; Wang et al., 2007; Yang et al., 2008).

Achten and Hofmann (2009) collected and summarized the PAH content of 39 types of coal (Table

11). Both the total and United States Environmental Protection Agency (EPA)-PAH concentration

levels are included in this table, and are expressed as mg/kg coal and as weight/weight percentage

(w/w %). The list of 16 EPA priority PAHs is often used as reference list for measurement and

assessment of this group of compounds in the environment. A summary of the 16 EPA PAHs and

their official classification under the Dangerous Substances Directive (DSD) and classification,

labelling and packaging (CLP) is shown in Table 12.

Acenaphthylene and indeno(1,2,3-cd)pyrene are the only two of the 16 EPA-PAHs that are not

classified (no Annex VI classification; no self-classification). There are seven EPA-PAHs with an

official classification of Aquatic Acute 1, Aquatic Chronic 1; only one of them (benzo(a)anthracene)

has an additional M-factor of 100, indicating that the acute toxicity (ERVacute) is situated between 1

µg/L and 10 µg/L.

The Annex VI classification is based on acute data; therefore, no conclusions on the ERVchronic can be

made. Assuming that a classification based on chronic ecotoxicity data would lead to a similar

outcome (Aquatic Chronic 1, M-100), the ERVchronic for benzo(a)anthracene is situated between 0.1

µg/L and 1 µg


Table 11 Sum m ary of total and 16 EPA polycyclic arom atic hydrocarbon concentrations in coals

Type of coal Total PAHs EPA-PAHs

mg/kg % mg/kg %

High-volatile bituminous coal A, Elmsworth Gasfield, 10-11-71-11W6,

Canada

2429.1 0.243 152.1 0.015

High-volatile bituminous coal A, Elmsworth Gasfield, 10-03-70-10W6,

Canada

2412.3 0.241 136.6 0.014

Medium-volatile bituminous coal, Ruhr basin, Osterfeld, Germany 1037.2 0.104 153.3 0.015

Medium-volatile bituminous coal, Ruhr basin, Hugo, Germany 933.8 0.093 123.6 0.012

Low-volatile bituminous coal, Ruhr basin, Westerholt, Germany 1200.7 0.120 163.9 0.016

Low-volatile bituminous coal, Ruhr basin, Blumenthal, Germany 786.5 0.079 155.4 0.016

Low-volatile bituminous coal, Elmsworth Gasfield, 06-19-68-13W6,

Canada

546.4 0.055 98.6 0.010

Low-volatile bituminous coal, Ruhr basin, Haard, Germany 567.7 0.057 154.8 0.015

High-volatile bituminous coal, Wealden Basin, Nesselberg, Germany 656.2 0.066 43.1 0.004

High-volatile bituminous coal, Wealden Basin, Barsinghausen,

Germany

554.4 0.055 56.7 0.006

High-volatile bituminous coal, Saar, Ensdorf, Germany 165.9 0.017 50.5 0.005

Medium-volatile bituminous coal, Germany 68.0 0.007 22.4 0.002

Bituminous coal, Germany 127.6 0.013 28.7 0.003

Lignite A, Northern Great Plains, Beulah, USA 8.5 < 0.001 1.2 < 0.001

Lignite A, Northern Great Plains, Pust, USA 6.5 < 0.001 1.0 < 0.001

Sub-bituminous coal C, Northern Great Plains, Smith-Roland, USA 12.0 0.001 0.1 < 0.001

Sub-bituminous coal C, Gulf Coast, Bottom, USA 14.0 0.001 1.6 < 0.001

Sub-bituminous coal B, Northern Great Plains, Dietz, USA 14.0 0.001 0.8 < 0.001

Sub-bituminous coal B, Northern Great Plains, Wyodak, USA 5.4 < 0.001 0.3 < 0.001


Source: Achten and Hofmann, 2009 (data taken from Willsch and Radke, 1995; Radke et al., 1990; Pies et al., 2007; Stout and Emsbo-Mattingly, 2008; Stout et al.,

2002; Zhao et al., 2000; Chen et al., 2004; Püttmann, 1988)

Sub-bituminous coal A, Rocky Mountains, Deadman, USA 12.0 0.001 1.5 < 0.001

High-volatile bituminous coal C, Rocky Mountains, Blue, USA 77.0 0.008 5.3 < 0.001

High-volatile bituminous coal B, Eastern Coal, Ohio #4A, USA 60.0 0.006 8.2 < 0.001

High-volatile bituminous coal A, Rocky Mountains, Blind Canyon, USA 78.0 0.008 4.4 < 0.001

High-volatile bituminous coal A, Eastern Coal, Pittsburgh, USA 76.0 0.008 11.0 0.001

Medium-volatile bituminous coal, Rocky Mountains, Coal Basin M, USA 29.0 0.003 1.8 < 0.001

Low-volatile bituminous coal, Eastern Coal, Pocahontas #3, USA 20.0 0.002 3.8 < 0.001

Semi-anthracite, Eastern Coal, PA Semi-Anth. C, USA 5.9 < 0.001 2.1 < 0.001

Anthracite, Eastern Coal, Lykens Valley #2, USA 0.2 < 0.001 <0.1 < 0.001

High-volatile bituminous coal, Blind Canyon, USA 78.3 – –

High-volatile bituminous coal C-1, USA 7.5 < 0.001 0.5 < 0.001



High-volatile bituminous coal B-1, USA 1.6 < 0.001 0.3 < 0.001

High-volatile bituminous coal B-2, USA 12.7 0.001 2.4 < 0.001

High-volatile bituminous coal A-1, USA 13.7 0.001 5.4 < 0.001

High-volatile bituminous coal A-2, USA 27.6 0.003 6.4 < 0.001

Low-volatile bituminous coal, USA 1.2 < 0.001 0.3 < 0.001

Anthracite, China 2.5 < 0.001 1.8 < 0.001

Bituminous coal, Brazil 13.0 0.001 – –


Table 12 Overview of the environmental classification of the most relevant PAH

compounds

16 EPA-PAH

compounds

Environmental classification under DSD/CLP

Naphthalene Aq.Acute 1, Aq.Chronic 1

Acenaphthylene No official classification, no environmental self-classification

Acenaphthene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

Fluorene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

Phenanthrene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

Anthracene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

Fluoranthene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

Pyrene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

(M = 10)

Benzo(a)anthracene Aq.Acute 1, Aq.Chronic 1 (M = 100)

Chrysene Aq.Acute 1, Aq.Chronic 1

Benzo(b)fluoranthene Aq.Acute 1, Aq.Chronic 1

Benzo(k)fluoranthene Aq.Acute 1, Aq.Chronic 1

Benzo(a)pyrene Aq.Acute 1, Aq.Chronic 1

Dibenz(a,h)anthracene Aq.Acute 1, Aq.Chronic 1

Benzo(g,h,i)perylene No official classification; self-classification: Aq.Acute 1, Aq.Chronic 1

Indeno(1,2,3-c,d)pyrene No official classification; no environmental self-classification

For the remaining seven EPA-PAHs there is no official classification, but the compounds were self-

classified under CLP (Aq.Acute1, Aq.Chronic1). An additional chronic M-factor of 10 was assigned

to only one of these eight PAHs (pyrene). It can thus be concluded that for the majority of the EPA-

PAHs, the ERVacute is situated between 100 µg/L and 1000 µg/L, and that the ERVchronic is situated

between 10 µg/L and 100 µg/L.

1.4. ENVIRONMENTAL HAZARD ASSESSMENT OF COAL

1.4.1. HAZARD ASSESSM ENT OF TRACE ELEM ENTS IN COAL

The conservative worst-case concentration levels of trace metals in coal (see Table 6) are used as

a starting point for the prioritization of the most critical trace elements that may trigger an

environmental classification, resulting in the classification of coal as an HME. This assessment is

conducted with the MeClas tool (Metals Classification tool). This tool uses the most up-to-date


information on metal toxicity and bioavailability of various metal compounds and minerals, and can

be used for the derivation of a classification for a (multi)metallic complex material, hereby

following the mixture rules that are outlined in the Globally Harmonized System of Classification

and Labelling of Chemicals (GHS). The use of this tool ensures that the derived classification is

fully compliant with the principles, concepts and assumptions that are accepted by the various

metal commodities (e.g. European Copper Institute, International Copper Association, Lead

Development Association, etc.), and that the most recent toxicological and ecotoxicological data

and principles (industry or legislation) are taken into account.

Based on all information on trace elements in coal that is currently summarized (see Table 6), a

‘worst case’ coal sample has been generated: for each trace element the highest available

concentration in coal is taken forward in the composition. Table 6 also presents the fraction (in %)

of each element in coal, and also determines the maximum amount of each trace metal in coal at a

loading of 100 mg/L and 1 mg/L. It should be noted that the loading of 1 mg/L is relevant for Acute

1 and Chronic 1 classification purposes. Apart from iron, the highest percentage of a classified

trace metal in coal was found for zinc and was 0.7%.

With regard to the presence of a single classified substance in a mixture, the maximum allowed

concentrations that would not trigger an Aq.Chronic1 or Aq.Chronic2 classification (i.e.

classification criteria for an HME) can be summarized as follows:

• A substance with an Aq.Chronic2 classification will only trigger an Aq.Chronic2

classification in a mixture when present at concentration levels of 25% or higher (and no

other substances with an Aq.Chronic1 or Aq.Chronic2 classification are present in the

mixture). All worst-case trace metal concentrations are well below 1%; therefore, none of

the metals with an Aq.Chronic.2 classification (e.g. Sn) will directly result in an Aq.Chronic2

classification for coal.

• A substance with an Aq.Chronic1 classification and M-factor 1 will only trigger an

Aq.Chronic2 classification in a mixture when present at concentration levels of 2.5% or

higher (and no other substances with an Aq.Chronic1 or Aq.Chronic2 classification are

present in the mixture). All worst-case trace metal concentrations are well below 1%;

therefore, none of the metals with a Aq.Chronic.1 classification and M-factor 1 (e.g. Zn, Cu)

will directly result in an Aq.Chronic2 classification for coal.





present in the mixture). Such a concentration level is only observed for Zn (0.7%), but as

this metal does not have an M-factor of 10, it will not trigger an environmental

classification. All elements with an M-factor of 10 are present at concentration levels

below 0.25%, and will therefore not directly result in an Aq.Chronic2 classification for coal.




present in the mixture). An M-factor of 100 is relevant for Ag, Cd and Hg, but the highest

worst-case concentration for these elements is 0.00002%, 0.0065% and 0.003%,

respectively, i.e. well below the critical concentration level of 0;05%. As such, none of these

three highly toxic elements will directly result in an Aq.Chronic2 classification for coal.

The combined hazard classification of various elements, however, may trigger a classification, and

this can be assessed with the output of the MeClas calculation. The output of this exercise is

presented in Figure 1 and Table 13. Figure 1 shows the Tier-0 output of the MeClas calculation

(relevant end points for environmental classification only). With the Tier-0 assumptions (100%

bioavailability plus each element is present under its most toxic from), no Aq.Acute1 classification

is derived. Under GHS, however, a worst-case coal sample would be classified as Aq.Acute2 (not

relevant for the International Convention for the Prevention of Pollution from Ships (MARPOL)).

Figure 1: M eClas output of the TIER-0 environmental classification of a worst-case

coal sample


For the chronic end point, however, the combination of a worst-case coal composition with

(unrealistic) worst-case bioavailability assumptions (100% solubility of trace elements in coal)

may lead to an overly conservative Aq.Chronic2 classification.

As both acute and chronic assessments are based on the same set of trace element concentration

levels, this analysis indicates that the chronic assessment evaluation is the most critical one, and,

hence, that a coal sample that has no environmental classification for the chronic endpoint will also

have no Aq.Acute1 classification.

Table 13 gives a summary of the relative contribution of each element to the Tier-0 Aq.Chronic2

classification. Again, it should be stressed that this Chronic 2 classification is the result of a worst-

case trace element composition combined with overly conservative bioavailability assumption

(100% bioavailability of these trace elements in water); this classification can therefore not be

taken forward as such for coal samples in general.

Table 13 M ain trace elements that determine the TIER-0 classification of a worst-

case coal sample (maximum concentration for each classified trace element)

M ajor contributors (> 2.5% ) M inor contributors (0.5–2.5% )

Element (1) Contribution to the

Aq.Chronic 2

classification

Element Contribution to the

Aq.Chronic 2

classification

Zn (as ZnSO4) 48.6% Co (as

CoSO4)

1.7%

Cd (as CdSO4) 33.8% Cu (as CuSO4) 1.7%

Hg 8.2% Ni (as NiSO4) 0.7%

Pb 2.53% Cr (as CrO3) 0.5% (1) In the TIER-0 classification, each element is considered to be present under its most toxic form

(e.g. CdSO4 for cadmium).

The calculated Aq.Chronic2 classification is predominantly driven by four trace elements:

cadmium, mercury, lead and zinc, with the latter being the most important contributor. Less critical

elements, but still representing approximately 5% of the total Aq.Chronic2 contribution, are

cobalt, copper, chromium and nickel. All other elements contribute less than 0.1% to the

Aq.Chronic2 classification and are therefore not critical for assessing the environmental

classification of coal.


As mentioned before, the Tier-0 approach assumes that all trace elements in coal are bioavailable,

i.e. will be released to the aqueous medium (100% soluble). This is an unrealistic assumption as the

trace metals are embedded into the coal matrix and are not expected to be released (or only a very

limited fraction). For metals, the environmental classification can be further refined by only taking

the soluble fraction into account (= bioavailable fraction). Standard methods for the determination

of the soluble fraction have been developed and are outlined in the OECD N.29 Guidance document

(OECD, 2002). These so-called Transformation/Dissolution Protocol (T/DP) tests have been

included in the GHS guidance for assessing the hazard of sparingly soluble metal compounds and

metal-containing mixtures.

Several WCA members conducted T/DP tests with various coal samples. Due to the low

concentrations in the coal samples – often below 10 mg/kg – the maximum released amount of

trace metal in a typical acute T/DP test (seven-day exposure of a 100 mg coal sample in 1 L of

test medium) is already below the typical detection limits of standard analytical laboratories

(i.e. 1 µg/L or lower). Therefore, it is not possible to derive meaningful release factors for the

majority of trace elements.

With regard to zinc (the most critical element that determines the Aq.chronic2 classification of the

worst-case coal sample), there were three WCA members that measured Zn levels in various coal

samples (n = 18), but Zn levels in all T/DP test media were too low to be determined (value below

the limit of quantification); therefore no release factors could be determined. The Zn levels in the

tested samples are several orders of magnitude below the worst-case concentration of

7000 mg/kg that is used in the Tier-0 classification; consequently, the coal samples that were

evaluated in the T/DP tests would not be classified for the environment.

Similar conclusions can be drawn for all the other elements that are considered critical for the

environmental classification of coal (Cd, Hg, Pb, but also Co, Cr, Cu, Ni); when measured in T/DP

test media, the levels were found to be below the limit of quantification and no reliable release

factor could be established.

A summary of the provided T/DP data is given in the Annex.


