Upload
others
View
3
Download
0
Embed Size (px)
Citation preview
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
Stapelplein 70 box 104 9000 Gent, Belgium
+32 9 265 8758
www.arche-consulting.be [email protected]
World Coal Association
5th Floor, Heddon House 149-151 Regent Street London W1B 4JD, UK
+44 (0) 207 851 0052
www.worldcoal.org [email protected]
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 3
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
4 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 5
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
6 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 7
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.
8 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 9
• 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
10 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
(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,
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 11
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)
12 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 13
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)
14 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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)
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 15
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
16 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 17
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)
18 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 19
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.
20 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 21
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
22 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 23
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
24 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 25
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).
26 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 27
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
28 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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 C-2, USA 3.4 < 0.001 0.4 < 0.001
High-volatile bituminous coal C-3, USA 2.4 < 0.001 0.3 < 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 – –
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 29
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
30 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 31
• A substance with an Aq.Chronic1 classification and M-factor 10 will only trigger an
Aq.Chronic2 classification in a mixture when present at concentration levels of 0.25% or
higher (and no other substances with an Aq.Chronic1 or Aq.Chronic2 classification are
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.
• A substance with an Aq.Chronic1 classification and M-factor 100 will only trigger an
Aq.Chronic2 classification in a mixture when present at concentration levels of 0.025% or
higher (and no other substances with an Aq.Chronic1 or Aq.Chronic2 classification are
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
32 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 33
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.
34 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 35
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.
36 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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)
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 37
Table 14 continued
Sam ple code
S #9 S #10 S #11 S #12 S #13 S #14 S #15 S #16
µg/L ( loading of 100 mg/L)
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)
38 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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).
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 39
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.
40 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 41
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).
42 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 43
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
44 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 45
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.
46 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 47
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
48 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 49
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,
50 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 51
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.
52 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
• 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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 53
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
54 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 55
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
56 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 57
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
58 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 59
• 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
60 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 61
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
62 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 63
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.
64 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 65
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
66 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
(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
Hendryx et al. (2010)
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
Hendryx et al. (2012)
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 67
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.
68 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 69
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
70 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 71
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
72 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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).
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 73
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
74 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 75
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
76 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 77
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.
78 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
4. REFERENCES
Acheson ED, Cowdell RH, Rang EH (1981). Nasal cancer in England and Wales: an occupational
survey. Br. J. Ind. Med. 38: 218–224.
Achten C, Hofmann T, (2009). Native polycyclic aromatic hydrocarbons (PAH) in coals – a hardly
recognized source of environmental contamination. Sci.Total Environ. 407: 2461–2473.
Ahern M, Mullett M, Mackay K, Hamilton C (2011a). Residence in coal-mining areas and low-birth-
weight outcomes. Matern. Child Health J. 15: 974c979.
Ahern MM, Hendryx M, Conley J, Fedorko E, Ducatman A, Zullig KJ (2011b). The association
between mountaintop mining and birth defects among live births in central Appalachia, 1996-
2003. Environ. Res. 111: 838–846.
Ahrens MJ, Morrisey DJ, (2005). Biological effects of unburnt coal in the marine environment.
Oceanogr. Mar. Biol.: an Annual Review 43: 69–122.
Amandus HE, Shy C, Wing S, Blair A, Heineman EF (1991). Silicosis and lung cancer in North
Carolina dusty trades workers. Am. J. Ind. Med. 20: 57–70.
Amandus RE, Castellan RM, Shy C, Heineman EF, Blair A (1992). Re-evaluation of silicosis and lung
cancer in North Carolina dusty trades workers. Am. J. Ind. Med. 22: 147–153.
Ames RG (1983). Gastric cancer and coal mine dust exposure. A case-control study. Cancer 52:
1346–1350.
Ames RG, Amandus H, Attfield M, Green FY, Vallyathan V (1983). Does coal mine dust present a
risk for lung cancer? A case-control study of U.S. coal miners. Arch. Environ. Health. 38: 331–
333.
Ames RG, Gamble JF (1983) Lung cancer, stomach cancer, and smoking status among coal miners.
A preliminary test of a hypothesis. Scand. J. Work Environ. Health 9: 443–448.
ANZECC (2000). Australian and New Zealand guidelines for fresh and marine water quality.
National water quality management strategy. Wellington and Canberra: Australian and New
Zealand Environment and Conservation Council and Agriculture and Resource Management
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 79
Council of Australia and New Zealand. Online. Available at:
www.mfe.govt.nz/publications/water/anzecc-water-quality- guide-02/index.html (accessed
30 June 2004).
Armstrong BK, McNulty lC, Levitt Ll, Williams KA, Hobbs MST (1979). Mortality in gold and coal
miners in Western Australia with special reference to lung cancer. Br. J. Ind. Med. 36: 199–205.