1.4.2. ENVIRONM ENTAL HAZARD ASSESSM ENT OF PAHS IN COAL

A complex mixture of compounds that contains Acute1/Chronic1 compounds is considered as

Acute1/Chronic1 when the contribution of these compounds in the mixture exceeds 25%. The data

in Table 14 show that the highest measured EPA-PAH content was 153 mg/kg, which corresponds

to 0.015%, i.e. several orders of magnitude below the critical threshold of 25%. Application of a

worst-case M-factor of 100 (assuming that benzo(a)anthracene is the only EPA-PAH in coal) would

result in a contribution of 100*0.015% = 1.5%. This is still below the cut-off value of 25%.

As mentioned before, an Aq.Chronic1 substance in a mixture will only trigger an Aq.Chronic2

classification of that mixture when the Aq.Chronic1-fraction * M-factor * 10 exceeds 25%. For a

coal sample with an EPA-PAH content of 0.015%, no Aq.Chronic2 classification is applicable, even

when a worst-case M-factor of 100 is considered (100*10*0.015% = 15% < 25%).

Assuming that the vast majority of PAHs in a coal sample are categorized as

Aq.Acute1/Aq.Chronic1 (M-factor 1), then a coal sample would only be classified as

Aq.Acute1/Aq.Chronic1 when it contains 250,000 mg/kg PAHs (25%); this cut-off threshold is a

factor of 103 times higher than the highest reported total PAH content of 2,429 mg/kg coal (Table

14). Application of an M-factor of 100 would still result in a concentration that is (marginally)

lower than 25% (i.e. 24.3%).

An Aq.Chronic2 classification is relevant if the content of the PAHs would be higher than

25,000 mg/kg (assuming an M-factor of 1 for all PAHs). This is not the case for any of the coal

samples that are presented in Table 14. Only if all PAHs had an M-factor of 100 would an

Aq.Chronic2 classification be applicable. This is, however, not the case as only one PAH with M-

factor of 100 has been identified, and even if the concentration of EPA-PAHs was solely due to

the presence of this specific PAH (benzo(a)anthracene), then the overall contribution would be

limited (152/2430 = 6.3%).

It can thus be concluded that based on the mixture rules, assuming worst-case classifications and

assuming that all PAH in coal is bioavailable, there is no need to assign an environmental

classification based on the PAH content of coal samples. Based on the typical environmental

classification of PAHs (Aq.Acute1/Aq.Chronic1; M-factor of 1), the ‘Chronic2 fraction’ is 0.15%. An


Aq.Chronic2 classification is only applicable when 25% is reached; the PAH contribution, however, is

less than 1% and will therefore not trigger an environmental classification. It should be stressed that

this is based on 100% bioavailability of PAH, which is an unrealistic worst-case assumption in itself.

It is also noteworthy that under GHS (and national/regional regulations that are based on GHS), an

Aq.Acute1/Aq.Chronic1 compound only has to be taken into account if its concentration in the

mixture exceeds 0.1% (or 0.1% divided by its M-factor). The total amount of classified EPA-PAHs

is well below this cut-off value (0.015%), and concentrations of individual PAHs are most likely

even several orders of magnitude below the cut-off value. This supports the overall conclusion that

the presence of PAHs in coal does not trigger an environmental classification.

1.4.3. DATA PROVIDED BY W CA M EM BERS

WCA members have measured the concentration levels of PAHs in coal sample solutions, and these

data can be used as supportive information to demonstrate that the maximum released amount of

(individual) PAHs are well below their acute/chronic ecotoxicity reference values (assumption:

100% bioavailability).

A total of 18 different PAHs were measured in solutions of 16 different coal samples, and were

subsequently assessed according to the principles that were outlined in section 1.4.2. The

guidance for evaluating the solubility of a compound/mixture recommends that bulk materials are

tested using the smallest commercially sold size range. However, in the case of coal, testing

without further particle size reduction would not be practical due to the sample sizes involved.

Taking the coal density into account, it was determined that the creation of a 2L dissolution test

solution with a concentration of 100 mg/L coal and a minimum of 50 particles (statistically valid

number), the coal particles had to have a maximum diameter of 1 mm.

The different replicates were placed on a tumbler (approx. 30 rpm at 20°C), and PAH levels were

measured after seven days. The results of this monitoring exercise are reported in Table 14.


Table 14 Concentration of 18 PAHs after a seven-day dissolution period – values between brackets are estimated below

reporting l imit

Sam ple code

S #1 S #2 S #3 S #4 S #5 S #6 S #7 S #8

µg/L ( loading of 100 mg/L)

1-methylnaphthalene 0.063 0.013 0.062 (0.088) 0.051 0.024 0.046 0.047

2-methylnaphthalene 0.093 (0.0085) 0.087 (0.092) 0.058 0.022 0.058 0.058

Acenaphthene n.d. n.d. n.d. n.d. (0.005) n.d. n.d. n.d.

Acenaphthylene n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Anthracene n.d. n.d. (0.0023) (0.0027) (0.0076) n.d. 0.028 n.d.

Benz(a)anthracene (0.0023) n.d. n.d. (0.0038) (0.003) n.d. n.d. (0.0038)

Benzo(a)pyrene n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Benzo(b)fluoranthene n.d. n.d. n.d. n.d. n.d. n.d. (0.0033) (0.0044)

Benzo(gh)perylene (0.005) n.d. (0.0026) n.d. (0.0042) n.d. (0.0047) (0.0058)

Benzo(k)fluoranthene 0.012 (0.0099) (0.0092) 0.012 0.011 0.012 (0.0091) 0.010

Chrysene (0.0046) (0.0036) (0.0028) (0.005) (0.0026) n.d. (0.0036) (0.0044)

Dibenz(ah)anthracene n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Fluoranthene n.d. n.d. n.d. n.d. (0.0062) n.d. n.d. (0.0041)

Fluorene (0.0051) (0.0082) 0.01 (0.0051) (0.0076) (0.002) (0.0051) (0.004)

Indeno(123,cd)perylene n.d. (0.0024) (0.0024) n.d. n.d. n.d. (0.0027) (0.0027)

Naphthalene 0.046 (0.0078) 0.058 0.024 0.051 0.017 0.045 0.05

Phenanthrene 0.033 0.022 0.033 0.015 0.029 0.013 0.024 0.024

Pyrene (0.0043) n.d. n.d. n.d. (0.0068) n.d. n.d. (0.0051) n.d.: not detected at reporting limit (0.01 µg/L)


Table 14 continued

Sam ple code

S #9 S #10 S #11 S #12 S #13 S #14 S #15 S #16


1-methylnaphthalene (0.0046) (0.053) 0.025 0.089 0.012 0.016 0.024 0.042

2-methylnaphthalene (0.0048) (0.0066) 0.025 0.13 0.013 0.018 0.027 0.06

Acenaphthene n.d. n.d. n.d. (0.0019) n.d. n.d. n.d. n.d.

Acenaphthylene n.d. n.d. n.d. (0.0016) n.d. n.d. n.d. (0.0019)

Anthracene (0.0027) (0.0027) n.d. n.d. n.d. n.d. (0.004) (0.0047)

Benz(a)anthracene n.d. n.d. n.d. (0.0034) n.d. n.d. n.d. (0.0033)

Benzo(a)pyrene n.d. (0.0027) n.d. n.d. n.d. n.d. n.d. n.d.

Benzo(b)fluoranthene (0.0073) n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Benzo(gh)perylene n.d. n.d. n.d. (0.0037) n.d. n.d. n.d. n.d.

Benzo(k)fluoranthene (0.0078) (0.0078) 0.011 0.011 (0.0076) 0.011 (0.0088) (0.0091)

Chrysene n.d. (0.0057) n.d. (0.0043) n.d. n.d. (0.0025) (0.0053)

Dibenz(ah)anthracene n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Fluoranthene n.d. n.d. n.d. (0.004) n.d. n.d. (0.0052) (0.0063)

Fluorene n.d. (0.004) (0.0043) (0.0058) (0.0022) (0.0024) (0.0048) (0.0053)

Indeno(123,cd)perylene (0.0019) (0.0021) n.d. n.d. n.d. n.d. (0.0025) n.d.

Naphthalene 0.019 0.013 0.029 0.13 0.024 0.017 0.026 0.056

Phenanthrene (0.0031) 0.012 0.017 0.032 (0.043) (0.0062) 0.01 0.017

Pyrene n.d. n.d. n.d. (0.0054) n.d. n.d. (0.004) (0.0051) n.d.: not detected at reporting limit (0.01 µg/L)


A summary of the min-max range for each PAH is given in Table 15. The highest value is then

translated to a concentration at a loading of 1 mg/L (relevant loading for acute and chronic

classification purposes) and compared to the threshold that is determined for each PAH. The

highest value is then translated to a concentration at a loading of 1 mg/L (relevant loading for

acute and chronic classification purposes) and compared to the threshold that is determined for

each PAH:

• Aq.Acute1: threshold of 100 µg/L

• Aq.Acute1, M = 100: threshold of 1 µg/L

• Aq.Chronic1: threshold of 10 µg/L

• Aq.Chronic1, M = 10: threshold of 1 µg/L

• Aq.Chronic1, M = 100: threshold of 0.1 µg/L

• Aq.Chronic2: threshold of 100 µg/L (methylnaphthalene; self-classification under CLP).

The highest recorded concentration level for each PAH at a loading of 1 mg/L is several orders of

magnitude below the concentration that would trigger a classification, i.e. no acute or toxic effects

are expected when aquatic organisms are exposed to these levels of PAH concentration levels. The

highest concentration at a loading of 1 mg/L was found for 2-methylnaphthalene and naphthalene,

and was 1.3 ng/L. This concentration is almost four orders of magnitude lower than the

concentration that is expected to cause a significant chronic toxic effect (1.3 ng/L vs 10 µg/L).


Table 15 M in-max concentration of PAHs in 16 coal samples after a seven-day

dissolution period; comparison of theoretically derived concentrations for a 1 mg/L

loading with acute/chronic classification threshold values – values between

brackets are estimated below reporting l imit

M in-max (µg/L) M ax at

loading of 1

mg/L (in µg/L)

Acute

ERV (1)

(µg/L)

Chronic

ERV (1)

(µg/L)

1-methylnaphthalene (0.0046)–0.089 0.00089 – 100

2-methylnaphthalene (0.0048)–0.13 0.0013 – 100

Acenaphthene (0.0019–0.005) (0.00005) 100 10

Acenaphthylene (0.0016–0.0019) (0.000019) – –

Anthracene (0.0023)–0.028 0.00028 100 10

Benz(a)anthracene (0.0023–0.0038) (0.000038) 1 0.1

Benzo(a)pyrene (0.0027) (0.000027) 100 10

Benzo(b)fluoranthene (0.0033–0.0073) (0.000073) 100 10

Benzo(gh)perylene (0.0026–0.0058) (0.000058) 100 10

Benzo(k)fluoranthene (0.0076)–0.012 0.00012 100 10

Chrysene (0.0025–0.0057) (0.000057) 100 10

Dibenz(ah)anthracene n.d. n.d. 100 10

Fluoranthene (0.004–0.0063) (0.000063) 100 10

Fluorene (0.002–0.0082) (0.000082) 100 10

Indeno(123,cd)perylene (0.0019–0.0027) (0.000027) – –

Naphthalene (0.0078)–0.13 0.0013 100 10

Phenanthrene (0.0031–0.043) (0.00043) 100 10

Pyrene (0.004–0.0068) (0.000068) 100 1 (1) Worst case assumption; based on reported classification.

The measured PAH concentrations confirm that the released amounts of PAH after a seven-day

solubility experiment do not justify an environmental classification that is driven by the presence

of PAHs.

In addition, a second company conducted a similar seven-day dissolution test with a coal sample

and analysed the dissolution medium for the same set of 18 PAHs. All measurements were below

the detection limit of 0.025 µg/L, confirming the findings that released PAH levels are well below

concentration levels that would trigger any classification for the environment.


2. RESULTS OF ECOTOXICOLOGICAL EXPERIMENTS WITH

COAL SAMPLES

No industry-sponsored toxicological or ecotoxicological test results with coal samples were

provided by members of the WCA. A search of open literature revealed that most data use the

fly ash as test substance in ecotoxicological tests; the remains of the coal burning process,

however, will contain markedly higher concentration levels of metals than what is found in raw

coal, and data are therefore not relevant for classification purposes of raw coal. Ahrens and

Morrisey (2005), however, published a review on the biological effects of unburnt coal in the

marine environment and made a clear distinction between the physical and the chemical

effects of coal on marine organisms. The hazard assessment of a substance, however, should

only be based on chemical effects.

Various direct and indirect physical effects of coal have been identified. Increased concentrations

of suspended particulate coal in the water column may cause abrasion of animals and plants living

on the surface of the seabed or on structures such as rocks or wharf piles, or destruction of the

normal habitat such as infilling of crevice habitats that reduce abundance and diversity of soft-

sediment assemblages. Such effects were reported for, for example, the green alga Ulva lactuta,

the polychaete Arenicola marina, the Dungeness crab Cancer magister, the fathead minnow

Pimephales promelas, the rainbow trout Oncorhynchus mykiss gairdneri (and O. clarkii) and the

brown trout Salmo trutta (Pautzke, 1937; Herbert and Richards, 1963; Williams and Harcup, 1974;

Hughes, 1975; Pearce and McBride, 1977; Emerson and Zedler, 1978; Gerhart et al., 1981; Hillaby,

1981; Kendrick, 1991; Hyslop et al., 1997; Hyslop and Davies, 1998, 1999), whereas impact on

diversity and abundance of sediment organisms was reported by, for example, Shelton (1973),

Scullion and Edwards (1980), Norton (1985), Johnson and Frid (1995), Chapman et al. (1996), Holte

et al. (1996) and Barnes and Frid (1999). Particles of coal in suspension will also reduce the

amount, and possibly the spectral quality (Davies-Colley and Smith, 2001), of light that reaches the

seabed or other underwater surfaces, in a manner similar to other suspended particles (Moore,

1977). This, in turn, may affect growth of plants such as seaweeds, seagrasses, and microalgae on


the surfaces of sediments and rocks (e.g. Duarte, 1991; Preen et al., 1995; Vermaat et al., 1996;

Moore et al., 1997; Terrados et al., 1998; Longstaff and Dennison, 1999). Deposition of coal dust

on the surface of plants above and below water may also reduce photosynthetic performance, and

suspended particles in general may clog feeding and respiratory organs of a wide range of marine

animals, reducing efficiency of feeding and respiration and possibly damaging the organs (see

reviews by Newcombe and MacDonald, 1991; Newcombe and Jensen, 1996; Wilber and Clarke,

2001). Suspended sediments can also cause mortality of eggs and larvae of fishes and benthic

invertebrates (Auld and Schubel, 1978; Wilber and Clarke, 2001). As coal settles out of suspension

onto the seabed, its most direct effect is likely to be smothering of animals and plants. Indirect

effects, however, are filling with coal of rocky crevices that act as important habitats, or impact on

higher trofic levels that depend on affected, lower levels as food source.

Ahrens and Morrisey (2005) also stated that there is surprisingly little published evidence

demonstrating direct toxic effects of unburnt coal on marine organisms and communities. The

absence of scientific evidence seems to uphold the hypothesis that unburnt coal is an

ecotoxicologically relatively inert substance (Chapman et al., 1996), and the majority of the few

studies that investigated the potential toxic effects of unburnt coal (or its leachates) on marine

organisms concluded that unburnt coal (or its leachates) is not acutely or chronically toxic. Bender

et al. (1987), for instance, convincingly demonstrated the absence of acute toxicity (mortality) for

the oyster Crassostrea virginica when exposed to 1 mg/L and 10 mg/L of coal dust. Their

interpretation on the absence of effects on shell growth (chronic effect), as well as their finding

that PAHs were not accumulated during the exposure period, may be less conclusive as the oysters

originated from a location that already contained high levels of PAHs (Ahrens and Morrisey, 2005).

Hillaby (1981) also found no direct acute effects (mortality) when exposing crabs to coal dust

under laboratory conditions. The presence of coke particles (both thermochemically modified coal

products as well as unburnt coal) in sediments did not cause any adverse effects (i.e. mortality) on

the amphipod Rhepoxynius abronius or on the sand dollar Dendraster excentricus (Paine et al.,

1996). One additional study (Shaw and Wiggs, 1980) suggested accumulation of PAHs in deposit

feeding clams (Macoma balthica) when exposed to coal, but as organisms were not depurated

before analysis, the PAHs could have originated from coal particles in the digestive track (and not

PAHs that were actually assimilated in the tissue).


With regard to freshwater species, Carlson et al. (1979) exposed fathead minnow (Pimephales

promelas) for 3 to 24 weeks to centrifuged leachates of coal dust (loading of 6.3 g/L). Test

organisms showed no increased mortality, no reduced growth and no significant accumulation of

PAHs. The spawning success, however, was somewhat lower in two- to four-week exposures. When

exposed to uncentrifuged leachates (i.e. coal dust still present at a loading of 25 g/L), mortality

was 100%. It is noteworthy that the concentrations of coal dust are three to four orders of

magnitude higher than the highest concentration (of 1 mg/L) that would trigger a chronic

classification based on direct toxicity testing.

In addition, some beneficial/stimulatory effects were observed such as increased growth of algae

and duck-weed due to exposure of coal leachate or unfiltered coal slurry (Coward et al., 1978;

Gerhart et al., 1980).

Ahrens and Morrisey (2005) concluded that at levels of coal contaminations at which estimates of

bioavailable concentrations of contaminants might give cause for concern, acute physical effects

are likely to be much more significant. The general opinion in most papers that describe the risk of

coal to the marine environment is that coal may present a physical hazard in the marine

environment when present in sufficient quantities, but not a chemical one.

This conclusion, based on available ecotoxicological data that were generated with unburnt coal as test

substance, supports the conclusion that there is no need for an environmental classification of coal.


3. HUMAN HEALTH EFFECTS OF COAL AND COAL TRANSPORT:

REVIEW OF LITERATURE

3.1. INTRODUCTION

3.1.1. RELEVANCE OF EXISTING LITERATURE

A large body of literature exists on the health effects of coal. The majority of publications deal

with the effects of occupational exposure from coal mining. The most thoroughly studied health

effects are the lung effects seen in coal workers and these often relate to many years of exposure

to high levels of coal dust. For example, the association between diseases such as silicosis and lung

cancer and coal mining has been studied extensively.

Some publications consider coal mining itself as a contributing factor to disease development;

exposure can either result from occupational exposure or from living in a coal mining area.

Other publications consider exposure to certain constituents of coal, such as coal dust or

crystalline silica. The focus in this review is on the health effects caused by coal and coal dust,

rather than confining to particular constituents of coal. However, some notes on the health

hazards from exposure to fine particles of crystalline silica are mentioned in the annex to this

document (cf. Annex IV).

With respect to coal dust, the important fraction is that portion of airborne dust that is capable of

entering the gas-exchange regions of the lungs when inhaled. By convention, this fraction is made

up of particles with an aerodynamic diameter less than 10 µm. The smaller the particles, the less

likely are they that they will be trapped in the nose and throat and the more likely they will reach

the lungs and thus present a health hazard.

Although the publications on the health effects of coal mining provide an interesting source of

information, they may not all be indicative of health hazards posed by transportation of bulk coal

overseas. Particularly in underground mining, dust concentrations might be very high and many

studies consider exposures from the past, when less strict occupational exposure limits were


applicable. Apart from coal dust, miners might also have been exposed to diesel exhaust, toxic

gases from mine fires and chemicals such as isocyanates (Petsonk et al., 2013). Depending on the

area that was mined, coal miners may also have been exposed to varying levels of silica. For

example, as thicker coal seams are starting to get depleted, the mining of thinner seams expands

and coal miners are increasingly exposed to silica from adjacent rock (Laney et al., 2010), which has

been associated with health hazards (cf. Annex IV).

Of note, data on the health effects of combusted coal are beyond the scope of this literature

review, as they are irrelevant to bulk transport of coal.

3 .1.2. UN GHS CRITERIA FOR CLASSIFICATION

Classification as Mutagenic, Carcinogenic, Toxic for Reproduction or as STOT-RE is decisive in

determining whether a substance is an HME under the MARPOL Convention and affects the

categorization under the IMSBC Code. Therefore, the basis of the classification into these

categories according to UN GHS is discussed below.

3.1.2.1. GERM CELL M UTAGENICITY

Mutations are permanent changes in the amount or structure of the genetic material in a cell. It is

important to make a distinction between germ cell mutations and somatic mutations. Germ cell

mutations are those that occur in the egg or sperm cells and therefore can be passed on to

offspring. Somatic mutations are those that happen in other cell types, and therefore cannot be

transmitted to the next generation.

Mutagenic substances give rise to an increased occurrence of mutations. Genotoxicity tests are

usually taken as indicators for mutagenic effects. However, genotoxicity is a broader term than

mutagenicity. Genotoxicity refers to the ability of a substance to interact with DNA and/or the

cellular apparatus that regulates the fidelity of the genome. Mutagenicity refers to the induction

of permanent transmissible changes in the structure of the genetic material.


Hazard classification for germ cell mutagenicity primarily aims to identify substances causing

heritable mutations or being suspected of causing heritable mutations. Where there is evidence of

only somatic cell genotoxicity, substances are classified as suspected germ cell mutagens.

Classification as a suspected germ cell mutagen may also have implications for potential

carcinogenicity classification.

For the purpose of classification for germ cell mutagenicity, substances are allocated to one of

two categories, as explained in Table 16.

Table 16 Hazard categories for germ cell m utagens

Category Criteria

Category 1 Substances are classified in Category 1 if they are known to induce heritable

mutations or are regarded as if they induce heritable mutations in the germ cells of

humans.

Category 1 A: substances known to induce heritable mutations in the germ cells of humans.

Classification is based on positive evidence from human epidemiological studies.

Category 1 B: substances to be regarded as if they induce heritable mutations in the germ cells of humans.

Classification is based on:

• positive result(s) from in vivo heritable germ cell mutagenicity tests in

mammals; or

• positive result(s) from in vivo somatic cell mutagenicity tests in

mammals, in combination with some evidence that the substance has

potential to cause mutations to germ cells; or

• positive results from tests showing mutagenic effects in the germ cells

of humans, without demonstration of transmission to progeny; for

example, an increase in the frequency of aneuploidy in sperm cells of

exposed people.


Category 2 Substances that cause concern for humans owing to the possibil ity

that they m ay induce heritable m utations in the germ cells of hum ans.

A substance is classified in Category 2 based on evidence obtained from

experiments in mammals and/or in some cases from in vitro experiments (e.g.

somatic cell mutagenicity tests in vivo, or other in vivo somatic cell genotoxicity

tests that are supported by positive results from in vitro mutagenicity assays).

Classification for heritable effects in human germ cells is made on the basis of well-conducted,

sufficiently validated tests. Test results are considered from experiments determining mutagenic

and/or genotoxic effects in germ and/or somatic cells of exposed animals. Mutagenic and/or

genotoxic effects determined in in vitro tests shall also be considered. Evaluation of the test

results should be done using expert judgement and all the available evidence should be weighed in

arriving at a classification. The relevance of the route of exposure used in the study compared to

the most likely route of human exposure should also be taken into account.

3.1.2.2. CARCINOGENICITY

Chemicals are defined as carcinogenic if they induce tumours, increase tumour incidence and/or

malignancy or shorten the time to tumour occurrence. Benign tumours that are considered to have

the potential to progress to malignant tumours are generally considered along with malignant

tumours.

Classification of a substance as a carcinogen is based on consideration of the strength of the

evidence of the available data (weight of evidence). Carcinogens may be identified from

epidemiological studies, from animal experiments or other means, such as (Quantitative)

Structure-Activity Relationship ((Q)SAR) analyses or extrapolation from structurally similar

substances (read-across). In addition, some information on the carcinogenic potential can be

inferred from in vivo and in vitro tests, such as germ cell and somatic cell mutagenicity studies.

For the purpose of classification for carcinogenicity, substances are allocated to one of the two

categories outlined in Table 17. Expert judgement is generally required. Among others, the


International Agency for Research on Cancer (IARC, 2006) provides a basis for systematic

assessments that may be performed in a consistent fashion internationally. Hence, there is a

strong link between the GHS/CLP and IARC classification criteria (cf. Table 20).

Table 17 Hazard categories for carcinogens

Category Criteria

Category 1 A substance is classified in Category 1 for carcinogenicity on the basis of

epidemiological and/or animal data.

Category 1 A: known human carcinogens

Classification is largely based on human evidence, e.g. human studies that establish

a causal relationship between human exposure to a substance and the development

of cancer.

Category 1 B: presumed human carcinogens

Classification is largely based on animal evidence, e.g. animal experiments for

which there is sufficient evidence to demonstrate animal carcinogenicity .

Category 2 Suspected hum an carcinogens

A substance is classified in Category 2 for carcinogenicity based on limited

evidence of carcinogenicity in human studies or from limited evidence of

carcinogenicity in animal studies.

It is recognized that genetic events are central in the overall process of cancer development.

Therefore, evidence of mutagenic activity in vivo may indicate that a substance has a potential for

carcinogenic effects. In general, if a substance is mutagenic, then it will be considered to be

potentially carcinogenic in humans; however, mutagenicity data alone are insufficient information

to justify a carcinogen classification.

It should be taken into account that some modes of action of tumour formation are not relevant to

humans. Carcinogenic chemicals have conventionally been divided into two categories according

to their presumed mode of action: genotoxic or non-genotoxic. Evidence of genotoxic activity is


gained from studies on mutagenic activity. Genotoxic chemicals cause a change in the primary

sequence of the DNA, either by directly interacting with DNA, or following interaction with other

cellular processes. Non-genotoxic modes of action of carcinogenesis include epigenetic changes,

i.e. effects that do not involve alterations in DNA but that may influence gene expression, altered

cell–cell communication, etc. For the classification as carcinogenic, the lack of genotoxicity is an

indicator that mechanisms not relevant to humans might be operating.

3.1.2.3. REPRODUCTIVE TOXICITY

Reproductive toxicity includes adverse effects on sexual function and fertility in adult males and

females, as well as developmental toxicity in the offspring. Of note, the induction of genetically

based heritable effects in the offspring is addressed under the separate hazard class of germ cell

mutagenicity (cf. 3.1.2.1).

In this classification system, reproductive toxicity is subdivided under two main headings:

• Adverse effects on sexual function and fertility. For example:

o alterations to the female and male reproductive system

o adverse effects on onset of puberty

o gamete production and transport

o reproductive cycle normality

o sexual behaviour

o fertility

o parturition

o pregnancy outcomes

o premature reproductive senescence.

• Adverse effects on development of the offspring. Classification under the heading of

developmental toxicity is primarily intended to provide a hazard warning for pregnant

women, and for men and women of reproductive capacity. The major manifestations of

developmental toxicity include:

o death of the developing organism


o structural abnormality

o altered growth

o functional deficiency.

Importantly, adverse effects on fertility and reproductive performance are not taken into account

when seen at dose levels causing systemic toxicity.

Adverse effects on or via lactation are included under reproductive toxicity, but for classification

purposes such effects are treated separately. This is because it is desirable to be able to classify

substances specifically for an adverse effect on lactation so that a specific hazard warning about

this effect can be provided for lactating mothers. This classification is intended to indicate when a

substance may cause harm due to its effects on or via lactation. This can be due to the substance

being absorbed by women and adversely affecting milk production or quality, or due to the

substance (or its metabolites) being present in breast milk in amounts sufficient to cause concern

for the health of a breastfed child.

Table 18 Hazard categories for reproductive toxicants

Category Criteria

Category 1 Substances are known to have produced an adverse effect on sexual function and

fertility, or on development in humans or when there is evidence from animal

studies, possibly supplemented with other information, to provide a strong

presumption that the substance has the capacity to interfere with reproduction in

humans.

Category 1A: known human reproductive toxicant

Classification is largely based on evidence from humans.

Category 1B: presumed human reproductive toxicant

Classification is largely based on data from animal studies.

Category 2 Suspected hum an reproductive toxicant

Classification is based on some evidence from humans or experimental animals,


possibly supplemented with other information, of an adverse effect on sexual

function and fertility, or on development.

Additional

category

Adverse effects on or via lactation

3.1.2.4. SPECIFIC TARGET ORGAN TOXICITY – REPEATED EXPOSURE

Specific Target Organ Toxicity – Repeated Exposure (STOT-RE) means all significant health

effects specific to a certain target organ, arising from repeated exposure to a substance or

mixture. It includes both reversible and irreversible toxicity, immediate as well as delayed.

The information required to evaluate specific target organ toxicity comes either from repeated

exposure in humans, such as exposure at home, in the workplace or environmentally, or from

studies conducted in experimental animals. Relevant information for humans may be available

from case reports, epidemiological studies, medical surveillance and reporting schemes, and

national poisons centres. The standard animal studies in rats or mice that provide this information

are 28-day, 90-day or lifetime studies (up to two years) that include haematological,

clinicochemical and detailed macroscopic and microscopic examination to enable the toxic effects

on target tissues/organs to be identified.

Other long-term exposure studies, such as on carcinogenicity, neurotoxicity or reproductive

toxicity, might also provide evidence of specific target organ toxicity that could be used in the

assessment of classification. However, STOT-RE classification is only assigned where the

observed toxicity is not covered more appropriately by another hazard class such as

Carcinogenicity or Reproductive Toxicity.


Table 19 Hazard categories for Specific Target Organ Toxicity – Repeated

Exposure

Category Criteria

Category 1 Substances that have produced significant toxicity in humans or that, on the basis

of evidence from studies in experimental animals, can be presumed to have the

potential to produce significant toxicity in humans following repeated

exposure.

Classification is based on reliable and good-quality evidence from human cases or

epidemiological studies, or on observations from appropriate studies in

experimental animals, in which significant and/or severe toxic effects of relevance

to human health were produced at generally low-exposure concentrations.