ASTM D388-12 (2012). Standard classification of coals by rank. American Society for Testing and
Materials.
Attfield MD (1992). British data on coal miners' pneumoconiosis and relevance to US conditions.
Am. J. Public Health 829789–829783.
Attfield MD and Althouse RB (1992). Surveillance data on US coal miners' pneumoconiosis, 1970
to 1986. Am. J. Public Health 82: 971–977.
Attfield MD and Castellan RM (1992). Epidemiological data on US coal miners' pneumoconiosis,
1960 to 1988. Am. J. Public Health 82: 964–970.
Attfield MD and Kuempel ED (2008). Mortality among U.S. underground coal miners: a 23-year
follow-up. Am. J. Ind. Med. 51: 231–245.
Attfield MD and Morring K (1992). An investigation into the relationship between coal workers'
pneumoconiosis and dust exposure in U.S. coal miners. Am. Ind. Hyg. Assoc. J. 53: 486–492.
Attfield MD and Seixas NS (1995). Prevalence of pneumoconiosis and its relationship to dust
exposure in a cohort of U.S. bituminous coal miners and ex-miners. Am. J. Ind. Med. 27: 137–
151.
Attfield MD and Wagner GR (2007). Respiratory disease in coal miners. In: Rom WN, ed.,
Environmental and occupational medicine. 4th ed. Philadelphia: Lippincott, Williams and
Wilkins.
Atuhaire LK, Campbell MJ, Cochrane AL, Jones M, Moore F (1986). Gastric cancer in a South Wales
valley. Br. J. Ind. Med. 43: 350–352.
Auld AH and Schubel JR (1978). Effects of suspended sediment on fish eggs and larvae: a
laboratory assessment. Est. Coast. Mar. Sci. 6: 153–164.
80 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Barnes N and Frid CLJ (1999). Restoring shores impacted by colliery spoil dumping. Aquatic
Conservation: Mar. Fresh. Ecosystems 9: 75–82.
Bender ME, Roberts MH, de Fur PO (1987). Unavailability of polynuclear aromatic hydrocarbons
from coal particles to the eastern oyster. Environ. Pollut. 44: 243–260.
Boitelle A, Gosset P, Copin MC, Vanhee D, Marquette CH, Wallaert B, Gosselin B, Tonnel AB (1997).
MCP-1 secretion in lung from nonsmoking patients with coal worker's pneumoconiosis. Eur.
Respir. J. 10: 557–562.
Borm P, Brown T, Donaldson K, Rushton L (2009). Review and hazard assessment of the health
effects of respirable crystalline silica (RCS) exposure to inform classification and labelling
under the global harmonised system: overview report. In: Sponsor: EUROSIL – European
Association of Industrial Silica Producers, ed. Brussels, 2009: 1–35.
Borm PJA, Höhr D, Steinfartz Y, Zeittrger I, Albrecht C (2000). Chronic inflammation and tumor
formation in rats after intratracheal instillation of high doses of coal dusts, titanium oxides
and quartz. Inhal. Toxicol. 12: 225–231.
Brown AM, Christie D, Taylor R, Seccombe MA, Coates MS (1997). The occurrence of cancer in a
cohort of New South Wales coal miners. Aust. N. Z. J. Public Health 21: 29–32.
Brown GM and Donaldson K (1989). Inflammatory responses in lungs of rats inhaling coalmine dust:
enhanced proteolysis of fibronectin by bronchoalveolar leukocytes. Br. J. Ind. Med. 46: 866–
872.
Brown T and Rushton L (2009). A review of the literature of the health effects of occupational
exposure to crystalline silica: silicosis, cancer and autoimmune diseases. In: Sponsor: EUROSIL
– European Association of Industrial Silica Producers, ed. Brussels, 2009: 1–178.
Burgess G, Turner S, McDonald JC, Cherr NM (1997). Cohort mortality study of Staffordshire
pottery workers: radiographic validation of an exposure matrix for respirable crystalline silica
(Abstract). ln: Cherry NM and Ogden TL, eds., lnhaled particles VIII, Occupational and
environmental implications for human health, 26–30 August 1996, Robinson College,
Cambridge, UK: Elsevier Science Ltd.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 81
Busch RH, Filipy RE, Karagianes MT, Palmer RF (1981). Pathologic changes associated with
experimental exposure of rats to coal dust. Environ. Res. 24: 53–60.
Cabarcas-Montalvo M, Olivero-Verbel J, Corrales-Aldana H. (2012). Genotoxic effects in blood
cells of Mus musculus and Iguana iguana living near coal mining areas in Colombia. Sci. Total
Environ. 416: 208–14.