Category 2 Substances that, on the basis of evidence from studies in experimental

animals can be presumed to have the potential to be harm ful to human

health following repeated exposure.

Classification is based on observations from appropriate studies in experimental

animals in which significant toxic effects, of relevance to human health, were

produced at generally moderate-exposure concentrations.

In addition to the classification into Category 1 or 2, attempts are made to determine the primary

target organ of toxicity and classify for that purpose.

3.2. LITERATURE REVIEW

The aim of this literature review is to give an up-to-date summary of the available literature on the

human health hazards of coal. The emphasis lies on those human health hazards that may impact

the classification of coal under IMSBC and MARPOL.

Data from both animal studies and epidemiological data are considered:

• Data from animal studies have the advantage that the source and extent of exposure is well

characterized.


• On the other hand, animal studies might have been performed with particularly susceptible

animals, for a short duration and/or on a small scale.

• Human cohort studies2 often comprise a wide range of populations, with varying exposure

conditions and confounding variables, such as smoking.

• For case-control studies,3 the difficulty lies in gathering reliable information about

the exposure in the past. There may be biases in remembering exposure types,

dates and durations.

In addition, some confounding factors are typical of studies comprising coal miners

(Jenkins et al., 2013):

• Occupational studies of coal miners may suffer from the ‘healthy worker effect’. This is an

effect whereby only those individuals who are of greater health engage and continue to be

employed in such a physically demanding profession.

• Coal miners are subject to a considerable number of long-term studies of health and health

outcomes. This might result in a greater surveillance, and thus identification of disease,

than experienced by the general population.

Another factor to take into consideration while reviewing literature addressing the link between

exposure and human health effects is the publication bias. Studies confirming a link between

exposure and health effects are more likely to attract attention, whereas studies showing no

association might suffer from under-reporting or under-publishing.

3 .2.1. ROUTE OF EXPOSURE

The most thoroughly studied health effects caused by exposure to coal are the lung effects seen

after chronic inhalation of coal dust. Studies reporting health effects after dermal or oral exposure

2 A cohort study is an observational study where a group (cohort) of people is followed over time (e.g. for

cancer development). The study can either be conducted prospectively or retrospectively from archived

records. Distinction is made between groups of exposed and non-exposed individuals. 3 A case control study is an observational study in which two existing groups, differing in outcome, are

identified and compared on the basis of a supposed common cause (e.g. exposure to coal dust). This type of

trial requires fewer resources and is less time-consuming than a prospective cohort study.


to coal are virtually absent. Sartorelli et al. (2001) studied the penetration of PAHs from coal dust

through human skin. They found that the PAHs are poorly absorbed through the skin and, hence,

that their bioavailability and potency to induce health effects is low. In addition, publications are

available on the health effects of dermal exposure to coal tar, coal fly ash, coal combustion

residues, etc. However, their composition and the associated health effects are of little relevance

to bulk transported coal. Overall, there is no evidence that dermal or oral exposure to coal during

bulk transport of coal overseas would adversely affect human health, either acutely or after long-

term exposure.

3 .2.2. HUM AN HEALTH EFFECTS OF INHALATION EXPOSURE TO COAL

The inhalation route of exposure is the most relevant for coal (dust). The publications discussed

below for germ cell mutagenicity, carcinogenicity, reproductive toxicity and specific target organ

toxicity after repeated exposure therefore all relate to this route of exposure.

3.2.2.1. GERM CELL M UTAGENICITY

Over the years, several research groups have investigated the link between coal mining activity

and potentially genotoxic effects in animals as well as humans. A selection of relevant publications

is summarized below.

In vitro studies

In 1997, the IARC Monograph on the Evaluation of Carcinogenic Risks to Humans from exposure to

silica, some silicates, coal dust and para-aramid fibrils (IARC, 1997) reported five studies

investigating the mutagenicity of a variety of coal dust extracts in the pre-incubation variant of

the Ames assay using several strains of Salmonella typhimurium. Non-nitrosated extracts were

either non-mutagenic or very weakly mutagenic, while nitrosated extracts of bituminous or sub-

bituminous coal dusts and lignite were positive in this test. Nitrosated extracts of peat and


anthracite were negative. It was concluded that nitrosation of coal dusts at acidic pH may

contribute to the development of gastric cancer in coal miners (Green et al., 1983; Whong et al.,

1983; Krishna et al., 1987; Hahon et al., 1985; Stamm et al., 1994).

In addition, the IARC Monograph (IARC, 1997) reported studies on the ability of coal dusts to

transform mammalian cells. The results were somewhat conflicting: Yi et al. (1991) found that coal

dust from Jiayang, China, did not induce foci in Syrian hamster embryo ceIls, whereas Wu et al.

(1990) found that extracts of non-nitrosated and nitrosated sub-bituminous coal dust from New

Mexico, USA, did transform BALB/c-3T3 cells.

Furthermore, it was shown that nitrosated extracts of sub-bituminous coal dust were mutagenic in

mouse lymphoma cells, promoted sister chromatid exchange in Chinese hamster ovary cells

(Tucker et al., 1984) and induced micronuclei in BALB/c-3T3 cells (Gu et al., 1992). Non-nitrosated

extracts were not tested in these studies.

Two studies examined the induction of sister chromatid exchange in normal human peripheral

blood lymphocytes exposed to a variety of coal dust extracts in vitro. Organic solvent extracts of

sub-bituminous coal dust induced chromosomal aberrations that were increased by exposure to

extracts from nitrosated coal dust. Organic solvent extracts of bituminous or sub-bituminous coal

dusts, lignite and peat induced sister chromatid exchange; anthracite extracts were negative. In

contrast, water solvent extracts of bituminous coal dust, lignite and peat were positive in this

assay while water solvent extracts of sub-bituminous coal dust and anthracite were negative

(Tucker et al., 1984; Tucker and Ong, 1985).

Animal studies

Green et al. (1983) and Ong et al. (1985) conducted genotoxicity studies with mice and rats to

evaluate the potential mutagenic hazard associated with exposures of coal miners to diesel

emission particulates and coal dusts. The levels of respirable particulates were maintained at

2 mg/m3 and the exposure period ranged from three months to two years. Mutagenic activity

was assessed with the Ames Salmonella/microsome assay system; results indicated a

mutagenic potential for extracted diesel emission particulates, but not for coal dust.

Mutagenic compounds were not found in the urine of the exposed animals, nor were sister


chromatid exchanges detected in peripheral lymphocytes. Bone marrow cells were analysed for

micronuclei in both polychromatic and normochromatic erythrocytes; no increase in

micronuclei was detected in rats exposed for 24 months.

In more recent years, da Silva et al. (2000) performed a study over a two-year period on Ctenomys

torquatus, a fossorial rodent. In comet and micronucleus assays, peripheral blood isolated from

animals found in and near a strip coal mine region in Brazil was compared to that from animals in a

control region. Results indicated that coal and derivatives induced DNA and chromosomal lesions

in rodent cells. Quantitative differences between field exposures (within strip coal mine region

greater than near a strip coal mine) were also observed.

In 2007, León et al. investigated potential genotoxic effects of coal mining activity in peripheral

blood cells of wild rodents (Rattus rattus and Mus musculus). The blood cells of animals from a coal

mining area in Colombia were compared to animals from a control area in a comet assay. Evidence

was found that exposure to coal results in elevated primary DNA lesions. DNA damage index,

migration length and percentage damaged cells all showed statistically significant higher values in

mice and rats from the coal mining area in comparison to animals from the control area.

In a study reported by Cabarcas-Montalvo et al. (2012), the comet assay in peripheral blood cells

and the micronucleus test in blood smears were again used to evaluate potential genotoxic effects

derived from exposure to coal mining activities on wild populations of Mus musculus and Iguana

iguana. Four locations in Colombia were evaluated: two municipalities located near coal mining

fields and two cities used as reference sites, localized at a distance of 100 km and 200 km from

the mines respectively. Animals collected in close proximity to coal mining areas showed highest

percentages of DNA damage for both species, evidencing that living around coal mining fields may

result in an increase of DNA lesions in blood cells of rodents and reptiles. The results for

micronucleus test were conflicting, possibly as a result of infection found by blood parasites.

Human studies

Epidemiological studies addressing the potential mutagenicity of coal (dust) are also available. The

IARC Monograph (IARC, 1997) reported a study by ⇧rám et al. (1985), investigating four groups of

23–31 men and women in the soft coal open-cast mining industry in Czechoslovakia. One group


was employed in stripping operations 20 m–50 m from the mine surface, another group in digging

operations 50 m–80 m from the mine surface, another in a coal cleaning plant and the final group

had no known occupational exposure to known chemical mutagens. Peripheral blood lymphocytes

stimulated with phytohaemagglutinin were scored for chromatid or chromosome breaks and

exchanges. The frequency of aberrant cells was elevated only in the workers employed in digging

operations. Coal dust alone could hardly be responsible for the rise in chromosomal aberrations.

Exposure to fumes and fires leading to formation of PAHs in the soft coal open-cast mining

operation was considered to be responsible for increased chromosomal aberrations in this group

(⇧rám et al., 1985).

Schins et al. (1995) measured the 7-hydro-8-oxo-2'-deoxyguanosine (8-oxodG) to deoxyguanosine

(dG) ratio as a marker for oxidative DNA damage in peripheral blood lymphocytes of 38 retired coal

miners (30 healthy and 8 with coal miners' pneumoconiosis) and 24 age-matched non-exposed

controls. This ratio was significantly higher in miners than in the control group. Neither age nor

smoking status was related to the extent of oxidative DNA damage. Among the miners, no

difference was observed between those with or without pneumoconiosis. It was concluded that the

elevated oxidative DNA damage in peripheral blood lymphocytes can be explained by increased

oxidative stress induced by coal dust in the lungs and/or the presence of stable coal dust radicals

in the lymph nodes (Dalal et al., 1991).

Exploring this further, Ulker et al. (2008) performed sister chromatid exchange and micronucleus

tests on peripheral blood lymphocytes isolated from CWP (coal workers’ pneumoconiosis)

patients, coal workers and unexposed controls. The purpose of this study was to investigate the

genotoxic risk in pneumoconiotic patients and in those with occupational exposure to coal dust.

Interestingly, both sister chromatid exchange and micronucleus frequencies in CWP patients were

found to be significantly higher than in coal worker and unexposed groups, in line with the

hypothesis that the chronic inflammation characterizing CWP provides a setting for oxidative

stress and formation of free radicals. In contrast, no differences were observed in the sister

chromatid exchange and micronucleus frequencies in coal workers and unexposed groups,

suggesting that the development of CWP leads to a significant induction of cytogenetic damage in

peripheral lymphocytes.


A cytogenetic monitoring study was carried out on a group of workers from a bituminous coal mine

in Turkey to investigate the genotoxic risk of occupational exposure to coal mine dust (Donbak et

al., 2005). Cytogenetic analysis (for sister chromatid exchanges and chromosomal aberrations)

and micronucleus tests were performed on a strictly selected group of 39 workers, compared to 34

controls matched for gender, age and habit. The frequency of both sister chromatid exchanges and

chromosomal aberrations appeared significantly higher in coal miners than in controls, and

increased with years of exposure. Similarly, there was a significant increase in the frequency of

total micronuclei in exposed group as compared to the control group. It was concluded that

occupational exposure to coal mine dust leads to a significant induction of cytogenetic damage in

peripheral lymphocytes of workers engaged in underground coal mining.

León-Mejía et al. (2011) evaluated the genotoxic effects in a population exposed to coal residues

from an open-cast mine in Colombia. A hundred exposed workers and a hundred non-exposed

control individuals were included in this study. The exposed group was divided according to

different mining area activities:

• transport of extracted coal

• equipment field maintenance

• coal stripping

• coal embarking.

Blood samples were taken to investigate biomarkers of genotoxicity using the comet assay and

chromosome damage as micronucleus frequency in lymphocytes. Both biomarkers showed

statistically significantly higher values in the exposed group compared to the non-exposed control

group. No difference was observed between the exposed groups executing different mining

activities. These results indicate that exposure to coal mining residues may result in an increased

genotoxic exposure in coal mining workers.

Kvitko et al. (2012) evaluated genotoxic effects in Brazilian coal miners. The study included 44 coal

miners and 65 individuals not exposed to coal. Blood samples were collected and DNA damage was

evaluated using the comet assay. Coal miner blood cells had a significantly higher damage index

and damage frequency. In addition, a micronucleus test was performed on epithelial buccal cells

from 28 coal miners and 54 individuals not exposed to coal. This test indicated a significant


increase in nuclear bud frequency and binucleated cells in the exposed group, an increased cell

death frequency and a decreased proliferative potential.

Rohr et al. (2013) evaluated the potential genotoxic effects of coal and oxidative stress resulting

from exposure to coal. This study involved 71 males occupied in coal mining in Brazil and 57

unexposed individuals. The exposed group had a significantly increased damage index and damage

frequency, as assessed using the comet assay, and increased micronucleus and nucleoplasmic

bridge frequencies. In addition, higher superoxide dismutase (SOD) levels were measured in the

exposed group. SOD enzymes form a defence mechanism against reactive oxygen species, which

are produced by inflammatory cells.

Conclusion on germ cell mutagenicity

The available data on coal dust genotoxicity/mutagenicity were checked against the UN GHS

criteria for classification as a germ cell mutagen.

In order for a classification as a germ cell mutagen Category 1 (A or B) to apply, both evidence

demonstrating the mutagenicity of the compound in vivo and evidence showing that the mutations

can occur in germ cells and thus can be transferred to future generations is required. On the basis

of the absence of any publications addressing the targeting of the germ cells, a Category 1

classification can be excluded.

Where there is evidence of only somatic cell mutagenicity, classification as a germ cell mutagen

Category 2 is applicable. Hence, the key question is whether the available data in somatic cells are

sufficiently coherent to conclude that coal (dust) is mutagenic. In vitro studies as well as animal

and human studies have been conducted to this end. Overall, it cannot be concluded firmly from the

available data that coal (dust) is mutagenic, for the following reasons:

• In vitro data: some of the studies indicate a potential for mutagenicity, but only under

specific circumstances, e.g. depending on the source/composition of the coal dust (e.g. Wu

et al., 1990; Yi et al., 1991) or only after nitrosation (e.g. Whong et al., 1983). It is

conceivable that nitrosation of coal dust occurs in the acid environment of the stomach;

however, to date there is no evidence from in vivo experiments.


• Animal data: whereas some of the available studies demonstrate the absence of any

mutagenic effect (Green et al., 1983; Ong et al., 1985), others report a positive result (da

Silva et al., 2000; León et al., 2007; Cabarcas-Montalvo et al., 2012).

• Human studies: especially in recent years, studies have been published examining the

genotoxic effects of occupational exposure to coal mine dust, albeit on a relatively small

scale (typically, groups of about 30 persons). A number of studies showed increased

genotoxic effects from coal dust exposure (e.g. Donbak et al., 2005; León-Mejía et al.,

2011). In other studies, in contrast, it was concluded that not coal dust but exposure to

fumes and fires was responsible for the increased number of chromosomal aberrations

observed in a subset of the miners (⇧rám et al., 1985), or that cytogenic damage lies at the

basis of any observed mutagenic effects (e.g. Ulker et al., 2008). Indeed, coal dust

exposure may lead to chronic inflammation (e.g. in coal workers with CWP, cf. 0), setting the

scene for oxidative stress, which is associated with the overgeneration of reactive oxygen

species (ROS) and subsequent DNA damage (Rohr et al., 2013). Hence, the mutagenic

effects seen in coal workers are more likely to be a consequence of the inflammatory

response elicited in the lungs following inhalation of coal dust, rather than being a primary

effect of the exposure to coal dust.

Taking into account all available data from in vitro, animal and human studies and applying a weight

of evidence approach, it is concluded that classification of coal dust as a germ cell mutagen

Category 2 is not justified. Of note, the German MAK working group came to a similar conclusion in

2002 (MAK, 2002).

3.2.2.2. CARCINOGENICITY

The International Agency for Research on Cancer (IARC), which is an agency of the World Health

Organization (WHO), is regarded as an authority when it comes to classification of substances as

carcinogenic to humans. In 1997, the IARC published a Monograph on the Evaluation of

Carcinogenic Risks to Humans from exposure to silica, some silicates, coal dust and para-aramid

fibrils (IARC, 1997). Their work provides a comprehensive evaluation of the available data at that


time regarding the carcinogenicity of inhaled exposure to these compounds. They aimed at

classifying the compounds into one of the categories outlined in Table 20. This classification is a

matter of scientific judgement, reflecting the strength of the evidence derived from studies in

humans and in experimental animals and from other relevant data.

Table 20 Categories for carcinogenicity as defined by the IARC

Category Criteria

Group 1 The agent is carcinogenic to humans. There is sufficient evidence of

carcinogenicity in humans.

Group 2 This category includes agents for which the degree of evidence of carcinogenicity in

humans is almost sufficient, as well as those for which there are no human data but

for which there is evidence of carcinogenicity in experimental animals. Agents are

assigned to either Group 2A or Group 2B.

Group 2 – the agent is probably carcinogenic to hum ans. This category is

used when there is limited evidence of carcinogenicity in humans and sufficient

evidence of carcinogenicity in experimental animals.

Group 2B – the agent is possibly carcinogenic to humans. This category is

used for agents, mixtures and exposure circumstances for which there is limited

evidence of carcinogenicity in humans and less than sufficient evidence of

carcinogenicity in experimental animals.

Group 3 The agent is not classifiable as to its carcinogenicity to humans. This

category is used most commonly for agents for which the evidence of

carcinogenicity is inadequate in humans and inadequate or limited in experimental

animals. Agents that do not fall into any other group are also placed in this category.

Group 4 The agent is probably not carcinogenic to humans. This category is used for

agents or mixtures for which there is evidence suggesting lack of carcinogenicity in

humans and in experimental animals. In some instances, agents or mixtures for which

there is inadequate evidence of carcinogenicity in humans but evidence suggesting


lack of carcinogenicity in experimental animals, consistently and strongly supported

by a broad range of other relevant data, may be classified in this group.

The conclusion of the IARC Working Group on the classification of coal dust is summarized in Table

21. For coal dust, the degree of evidence based on human and animal data was inadequate. Coal

dust was therefore categorized as a Group 3 carcinogen, which essentially means that it is not

classifiable as to its carcinogenicity in humans.

Table 21 Sum m ary of IARC evaluation of carcinogenic properties of coal dust

Component Degree of evidence

of carcinogenicity

based on human data

Degree of evidence of

carcinogenicity based

on animal data

Overall evaluation

of carcinogenicity

to hum ans

Coal dust Inadequate Inadequate Group 3

Animal studies

In their assessment of coal dust carcinogenicity, the IARC Working Group reviewed a small number

of animal studies (Martin et al., 1977; Karagianes et al., 1981; Lewis et al., 1986). Coal dust was

tested both separately and in combination with other toxic particles, such as diesel exhaust. The

interpretation of the results of these studies was hampered by flaws in their design, as noted by

the IARC Working Group, such as short study duration, small number of animals analysed per group,

administration of excessively high doses and lack of details concerning histopathological findings.

Moreover, Oberdörster (1995) questioned whether the outcome of animal studies is useful to draw

conclusions for carcinogenesis in humans at all. Based on several studies with highly insoluble

nonfibrous particles of low cytotoxicity, including coal dust (Martin et al., 1977), it was concluded

that any highly insoluble particle of low cytotoxicity will cause lung tumours in rats if accumulating

chronically at high enough doses in the lung due to an overload response. This so-called ‘particle

overload’ is characterized by impaired lung clearance by the alveolar macrophages (AM) and

subsequent accumulation of the particles. Thus, the lung tumours observed in chronic rat studies at


very high particulate exposure concentrations may not be relevant for human extrapolation to low-

exposure concentrations. Evidence in humans suggests that particle-overloaded lungs, e.g. in coal

workers, respond primarily with fibrosis.

These finding were endorsed by Nikula et al. (1997) who found that relatively more particulate

material was retained in monkey than in rat lungs after long-term exposure. In addition, rats

retained a greater portion of the particulate material in lumens of alveolar ducts and alveoli.

Conversely, monkeys retained a greater portion of the particulate material in the interstitium.

Rats, but not monkeys, had significant alveolar epithelial hyperplastic, inflammatory and septal

fibrotic responses to the retained particles.

More recent studies by Borm et al. (2000) and Kolling et al. (2011) confirm the particle overload

theory. In the study by Borm et al. (2000), rats were instilled intratracheally with ground lean coal

(60 mg), coal mine dust (60 mg), DQ12 quartz (5 mg) and fine (60 mg) and ultrafine (30 mg) TiO2.

After 129 weeks, rats were killed, tumours detected by microscopy, and inflammation detected by

light microscopy after specific antibody staining for macrophages and granulocytes. Increased AM

and interstitial granulocytes were present in dust-treated animals. Both AM and granulocytes per

surface area were related to tumour incidence and can be interpreted as effects of overload. It was

concluded that coal dust is another poorly soluble, nontoxic dust, which at high enough dose rate

causes overload, inflammation and tumour response in the rat.

Kolling et al. (2011) repeatedly exposed rats to 10 mg of coal dust by intratracheal instillation.

Lung tumours were not detected. Pulmonary inflammatory responses to coal dust were very low,

indicating a mechanistic threshold for the development of lung tumours connected with particle-

related chronic inflammation. The positive control, crystalline silica, elicited the greatest

magnitude and progression of pulmonary inflammatory reactions, fibrosis and the highest

incidence of primary lung tumours (39.6%).

Epidemiological findings

There have been no epidemiological investigations on cancer risks in relation to coal dust per se.

There is, however, a large body of published literature concerning cancer risks potentially

associated with employment as a coal miner. Cancers of the lung and stomach have been


investigated most intensively among coal miners, with sporadic reports for other cancer sites. The

absence of information on the levels of specific components of coal mine dust (e.g. coal, quartz,

metals) further hinders interpretation of the epidemiological literature.

In 1997, the IARC Working Group concluded that the evidence from occupational cohort studies

for an association between coal mine dust and lung cancer has not been consistent; some studies

revealed excess risks (e.g. Rockette, 1977; Meijers et al., 1991), whereas others indicated cohort-

wide lung cancer deficits (e.g. Armstrong et al., 1979; Cochrane et al., 1979; Kuempel et al., 1995;

Swaen et al., 1995). There is no consistent evidence supporting an exposure-response relation for

lung cancer.

In contrast to the lung cancer findings, there have been reasonably consistent indications of

stomach cancer excess among coal miners, detected both in occupational cohort studies and in

community-based case-control studies (e.g. Armstrong et al., 1979; Cochrane et al., 1979; Coggon

et al., 1990; Gonzalez et al., 1991; Swaen et al., 1995). However, the IARC Working Group

concluded that there is no consistent evidence supporting an exposure-response gradient for coal

mine dust and stomach cancer (IARC, 1997).

In a more recent literature review, Jenkins et al. (2013) selected peer-reviewed

publications since 1980 explicitly examining the association between coal mining and

human cancer. In total, 34 publications met these criteria, 27 of which were studies of coal

mining as an occupational risk factor for cancer. The remaining seven publications were

ecological/cross-sectional studies of coal mining and associated cancer risk in the

surrounding population. The occupational studies comprised both studies examining

cohorts of coal miners and studies examining coal mining as a risk factor in case-control

analysis. The studies are summarized in Table 22.


Table 22 Sum m ary of 34 publications reviewed by Jenkins et al . (2013) on the

association between coal mining and human cancer

Reference Study details Findings

Occupational studies examining cohorts of coal miners (10)

Acheson et al. (1981)

Cross-sectional study among miners and quarrymen in England and Wales

Increased nasal cancer incidence among coal miners

Attfield and Kuempel (2008)

Cohort study of 8899 working coal miners from 31 mines in the US

No association between coal mine dust exposure and stomach/lung cancer mortality

Atuhaire et al. (1986)

Cohort study of 7939 men (miners and non-miners) in Wales

No association between coal mining and gastric cancer mortality

Brown et al. (1997)

Cohort study of 23,630 male coal industry workers in New South Wales (Australia)

No association between coal mining and incidence of all cancers; “no evidence of serious hazard for cancer in modern coal mines”

Kuempel et al. (1995)

Cohort study of 9078 male coal miners from 31 mines across the US

No association between coal mine dust exposure and stomach/lung cancer mortality

Miller and Jacobsen (1985)

Cohort study of c. 25,000 coal miners in England (compared to other men in coal mining regions of England and Wales)

Increased digestive system (m ostly stomach) cancer mortality among coal miners; no evidence for increased lung cancer

Miller and MacCalman (2010)

Cohort study of 17,820 British coal workers

Association between increased lung cancer mortality and exposure to coal mine dust with high quartz content; no association between (a.o.) stomach cancer mortality and coal mine dust exposure

Morfeld et al. (1997)

Cohort study of 4578 coal miners in Saar region (Germany)

No association between coal mining and lung cancer; some evidence for increased risk of stomach cancer

Swaen et al. (1995)

Cohort study of 3790 coal miners with abnormal chest X-rays in the Netherlands

Increased gastric cancer m ortality among coal miners with coal workers’ pneumoconiosis or other pulmonary pathology

Tomaskova et al. (2012)

Cohort study of Czech former coal miners with and without coal workers’ pneumoconiosis

Increased lung cancer incidence among coal miners with coal workers’ pneumoconiosis


Occupational studies examining coal mining as a risk factor (17)

Ames (1983) Case-control study of 184 coal miners with gastric cancer from the US NIOSH cohort database

Increased gastric cancer incidence for smokers only after exposure to coal dust/years of underground mining

Ames and Gamble (1983)

Cohort study of 184 coal miners with stomach/lung cancer from the US NIOSH cohort database

Association between coal mine dust exposure and increased stomach cancer incidence for miners with airway obstruction or long-term smoking

Ames et al. (1983)

Case-control study of 317 white male lung cancer deaths from the US NIOSH cohort database

No association between years of underground mining and lung cancer mortality

Coggon et al. (1990)

Case-control study of 95 stomach cancer cases and 190 controls in England

No association between coal mining and stomach cancer incidence

Cordier et al. (1993)

Case-control study of 1530 bladder cancer cases and controls recruited from seven hospitals in France

Increased bladder cancer incidence among coal miners

Goldberg et al. (1997)

Case-control study of 528 cases of hypopharynx/larynx cancer and 305 controls recruited from 15 hospitals in France

Increased hypopharynx/larynx cancer incidence among (coal) miners and quarrymen

Golka et al. (1998)

Case-control study of 926 men from an area of former coal, iron, steel industries in Germany

Increased bladder cancer incidence among hard-coal miners

Gonzalez et al. (1991)

Case-control study of 354 gastric cancer cases and 354 controls in Spain

Increased gastric cancer incidence among coal miners

Hosgood (2012)

Case-control study of 260 lung cancer cases and 260 age-matched controls (all farmers) in China

Increased lung cancer incidence among coal miners

Jöckel (1998)

Case-control study of 1004 lung cancer cases and 1004 matched controls recruited from hospitals in West Germany

No association between lung cancer incidence and coal mining

Lloyd et al. (1986)

Case-control study of 42 lung cancer cases and 42 matched controls in Scotland

No association between lung cancer incidence and occupational exposure to dust

Meijers et al. (1988)

Case-control study of 381 lung cancer cases and 381 controls recruited from one hospital in the Netherlands

No association between lung cancer incidence and coal mining

Schifflers et al. (1987)

Case-control study of 74 bladder cancer cases and 74 matched controls in Belgium

Increased bladder cancer incidence among coal miners, but not quite statistically significant

Swaen et al. Case-control study of 683 male No association between gastric cancer


(1987) gastric cancer cases and 683 controls in the Netherlands

and duration of coal mining occupation

Swanson et al. (1993)

Case-control study of 3792 lung cancer cases and 1966 colorectal cancer controls from the Detroit metropolitan area (US)

Trend of increased lung cancer incidence with increasing years of employment in coal mining

Une et al. (1995)

Cohort study of 1796 coal miners and 4022 non-miners in Japan

Increased m ortality from any cancer among coal miners; increased lung cancer mortality among coal miners with more than 15 years experience

Weinberg et al. (1985)

Case-control study of 176 stomach cancer cases and three control groups recruited from four counties in Pennsylvania (US)

No association between stomach cancer incidence and coal mining

Ecological/cross-sectional studies of coal mining and associated cancer risk in the surrounding population (7)

Christian et al. (2011)

Ecologic, population-based study in Kentucky (US)

Increased lung cancer incidence in several counties with high coal mining activity

Davies (1980)

Ecologic, population-based study among residents of 10 towns in Nottinghamshire (UK)

No association between stomach cancer mortality and residence in mining towns

Fernandez-Navarro et al. (2012)

Ecologic, population-based study in Spain

Association between high cancer mortality ( lung cancer, colorectal cancer, bladder cancer, leukaemia) and proximity to coal mining activity

Hendryx et al. (2008)

Ecologic, population-based study in the Appalachian region (US)

Increased lung cancer mortality in counties with heavy coal mining activity


Ecologic, population-based study in West Virginia (US)

Association between high cancer mortality (breast cancer, respiratory cancer and total cancer) with proximity to coal mining industry


Cross-sectional study among 773 adults in two rural communities in West Virginia (US), one of which a mountaintop mining area

Increase in self-reported incidence of cancer in coal mining areas

Minowa et al. (1988)

Ecologic, population-based study in Japan

Increased lung cancer mortality in administrative units with coal mining activity


The most-studied cancers related to coal mining were lung/trachea/bronchus/respiratory cancers

and digestive/gastric/stomach cancers. However, there is little consistency between the studies.

For the lung/trachea/bronchus/respiratory cancers, six studies showed an increased incidence and

equally six studies reported no increase. As for mortality, three studies showed an increase,

whereas eight reported no increase. For the digestive/gastric/stomach cancers, four studies

showed an increased incidence, whereas seven studies reported no increase. Furthermore, two

studies showed an increased mortality, whereas eight reported no increase.

Despite the absence of data on the composition of the inhaled coal dust, in some of the studies

that revealed an association between coal mining and cancer, it was noted that the workers had

been exposed to relatively high levels of silica (Une et al., 1995; Goldberg et al., 1997; Miller and

MacCalman, 2010). Noteworthy, inhaled crystalline silica (quartz or cristobalite) from occupational

sources has been categorized by the IARC Working Group as a Group 1 carcinogen (carcinogenic to

humans) based on sufficient evidence of carcinogenicity in humans and experimental animals

(IARC, 1997, 2012).

Despite the low number of studies examining the impact of coal mining on surrounding populations,

Table 22 shows that six of the seven studies concluded an increased cancer risk in association with

residence near coal mining. Jenkins et al. (2013) attributed this in part to publication bias, or the

tendency for coal mining regions to have high poverty rates. Some areas with both high cancer

rates and coal mining activity also face increased smoking, overweight and other cancer risk

factors (Hendryx et al., 2008; Hendryx et al., 2012).

Conclusion on carcinogenicity

The available data on coal dust carcinogenicity were checked against the UN GHS criteria for

classification as a carcinogen.

To justify the classification of a compound as carcinogenic Category 1, sufficient evidence should

be available from either human (Category 1A) or animal studies (Category 1B). If only limited

evidence is available (from human and/or animal studies), then a classification as carcinogenic

Category 2 is more appropriate.


In the case of coal (dust), a large body of literature is available investigating the relationship

between coal mining or coal dust exposure and tumour development. Both animal and

epidemiological studies have been conducted. Overall, the available data do not support a

classification of coal dust as a carcinogen, for the following reasons:

• Animal data: although there are animal studies showing increased cancer incidence

after coal dust exposure, the relevance of these studies, in particular those in rats,

has been questioned due to the ‘particle overload’ effect (Oberdörster, 1995). Indeed,

when exposed by inhalation to high enough levels of poorly soluble nonfibrous dusts

(such as coal dust), rats will develop lung tumours. However, these data are not

relevant for extrapolation to humans.

• Epidemiological data: the reported studies are at times contradictory, which prevents

making definitive conclusions about cancer risk due to coal mining. With respect to lung

cancer, the evidence from epidemiological studies for an association between coal mine

dust and lung cancer has not been consistent. Whereas some studies revealed excess risks

(e.g. Miller and MacCalman, 2010; Hosgood et al., 2012), others indicated cohort-wide lung

cancer deficits (e.g. Kuempel et al., 1995; Jockel 1998). In the case of gastric cancer, there

have been reasonably consistent indications of cancer excess among coal miners in both

cohort and case-control studies (e.g. Gonzalez et al., 1991; Swaen et al., 1995). However,

similar to lung cancer, there is no consistent evidence supporting an exposure-response

relation for coal mine dust and gastric cancer (IARC, 1997). Furthermore, the

epidemiological data relate to the activity of coal mining where other risk factors are

present than coal (dust) alone.

Overall, due to the contradictory results of research examining commonly studied cancer sites

(lung, stomach) and the paucity of studies examining other sites (Jenkins et al., 2013),

classification of coal dust as a carcinogen does not seem justified.


3.2.2.3. REPRODUCTIVE TOXICITY

In the IARC Monograph (IARC, 1997), the absence of data on the reproductive and developmental

effects of coal dust was indicated. More recently, however, population-wide studies on the effects

of coal mining on foetal development were published.

In a study published in Portuguese, Leite and Schüler-Faccini (2001) assessed the relationship

between coal mining and the reproductive health of populations living in small towns in southern

Brazil. Hospital records of 10,391 newborns (from 1985 to 1995) were analysed for birth defects.

Eight major birth defects were selected and their frequencies at birth were analysed and compared

to observed frequencies registered by the Latin American Collaborative Study of Congenital

Malformations. The results showed no increase in the frequencies of the birth defects studied, and

rule out the existence of potential reproductive hazards in this region.

Shanxi Province in northern China has one of the highest reported prevalence rates of neural tube

defects at birth in the world. Liao et al. (2010) selected Heshun, the county with the highest rate of

neural tube defects in Shanxi, as a study area and tested whether residence in a coal mining area

was a contributing factor. A neural tube defect cluster was detected in an area within 6 km of the

coal mines for almost every year during 1998–2005. Regression analysis revealed that there may

be an association between production in coal mines and prevalence of neural tube defects in coal

mine areas.

Ahern et al. (2011a) estimated the association between residence in coal mining environments and

low birth weight by means of a cross-sectional, retrospective analysis of 42,770 births in West

Virginia (US). After controlling for covariates, residence in coal mining areas posed an independent

risk of low birth weight. Living in areas with high levels of coal mining elevates the odds of a low-

birth-weight infant by 16%, and by 14% in areas with lower mining levels, relative to counties with

no coal mining.

Additionally, Ahern et al. (2011b) investigated birth defects in mountaintop coal mining areas,

compared to other coal mining areas and non-mining areas, of central Appalachia. In total,

1,889,071 live births from the period 1996–2003 were analysed. Children born in mountaintop

coal mining counties were 26% more likely to have a birth defect than those born in non-mining


areas, after adjusting for other risk factors such as maternal age, alcohol consumption and

diabetes and low socioeconomic status. Prevalences of circulatory and respiratory system birth

defects in mountaintop coal mining areas were nearly double those in other mining and non-mining

counties. Overall, from the comparison of the effects of mountaintop mining and conventional coal

mining, it was concluded that conventional mining is not a risk factor for increased birth defects.

Mountaintop mining, however, is not representative for exposure to coal during bulk transport, as

the explosive blasts required to flatten the mountain ridges and to expose coal seams result in the

release of many substances other than coal dust that may present a risk (e.g. silica, fine metals,

nitrogen dioxide, etc.).

Conclusion on reproductive toxicity

The available data were checked against the UN GHS criteria for classification as a reproductive

toxicant.

The classification of a compound as a reproductive toxicant (Category 1A, 1B or 2) relates to

adverse effects either on sexual function and fertility or on development of the offspring. Adverse

effects on or via lactation lead to a separate classification.

The number of studies investigating the effects of coal or coal dust on reproduction is low. Those

studies that are available are population-wide epidemiological studies assessing birth defects in

mining areas. Effects on fertility or lactation have been largely unexplored.

As for the birth effects, the evidence is conflicting, in that some studies indicate that there is an

effect (e.g. increased prevalence of neural tube defects, lower birth weight) (Liao et al., 2010;

Ahern et al., 2011a), while others demonstrate the absence of any adverse effect on reproduction

(e.g. no change in frequency of birth defects) (Leite and Schüler-Faccini, 2001).

In summary, indications of reproductive toxicity were only found in a limited number of human

studies. The available evidence is too weak to justify a classification of coal as a reproductive

toxicant. In addition, adverse effects on or via lactation have not been reported to date.


3.2.2.4. SPECIFIC TARGET ORGAN TOXICITY – REPEATED EXPOSURE

Literature data specifically addressing the health hazards from the transportation of bulk coal are

not available; however, epidemiological data relating to the health effects of coal mining are

collected on a systematic basis by several national authorities and are the subject of numerous

epidemiological studies. Occupational diseases commonly associated with coal mining activities

are those arising from chronic inhalation exposure to coal dust and clearly target the lungs:

pneumoconiosis, fibrosis and chronic airway diseases such as emphysema and chronic bronchitis

(Petsonk et al., 2013).

Coal workers’ pneumoconiosis (CWP) or black lung disease is a common affliction in coal miners

and results from the progressive build-up of inhaled coal dust in the lungs, similar to silicosis

resulting from the inhalation of crystalline silica dust. Most miners with simple CWP have no

symptoms or physical signs. Diagnosis is generally based on the radiographic classification of the

size, shape, profusion and extent of parenchymal opacities (Chong et al., 2006; Petsonk et al.,

2013). Shortness of breath is normally not seen, but studies of miners with CWP have

demonstrated a reduction in FEV1, the forced expiratory volume in one second (Seixas et al., 1993).

As the coal dust particles cannot be removed from the lungs, an inflammation reaction occurs and

the simple CWP may progress over time towards progressive massive fibrosis (PMF), a condition

characterized by the development of large fibrotic masses in the lungs due to exuberant fibroblast

activity (Boitelle et al., 1997). Diagnosis is based on determination of the presence of large

opacities (1 cm or larger) using radiography or the finding of specific lung pathology on biopsy or

autopsy (Chong et al., 2006; Petsonk et al., 2013). PMF may result in severe airways obstruction,

restrictive lung defects and congestive heart failure.

Another disease commonly associated with coal dust exposure is chronic obstructive

pulmonary disease (COPD) (Coggon and Newman Taylor, 1998). COPD is characterized by

persistent airflow limitation that is usually progressive and associated with an enhanced

chronic inflammatory response in the airways and the lung to noxious particles or gases. The

chronic inflammatory response may induce parenchymal tissue destruction (resulting in

emphysema, i.e. destruction of the air spaces where gas transfer occurs) and disrupt normal

repair and defence mechanisms (resulting in small airway fibrosis). These pathological changes


lead to air trapping and progressive airflow limitation, and in turn to breathlessness. COPD may

be associated with chronic bronchitis due to mucus hypersecretion (Vestbo et al., 2013). The

diagnosis is usually confirmed by spirometry.

Epidemiological findings

Numerous epidemiological studies in a variety of countries have consistently shown that the

development of CWP is related to exposure to respirable mixed coal mine dust (e.g. Hurley et al.,

1979; Jacobsen, 1979; Soutar et al., 2004; CDC, 2009). Similarly, the relationship between PMF

and past exposure to coal dust has been the subject of numerous publications (e.g. Maclaren and

Soutar, 1985; Wade et al., 2011).

The Coal Criteria Document (CCD) of the National Institute for Occupational Safety and Health

(NIOSH, 1995) provides a comprehensive overview of literature on the health effects of exposure

to coal mine dust at that time. It made note of studies of underground coal mining on CWP and PMF

in the US (Morgan et al., 1973; Attfield, 1992; Attfield and Seixas, 1995), in the UK (McLintock et

al., 1971; Shennan et al., 1981; Soutar and Hurley, 1986; Attfield and Althouse, 1992; Attfield and

Castellan, 1992) and in Germany (Reisner, 1971). More recent epidemiological studies include data

on both underground (e.g. Liu et al., 2009; Tor et al., 2010) and surface coal mining (CDC, 2012).

NIOSH in the US reported in 2011 that after a prolonged period of declining CWP prevalence,

surveillance data indicated that the prevalence was rising again, and that severe CWP was seen in

coal miners at relatively young ages. Multiple factors possibly contribute to the resurgence of this

disease, but according to the NIOSH report, an important explanation is the increase in crystalline

silica exposure (NIOSH, 2011). As the more productive seams of coal are being mined out, there is

a transition to mining thinner coal seams and mines with more rock intrusions. Crystalline silica is

commonly found in the rock strata surrounding coal seams, in concentrations much higher than

within the coal seam itself (Page, 2003). Concomitantly, there is an increased potential for

exposure to crystalline silica. For many years, it has been known that prolonged inhalation of fine

dust containing a proportion of crystalline silica can cause a specific type of lung damage called

silicosis (Petsonk et al., 2013) (see also Annex IV). In addition, exposure to crystalline silica dust

has been linked with CWP (Kuempel et al., 2003).


Interestingly, a similar resurgence of CWP as in the US was not reported by the Australian

underground coal mining industry, despite the higher levels of respirable coal mine dust in

Australian coal mines (Joy et al., 2012). As a potential explanation, Joy et al. (2012) put forward

that the coal seams mined in Australia are generally thicker than those mined in the US. As a result,

Australian coal workers are exposed to lower levels of respirable crystalline silica.

Based on these findings, it can be concluded that at least part of the cases of simple and

progressed pneumoconiosis in coal workers can be explained by exposure to respirable crystalline

silica (resulting from the mining activity), rather than to coal dust in general.

Coal constituents responsible for lung effects

Several publications attempted to elicit information on what constituents of coal dust predict the

development of lung diseases. Primarily, the levels of coal dust per se were shown to strongly

correlate with the prevalence of both simple CWP and PMF (Hurley et al., 1982; Attfield and

Morring, 1992).

Crystalline silica was found to be a minor contributor to CWP (Walton et al., 1977; Attfield and

Wagner, 2007). For example, Kuempel et al. (2003) showed in an analysis of lung inflammatory cell

counts from bronchoalveolar lavage in coal miners and non-miners that quartz dust was a

significant predictor of pulmonary inflammation and radiographic category of simple CWP. Against

this, epidemiologic research has not demonstrated a strong effect of crystalline silica on CWP

development in situations where silica levels are low (Attfield and Althouse, 1992; Attfield and

Castellan, 1992; Attfield and Seixas, 1995). However, in the case of exposure to excessive levels

of respirable crystalline silica due to mining of thinner coal seams, rapid progression of

pneumoconiosis was seen, as indicated above (Laney et al., 2010; NIOSH, 2011).

Apart from coal dust and silica, free radicals and bioavailable iron have been put forward as

potential mediators of human health effects of coal:

• Free radicals and coal rank: freshly fractured coal from siliceous rock has been found to

contain higher levels of free radicals and is more fibrogenic than aged particles (Dalal et al.,

1989; Dalal et al., 1995). Page and Organiscak (2000) linked the issue of coal rank, a known


risk factor for CWP development in the US, Britain, and Germany, with the potential for

higher levels of free radicals to be encountered where such coals are mined.

• Bioavailable iron: bioavailable iron has been found to predict coal mine dust toxicity (Zhang

et al., 2002; Huang et al., 2005; McCunney et al., 2009). It is formed in an oxidation reaction

from pyrite (FeS2) and subsequent hydrolysis.

Both factors, the amount of free radicals and the bioavailable iron, predominantly relate to the

mining activity rather than to the coal itself and are therefore of little relevance for the health

hazards during the bulk transport of coal.

Animal studies

Supplementing the epidemiological findings, a number of studies were conducted in animals to

characterize the relationship between coal dust exposure and potential human health effects. The

advantage of these studies is that the source and extent of exposure is well characterized.

Rats exposed for 20 months (6 hours/day, 5 days/week) at levels of 6.6 mg/ml and 14.9 mg/ml coal

dust from a mine developed lesions similar to simple CWP in humans. No advanced lesions such as

micro- or macronodules or infective granulomas were observed in these animals, but focal

bronchiolization occurred after exposure for 20 months (Busch et al., 1981).

In a summary of animal studies, Heppleston (1988) reviewed a study by Ross et al. (1962), who

exposed rats to dust levels of 60 mg/m3 (16 hours/day, 10 months) and quartz concentrations

from 5% to 40%. The experimental animals showed little fibrosis after exposure to mixtures with

5% and 10% quartz. However, rats exposed to 20% and 40% quartz–coal mixtures had fibrosis

and increased collagen content at the end of exposure. Both parameters appeared to be correlated

with the total quartz remaining in the lung 100 days after exposure. In other animal studies, a

fibrogenic role for quartz at concentrations noted in coal mine dust was not apparent (Woitowitz et

al., 1989). Also, the working group of the German MAK committee (Threshold Limit Value

Committee) summarized rat experiments with coal mine dust (MAK, 2002); experiments showed

far lower fibrogenic risks than expected from the experiments with pure quartz of the same mass

concentration. There was almost no correlation of fibrogenicity indices with varying quartz

contents of coal mine dusts. The high variability of coal mine dust fibrogenicity suggests


unidentified factors different from quartz (Woitowitz et al., 1989). As concluded by Heppleston

(1988), the concentration of coal dust and length of exposure remain the main determinants of

disease determinants.

Brown and Donaldson (1989) made observations in rats exposed to coal dust at a concentration of

10 mg/m3 in air for up to 52 days. Compared with controls, rats exposed to coal dust had a higher

proportion of neutrophils recovered at bronchoalveolar lavage (BAL) and significantly higher

concentrations of neutrophil elastase activity were found in their BAL fluid.

Donaldson et al. (1990) compared the bronchoalveolar leukocyte response to airborne coal

mine dust, quartz (positive control) and titanium dioxide (negative control). Groups of rats

were exposed to airborne mass concentrations of 10 mg/m3 and 50 mg/m3 of the dusts for

7 hours/day, 5 days/week for 2 to 75 days. Time- and concentration-dependent recruitment

of neutrophils and macrophages into the bronchoalveolar region was demonstrated after

inhalation of coal mine dust, but the magnitude of the response was not dependent on coal

rank or quartz content although the maximum quartz content in the dusts used was 6%.

Overall, the inflammatory response was much less than that produced by quartz alone at

similar airborne mass concentrations, and more than that produced by titanium dioxide.

In addition, in rats that were exposed for 32 or 75 days and were then allowed to recover for

64 days, there was marked progression of the leukocyte response with quartz and persistence

of the response with coal mine dust. Chronic recruitment of leukocytes to the lungs of

individuals inhaling coal mine dust was concluded to be an important factor in the development

of CWP.

Conclusion on specific target organ toxicity after repeated exposure

The available data on target organ (lung) toxicity after repeated exposure were checked against

the UN GHS criteria for classification.

Classification as STOT-RE relates to the ability of a compound to produce significant health

effects to a specific organ after repeated exposure. Reversible, irreversible, delayed and

immediate effects are all covered. If the available evidence comes from human epidemiological


studies, a STOT-RE Category 1 classification is warranted. In case the evidence comes from animal

studies only, a Category 2 classification is more appropriate.

In the case of coal (dust), a large body of literature is available investigating the relationship

between coal mining or coal dust exposure and lung diseases. Both animal and epidemiological

studies have been conducted. Overall, the available data support a classification of coal dust as

STOT-RE Category 1 for the following reasons:

• Epidemiological studies: numerous studies and monitoring programmes have established a

link between lung diseases (including pneumoconiosis, fibrosis and chronic airway diseases)

and long-term exposure to high levels of coal dust originating from mining activities (e.g.

NIOSH, 2011). Respirable crystalline silica, present in many coal dusts, is known to present

a hazard for silicosis development (cf. Annex IV) but cannot explain all cases of lung

diseases seen in coal workers.

• Animal studies: a large number of animal studies have been conducted with coal dust. These

studies mainly provide insight into the mechanisms leading to lung diseases after repeated

inhalation exposure to coal dust.

Overall, it can be concluded that coal dust may present a risk to human health after repeated

inhalation exposure and that classification as STOT-RE Category 1 is justified based on

epidemiological data. The lungs are the primary target organs.

3.3. SUMMARY AND CONCLUSION

This report reviews the available literature on the human health hazards of coal, in particular its

potential germ cell mutagenicity, carcinogenicity, reproductive toxicity and specific target organ

toxicity after repeated exposure.

Evidence in literature that would justify a classification of coal as a germ cell mutagen or

reproductive toxicant does exist although limited and/or contradictory. In contrast, numerous

publications investigate the relationship between exposure to coal (dust) and occupational

diseases, including coal workers’ pneumoconiosis (CWP), progressive massive fibrosis (PMF) and

cancers of the respiratory tract and digestive system.


Based on the available evidence, it was concluded that the evidence supporting an

association between coal mine dust and lung/stomach cancer is not consistent (IARC, 1997;

Jenkins et al., 2013).

In contrast, convincing evidence is available in literature for an association between long-term

exposure to coal dust and respiratory diseases such as CWP and PMF. Based on epidemiological

data, a classification of coal (dust) as STOT-RE Category 1 is therefore justified.

It is noted, however, that classification under GHS is hazard-based. The actual risk to human health

depends on the duration and level of exposure, which is likely to be different for workers involved

in the shipping of bulk coal than for underground coal miners.

The conclusions of this literature review have been summarized in Table 23.

Table 23 Classification of coal for human health hazards and implications for

categorization under maritime transport regulations

Dermal/oral route of

exposure

Inhalation route of

exposure

Germ cell mutagenicity Not classification No classification

Carcinogenicity No classification No classification

Reproductive toxicity No classification No classification

STOT-RE No classification STOT-RE Category 1 (inhalation, lungs)

Implications for

categorization under

maritime transport

regulations

Coal should not be considered as

hazardous to the marine

environment (target HME) under

the MARPOL Convention

Coal should be considered a

Group B cargo under the

IMSBC Code based on

human health hazards(1) (1) It is noted that coal is already considered a Group B cargo under the IMSBC Code based on its

physicochemical properties.


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5. ANNEXES

5.1. ANNEX I: SUMMARY OF THE ASTM COAL CLASSIFICATION SYSTEM

ASTM Standard D388-98a has put forward a classification of coal by rank, and the parameters

that define the ranking of a coal are fixed carbon limits, volatile matter limits and the gross

calorific value limits. In addition, the agglomerating character of a coal is also taken into account

up to a certain extent (see Table 24).

Table 24 Classification of coals by rank (1)

Class/group Fixed

carbon

l imits (dry,

mineral-

matter-free

basis) , %

Volatile

matter l imits

(dry, mineral-

matter-free

basis) , %

Gross caloric value l imits

(moist, (2) mineral-matter-free

basis)

Agglomerating

character

Btu/lb MJ/kg(3)

Equal

or

greater

than

Less

than

Greater

than

Equal

or

less

than

Equal or

greater

than

Less

than

Equal

or

greater

than

Less

than

Anthracitic

Meta-

anthracite

98 – – 2 – – – –

Non-

agglomerating Anthracite 92 98 2 8 – – – –

Semi-

anthracite(4)

86 92 8 14 – – – –

Bituminous coals

Low volatile 78 86 14 22 – – – –

Commonly

agglomerating(6)

Agglomerating

Medium

volatile

69 78 22 31 – – – –

High-volatile

A

– 69 31 – 14,000(5) – 32.6 –

High-volatile

B

– – – – 13,000(5) 14,000 30.2 32.6

High-volatile

C

– – – – 11,500 13,000 26.7 30.2

10,500 11,500 24.4 26.7

Sub-bituminous coals

Sub-

bituminous A

– – – – 10,500 11,500 24.4 26.7

Non-

agglomerating Sub-

bituminous B

– – – – 9500 10,500 22.1 24.4

Sub- – – – – 8300 9500 19.3 22.1


bituminous C

Lignitic

Lignitic A – – – – 6300 8300 14.7 19.3 Non-

agglomerating Lignitic B – – – – – 6300 – 14.7 (1 ) This classification only applies to coals that are composed mainly of vitrinite. (2) Moist refers to coal containing its natural inherent moisture but not including visible water on the surface

of the coal. (3) Megajoules per kilogram. To convert British thermal units per pound to megajoules per kilogram, multiply

by 0.002326. (4) If agglomerating, classify in low-volatile group of the bituminous class. (5) Coals having 69% or more fixed carbon on the dry, mineral-matter-free basis shall be classified according

to fixed carbon, regardless of gross calorific value. (6) It is recognized that there may be non-agglomerating varieties in these groups of the bituminous class, and

there are notable exceptions in the high-volatile C bituminous group.

The basis of the classification is according to fixed carbon and gross calorific value calculated to

the mineral-matter-free basis. The higher-rank coals are classified according to fixed carbon, on

the dry basis; the lower-rank coals are classified according to gross calorific value on the moist

basis, with the agglomerating character used to differentiate between certain adjacent groups.

5.2. ANNEX II : MODE OF OCCURRENCE OF METALS IN COAL

Table 25 provides an overview of the likely mode of occurrence of enriched trace elements in

coal, whereas Table 26 summarizes the other elements (depleted, similar). Both Dale (2009)

and Riley et al. (2005) also reported on modes of occurrence. Dale (2009) based his

conclusions on the outcome of density fractionation experiments (see Table 27). Although

there is a large overlap between the findings of both authors, there are still some significant

differences for some elements (e.g. B, Be, U).

Table 25 Likely mode of occurrence of enriched trace metals in coal

Element M ode of occurrence

Antimony In pyrite (FeS2) and accessory sulfides (co-crystallization), possibly organic

matter

Arsenic In pyrite (FeS2) (co-crystallization);(1) suggestion of some association to clay

minerals and phosphate minerals (Swaine, 1990)

Boron Organic association (plant material)

Cadmium In sphalerite ((Zn,Fe)S) (co-crystallization), some association with silicates

Lead In galena (PbS) (precipitation of lead sulfide in the anaerobic environment)


Mercury In pyrite (FeS2) (co-crystallization)

Molybdenum Not properly defined (probably sulfides)(2)

Selenium Organic association (plant material) and in pyrite (FeS2) (co-crystallization) and

accessory sulfides Sources: Riley et al, 2005; Dale, 2009 (1) Finkelman (1994. 1995) suggested that a minor amount of As and Cr may be organically bound. (2): Dale et al. (1999) reported that Mo is present in the monosulfides and pyrite and possibly associated with

organic matter.

Table 26 Likely mode of occurrence of non-enriched trace metals in coal

Element M ode of occurrence

Barium Phosphate minerals, carbonate minerals, sulfate minerals

Beryllium Organic association, clay minerals, silicates

Chromium Clay association, organic association?

Cobalt In pyrite, clay minerals, silicates some in accessory minerals

Copper Chalcopyrite (copper iron sulfide), silicates

Manganese In carbonate minerals, siderite (iron carbonate) and ankerite (calcium iron

carbonate), clay minerals

Nickel Not properly defined; associated with pyrite and organic matter (Finkelman,

1994, 1995) ; present in clays and carbonates (Swaine, 1990)

Uranium Organic association and in zircon (zirconium silicate), clay minerals, phosphate

minerals

Thorium In monazite (thorium phosphate), xenotime (yttrium phosphate) and zircon

(zirconium silicate)

Vanadium In clay minerals and some organic association

Zinc In sphalerite (ZnS) Sources: Riley et al, 2005; Dale, 2009.

Table 27 M odes of occurrence of trace elements using density fractionation

Element M ajor mode of occurrence

M inor mode of occurrence

Dale, 2009 Riley et al . , 2005 Dale, 2009 Riley et al . , 2005

Antimony Organic, sulfide Organic – Clay

Arsenic Sulfide Carbonate/oxide,

organic

Organic, clay Pyrite, clay

Beryllium Organic Clay,

carbonate/oxide

Clay Organic

Boron Organic Organic Clay Carbonate/oxide

Cadmium Sulfide Uncertain – Uncertain

Chromium Clay Clay, organic,

carbonate/oxide

Organic –

Cobalt Organic, clay,

sulfide, carbonate

Carbonate/oxide,

organic

– Clay


Copper Sulfide, clay,

carbonate

Carbonate/oxide,

organic

– Monosulfide, clay

Lead Sulfide Carbonate/oxide Clay Pyrite, clay

Mercury Sulfide Pyrite, organic – Monosulfide

Manganese Carbonate Carbonate/oxide Organic, sulfide –

Molybdenum Organic Organic, pyrite Sulfide –

Nickel Organic, clay,

sulfide

Clay, organic,

carbonate/oxide

– Pyrite

Selenium Sulfide Organic – Pyrite

Thorium Clay Clay,

carbonate/oxide

Phosphate Organic

Uranium Clay Organic Organic Clay,

carbonate/oxide

Vanadium Clay Clay Organic Organic

Zinc Sulfide Carbonate/oxide,

monosulfide

– Pyrite

5.3. ANNEX III : SUMMARY OF TRANSFORMATION/DISSOLUTION PROTOCOL

(T/DP) TEST DATA FOR COAL

A first company provided T/DP test for four different coal samples, each representing a different mining

site. Measured elements were Al, Cu and Pb. Table 28 gives a summary of the measured values after a

seven-day exposure period, and this for three different loadings (1 mg/L, 10 mg/L and 100 mg/L).

Table 28 Results of a seven-day T/DP test with four coal sam ples – tests

conducted in marine environment

Loading M ine Al (µg/L) Cu (µg/L) Pb (µg/L)

1 mg/L Mine A < 20 < 10 < 20

Mine B < 20 < 10 < 20

Mine C < 20 < 10 < 20

Mine D < 20 < 10 < 30

10 mg/L Mine A < 20 < 10 < 20

Mine B < 20 < 10 < 20

Mine C < 20 < 10 < 20

Mine D < 20 < 10 < 30

100

mg/L

Mine A 30 < 10 < 20

Mine B 20 < 10 < 20

Mine C 40 < 10 < 20

Mine D < 20 < 10 < 30


Aluminium was the only measured parameter for which the measured concentration exceeded the

detection limit; this was the case after a seven-day exposure period, and only in the T/DP test with

a 100 mg/L loading. This level was well below any known ecotoxicity reference value for this

element. Other elements were also measured, and here too, concentrations of metals were very

low and comparable to those in the blanks. This likely relates to:

• the trace elements of some constituents present in the reagent-grade salts used to

prepare the saltwater test solution

• the absence of leaching of metals from coal.

This company also conducted a T/DP test on a fifth sample; here, the concentration levels of 18

PAHs were also measured in the solution of a seven-day T/DP test (using seawater as test

medium). All levels were below detection limit (below 0.0250 µg/L). It should be stressed, however,

that within a regulatory context the T/DP test protocol is only applicable for metals, and not for

organic substances.

A second company assessed a suite of inorganic constituents (predominantly metallic elements)

during a seven-day dissolution test with two coal samples. A standard laboratory shaker table set

at a 100 revolutions per minute (rpm) oscillation rate was used in this testing, and all tests were

conducted at temperatures between 20°C and 25°C. The highest surface area product typically

used in commerce was obtained for testing, i.e. a 100 mg/L sample of 4-mesh coal was utilized in

these dissolution tests. Trace metal analyses of EPA priority pollutant and other metals were

conducted with US EPA Method 200.8 utilizing inductively coupled plasma mass spectrometry

(ICP-MS) ion collision techniques in order to obtain the lowest available detection limits in the

saltwater medium.

Table 29 Trace metal concentrations in the dissolution medium after a seven-day

exposure period

Element Blank

(µg/L)

7d dissolution of 100 mg

of Sample #1

(µg/L)

7d dissolution of 100 mg of

Sample #2

(µg/L)

Antimony 0.500 0 0.07

Arsenic 0.650 -0.03 0.07

Barium 3.29 -0.10 1.14


Beryllium 0.800 0 0

Cadmium 7.19 -0.12 0.55

Chromium 13.1 -5.53 -5.52

Copper 1.50 -0.07 0.11

Lead 0.660 -0.16 -0,10

Manganese 19.1 -0.47 1.17

Mercury 0.152 -0.02 -0,02

Nickel 60.1 -1.71 3.50

Selenium 1.50 0.01 0.24

Silver 0.250 0.002 0.03

Thallium 0.250 0.04 0.12

Vanadium 0.250 0 0

Zinc 10.0 0 0 Values in red were non-detectable at the method detection limit shown.

No significant increases of metal concentrations were observed in the solution of the coal sample

#1 (Table 29). The concentration levels were similar or marginally lower than the measured levels

in the blank solution prior to the test. The increase of thallium is due to an increased concentration

(estimated concentration; value above the MDL, but below the quantifiable reporting limit) in one

replicate after Day 4; all other measurements for thallium were below detection limit (including all

measurements after Day 7). A similar outlier after Day 4 was found for silver, resulting in the small

increase of 0.002 µg/L. All silver measurements after Day 7 were below the detection limit.

Most of the increases that are noted for Sample #2 are due to a higher value (potential outlier) in

one of the replicates after Day 4. Increased concentration levels were not observed after Day 7.

This is the case for antimony, arsenic, thallium and silver. The increase of nickel is most likely

related to the fact that the element is also measured in the blank at Day 7; therefore, the observed

increases after Day 7 are not reliable. It is noteworthy that no increase of nickel was noted in any

of the replicates after Day 4.

Selenium and manganese were the only elements for which a marginal increase was noted in most

replicates after Day 7. The measured levels can be explained by the presence of the element in the

coal sample, but concentration levels remain very low and are well below the concentration levels

that would trigger classification.


A third company conducted seven-day Transformation/Dissolution tests on 11 different coal

samples. The outcome of the analytical measurements showed that Zn, Cu and Pb levels in all

samples/all loadings (1 mg/L, 10 mg/L, 100 mg/L) were below the detection limit of 1 µg/L. Tests

were conducted in both freshwater and marine water.

The fourth company that supplied T/DP test data, conducted seven-day dissolution experiments

with 16 different coal samples at a loading of 100 mg/L. In total, 15 relevant trace elements were

analysed, and the measured concentrations in the test solution after a seven-day dissolution

period are presented in Table 30.

Table 30 Concentration of 14 trace elements after a seven-day dissolution period

– values between brackets are estimated below reporting l imit

Sample code

D-A D-B D-C D-D D-E D-F D-G D-H


Arsenic (0.0624) (0.13) (0.071) (0.067) (0.0937) (0.112) (0.057) (0.05)

Barium 1.49 (0.38) 0.92 (0.464) 1.74 1.64 0.87 1.11

Beryllium n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Boron n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Cadmium (0.196) (0.22) (0.19) (0.19) (0.186) (0.201) (0.18) (0.19)

Chromium (0.29) (0.16) (0.14) (0.198) (0.204) (0.225) (0.15) (0.14)

Copper n.d. n.d. n.d. n.d. n.d. 3.171 n.d. n.d.

Lead (0.064) (0.048) (0.07) n.d. n.d. n.d. (0.071) n.d.

Manganese 1.74 1.75 1.67 1.67 1.98 1.86 2.36 1.75

Mercury n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Nickel 3.11 2.64 2.68 3.24 3.37 3.22 2.72 3.5

Selenium (0.448) (0.42) (0.44) 0.532 0.508 (0.461) (0.39) (0.41)

Vanadium (0.092) (0.06) (0.065) (0.0586) (0.0474) (0.0691) (0.063) (0.09)

Zinc (3.02) (3.15) (5.31) (3.92) n.d. (4.19) (3.81) (4.14) n.d.: not detected at reporting limit

Table 30 continued

Sample code

D-I D-J D-K D-L D-M D-N D-O D-P


Arsenic (0.056) (0.074) (0.108) (0.101) (0.049) (0.0805) (0.081) (0.116)

Barium 15.6 1.12 0.77 1.86 3.99 (1.11) 1.8 3.15

Beryllium n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.


Boron n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Cadmium (0.067) (0.19) (0.146) (0.136) (0.2) (0.148) (0.22) (0.175)

Chromium (0.14) (0.43) (0.194) (0.229) (0.19) (0.189) (0.17) (0.226)

Copper n.d. n.d. (0.284) n.d. 1.83 n.d. n.d. n.d.

Lead n.d. (0.1) n.d. n.d. (0.24) n.d. n.d. n.d.

Manganese 1.71 1.76 1.68 1.65 1.72 1.63 1.7 1.7

Mercury n.d. n.d. n.d. n.d. n.d. n.d. n.d. n.d.

Nickel 2.56 2.87 3.13 3.11 2.91 3.14 2.91 3.34

Selenium (0.44) (0.44) (0.464) (0.434) (0.47) (0.439) (0.45) 0.521

Vanadium (0.19) (0.089) (0.111) (0.102) (0.099) (0.102) (0.11) (0.098

3)

Zinc (3.26) (3.7) (3.26) (5.07) (3.03) (3.7) (3.18) (3.63) n.d.: not detected at reporting limit

A summary of the min-max range for each trace element is given in Table 31. The highest value is

then translated to a concentration at a loading of 1 mg/L (relevant for acute and chronic

classification purposes). All values are well below 1 µg/L, and are several orders below their

acute/chronic ERV, i.e. no adverse effects are expected. None of these concentration levels are

expected to trigger an environmental classification.

Table 31 M in-max concentration of 14 element samples after a seven-day

dissolution period (n = 16 coal samples); estimation of the maximum concentration

for a 1 m g/L loading – values between brackets are estim ated below reporting l imit

M in-max (µg/L) M ax at loading of 1 mg/L (in µg/L)

Arsenic (0.049–0.116) (0.0016)

Barium (0.38)–15.6 0.156

Beryllium n.d. n.d.

Boron n.d. n.d.

Cadmium (0.067–0.22) (0.022)

Chromium (0.14–0.43) (0.0043)

Copper n.d.–3.17 0.0317

Lead n.d.–(0.24) (0.0024)

Manganese 1.65–2.36 0.0236

Mercury n.d. n.d.

Nickel 2.56–3.5 0.035

Selenium (0.39)–0.532 0.0053

Vanadium 0.0474–0.19) (0.0019)

Zinc (n.d. –5.31) (0.053) n.d.: not detected at reporting limit


5.4. ANNEX IV: HUMAN HEALTH HAZARDS OF CRYSTALLINE SILICA

(FINE FRACTION)

Coal dust is a complex and heterogeneous mixture. One of the components of coal dust is

crystalline silica, also known as quartz or cristobalite. The fine, respirable fraction of silica refers

to those particles with a diameter less than 10 µm. These are less likely to be trapped in the nose

and throat and are more likely to reach the lungs and thus present a health hazard. In particular,

lung diseases such as cancer and pneumoconiosis or fibrosis have been linked with long-term

inhalation exposure to crystalline silica.

Carcinogenicity

In 1997, the IARC Working Group concluded that inhaled crystalline silica from occupational

sources should be categorized as a Group 1 carcinogen (carcinogenic to humans) based on

sufficient evidence of carcinogenicity in humans and experimental animals. In addition, “in making

the overall evaluation, the Working Group noted that carcinogenicity in humans was not detected in

all industrial circumstances studied. Carcinogenicity may be dependent on inherent characteristics

of the crystalline silica or on external factors affecting its biological activity or distribution of its

polymorphs” (IARC, 1997).

The IARC decision to categorize crystalline silica as a Group 1 carcinogen greatly relied on

epidemiological studies, of which the following provided the least confounded investigations of an

association between occupational crystalline silica exposure and lung cancer risk:

• US gold miners (Steenland and Brown, 1995)

• Danish stone industry workers (Guénel et al., 1989a; Guénel et al., 1989b)

• US granite shed and quarry workers (Costello and Graham, 1988)

• US crushed stone industry workers (Costello et al., 1995)

• US diatomaceous earth industry workers (Checkoway et al., 1993)

• Chinese refractory brick workers (Dong et al., 1995)

• Italian refractory brick workers (Puntoni et al., 1985; Puntoni et al., 1988; Merlo et al.,

1991)


• United Kingdom pottery workers (Cherry et al., 1995; McDonald et al., 1995; Burgess et al.,

1997; Cherry et al., 1997; McDonald et al., 1997)

• Chinese pottery workers (McLaughlin et al., 1992)

• cohorts of registered silicotics from the US and Finland (Kurppa et al., 1986; Amandus et

al., 1991; Amandus et al., 1992; Partanen et al., 1994).

Not all of these studies demonstrated excess cancer risks. However, in view of the relatively large

number of epidemiological studies that have been undertaken, and given the wide range of

populations and exposure circumstances studied, some non-uniformity of results was expected. In

some studies, increasing risk gradients were observed in relation to cumulative exposure, duration

of exposure, the presence of silicosis and peak intensity exposure. For these reasons, the working

group concluded that overall, the epidemiological findings supported increased lung cancer risks

from inhaled crystalline silica resulting from occupational exposure and that the observed

associations could not be explained by confounding or other biases.

Importantly, some experts disagreed with the categorization of crystalline silica as a Group 1

carcinogen (Hessel et al., 2000). After the IARC’s 1997 evaluation, residual questions remained

about whether silicosis was a prerequisite for the development of silica-related lung cancer, about

the role of smoking, and the exact nature of the exposure-response relationship between silica

exposure and lung cancer.

Nevertheless, in 2012, when considerably more epidemiologic data were available, the IARC

reaffirmed their conclusion regarding silica (IARC, 2012). One of the studies supporting the IARC

conclusion was a pooled analysis by Steenland et al. (2001) of 10 large silica-exposed cohorts, all

of which had good-quality exposure data during the entire follow-up period. Together, these

cohorts included over 1000 lung cancer deaths. The pooled analysis found a significant positive

exposure-response relationship between cumulative silica exposure and lung cancer mortality.

In addition, a meta-analysis of studies with exposure-response data found results that were similar

to the earlier pooled analysis (Lacasse et al., 2009). This meta-analysis also found that studies with

and without controls for smoking yielded similar relative risks, suggesting that confounding from


smoking (e.g. the silica-exposed individuals smoked more than those not exposed to silica) was not

likely to explain the elevations in the relative risk.

Despite this new evidence, the higher relative risks among those with silicosis stimulated

continued debate about whether lung cancer should be interpreted solely as a consequence of the

fibrotic process rather than a direct effect of silica exposure, or if the higher risk among patients

with silicosis was simply a marker of higher exposure. A study by Liu et al. (2013) aimed at

addressing this question. They studied 34,000 tungsten miners, iron miners and pottery workers.

Data regarding silicosis (based on a medical surveillance programme) and smoking were available

for all cohort members. There were 546 lung cancer deaths and 5297 cases of silicosis. A positive

statistically significant exposure-response trend for lung cancer was noted. Furthermore, Liu et al.

(2013) stated that silicosis is not a requirement for lung cancer. In addition, their data indicate that

the relative risk for exposure to silica is similar in smokers and nonsmokers. Nonetheless, because

smoking is such a strong risk factor for lung cancer, the risks for silica exposure and smoking,

together, are high.

Based on these data, Steenland and Ward (2014) recently concluded that sufficient evidence

has now been gathered to support the IARC conclusion on the carcinogenicity of respirable

crystalline silica.

Specific target organ toxicity after repeated exposure

For many years, it is known that prolonged inhalation of fine dust containing a proportion of

crystalline silica can cause a specific type of lung damage called silicosis, an incurable occupational

disease marked by inflammation and scarring in the upper lobes of the lungs, with a high

prevalence in coal miners (Petsonk et al., 2013).

A hazard assessment of health effects caused by crystalline silica (and specifically the respirable

fine fraction) was commissioned by industrial minerals producers. The team of scientific experts

produced two reports (Borm et al., 2009; Brown and Rushton, 2009) that are not publicly available

but which were summarized in Morfeld (2010). A clear dose-response was demonstrated for

silicosis/pulmonary fibrosis in epidemiological investigations and in animal studies after repeated

exposure to crystalline silica (fine fraction). Therefore, Morfeld (2010) concluded that STOT-RE


Category 1 classification is warranted for crystalline silica (fine fraction). This classification

applies to the fine fraction of quartz and cristobalite only, because it is scientifically demonstrated

that it is only this fraction of crystalline silica, when made airborne, that may cause health effects.

A link between sil icosis and lung cancer?

In recent years, the mechanistic link between both diseases, silicosis and lung cancer, is beginning

to emerge (Steenland and Ward, 2014). Both silicosis and lung cancer are believed to result from

the strong inflammatory response that silica evokes in the lung. Inhaled silica causes both silicosis

and lung tumours in rats. When rat macrophages attempt to digest silica, they are themselves

killed, and their disintegration results in the release of oxidants and cytokines and leads to

persistent inflammation with elevated neutrophils. This in turns causes epithelial cell injury and

proliferation, resulting in fibrosis (silicosis) (IARC, 2012). The chronic inflammation and release of

oxidants is also thought to cause genotoxic damage to the lung epithelium, thereby increasing the

risk of lung cancer. These inflammatory cells also release several growth factors that may

contribute to the pathogenesis of silicosis and lung cancer. It seems likely that these mechanisms

also cause lung disease in humans (Steenland and Ward, 2014).

Position of the sil ica industry

The silica industry prepared a position paper on the classification of crystalline silica (fine

fraction), which is available via www.crystallinesilica.eu . It conducted a review and hazard

assessment of the health effects of crystalline silica (fine fraction). It jointly agreed on

classification of quartz and cristobalite (fine fraction) as STOT-RE Category 1 only, based on the

following arguments:

• health effects are limited to the fine fraction of crystalline silica

• despite the ubiquitous presence of crystalline silica in the environment, specific health

effects of crystalline silica (fine fraction) only appear at the workplace, not in the general

environment

• the route of exposure is by inhalation and the target organ is the lung


• silicosis is the main health effect of crystalline silica (fine fraction) exposure and it occurs,

in the vast majority of instances, only after long-term exposure to high concentrations

• any lung cancer excess risk is demonstrated only under high occupational exposures to

crystalline silica (fine fraction) and varies between different industries; no other cancer risk

is observed

• any cancer effect is indirect via inflammation, i.e. through silicosis; therefore, preventing

silicosis prevents lung cancer.

Applying the mixture rules of GHS/CLP classification, mixtures containing crystalline silica (fine

fraction) should be classified as STOT-RE Category 1 if the crystalline silica (fine fraction)

concentration is equal to, or greater than, 10%. This is in line with a publication showing that a

relevant silica-silicosis effect can be assumed to occur after repeated exposure to mixed

respirable dusts with mass percentages greater than 10% respirable crystalline silica (Laney and

Attfield, 2009; McCunney et al., 2009).

If the crystalline silica (fine fraction) concentration is between 1% and 10%, mixtures should be

classified as STOT-RE Category 2. If the crystalline silica (fine fraction) content is below 1%, no

classification is required.

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