Carlson RM, Oyler AR, Gerhart EH, Caple R, Welch KJ, Koppermann HL, Bodenner D, Swanson D
(1979). Implications to the aquatic environment of polynuclear aromatic hydrocarbons
liberated from Great Plains coal. Duluth, US. ES-EPA Report No. EPA-600/3-79-093.
CDC (Centers for Disease Control and Prevention) (2009). Coal workers' pneumoconiosis-related
years of potential life lost before age 65 years – United States, 1968-2006. MMWR Morb.
Mortal. Wkly Rep. 58: 1412–1416.
CDC (Centers for Disease Control and Prevention) (2012). Pneumoconiosis and advanced
occupational lung disease among surface coal miners-16 states, 2010-2011. MMWR Morb.
Mortal. Wkly Rep. 61: 431–434.
Chapman PM, Downie J, Maynard A, Taylor LA (1996). Coal and deodorizer residues in marine
sediments – contaminants or pollutants? Environ. Toxicol. Chem. 1: 638–642.
Checkoway H, Heyer NJ, Demers PA, Breslow NE (1993). Mortality among workers in the
diatomaceous earth industry. Br. J. ind. Med. 50: 586–597.
Chen Y, Bi X, Mai B, Sheng G, Fu J (2004). Emission characterization of particulate/gaseous phases
and size association for PAHs from residential coal combustion. Fuel 83: 781–790.
Cherry N, Burgess G, McNamee R, Turner S, McDonald JC (1995). Initial findings from a cohort
mortality study of British pottery workers. Appl. Occup. Environ. Hyg. 10: 1042–1045.
Cherry N, Burgess G, Turner S, McDonald JC (1997). Cohort mortality study on Staffordshire
pottery workers: nested case referent analysis on lung cancer. ln: Cherry NM, Ogden TL (Eds.),
Inhaled Particles VIII. Occupational and Environmental Implications for Human Health. Revised
Final Programme and Abstracts, 26-30 August 1996, Robinson College, Cambridge, UK,
Elsevier Science Ltd.
82 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Chong S, Lee KS, Chung MJ, Han J, Kwon OJ, Kim TS (2006). Pneumoconiosis: comparison of
imaging and pathologic findings. Radiographics 26: 59–77.
Christian WJ, Huang B, Rinehart J, Hopenhayn C (2011). Exploring geographic variation in lung
cancer incidence in Kentucky using a spatial scan statistic: elevated risk in the Appalachian
coal-mining region. Public Health Rep. 126: 789–796.
Clark MC, Swaine DJ? 1962. Trace elemnts in coal. New South Wales coal. CSIRO Div. Min. Chem.
Tech. Comm. No 45, pp 1-21.
Cochrane AL, Haley TJL, Moore F & Hole D (1979). The mortality of men in the Rhondda Fach, 1950-
1970. Br. J. Ind. Med. 36: 15–22.
Coggon D and Newman Taylor A (1998). Coal mining and chronic obstructive pulmonary disease: a
review of the evidence. Thorax 53: 398–407.
Coggon D, Barker DJ, Cole RB (1990) Stomach cancer and work in dusty industries. Br. J. Ind. Med.
47: 298–301.
Cordier S, Clavel J, Limasset JC, Boccon-Gibod L, Le Moual N et al. (1993). Occupational risks of
bladder cancer in France: a multicentre case-control study. Int. J. Epidemiol. 22: 403–411.
Costello J and Graham WGB (1988). Vermont granite worker's mortality study. Am. J. Ind. Med. 13:
483–497.
Costello J, Castellan RM, Swecker GS, Kullman Gl (1995). Mortality of a cohort of V.S. workers
employed in the crushed stone industry, 1940-1980. Am. J. Ind. Med. 27: 625–640.
Coward NA, Horton JW, Koch RG, Morden RD (1978). Static coal storage – biological and chemical
effects on the aquatic environment. Duluth, US. US-EPA Report No. 660/3-80-083.
da Silva J, de Freitas TRO, Heuser V, Marinho J, Erdtmann B (2000). Genotoxicity biomonitoring in
coal regions using wild rodent Ctenomys torquatus by Comet assay and micronucleus test.
Environ. Mol. Mutagen. 35: 270–278.
Dalal NS, Jafari B, Petersen M, Green FH, Vallyathan V (1991). Presence of stable coal radicals in
autopsied coal miners' lungs and its possible correlation to coal workers' pneumoconiosis.
Arch. Environ. Health 46: 366–372.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 83
Dalal NS, Newman J, Pack D, Leonard S, Vallyathan V (1995). Hydroxyl radical generation by coal
mine dust: Possible implication to coal workers’ pneumoconiosis. Free Radic. Biol. Med. 18:
11–20.
Dalal NS, Suryan MM, Vallyathan V, Green FH, Jafari B, Wheeler (1989). Detection of reactive free
radicals in fresh coal mine dust and their implication for pulmonary injury. Ann. Occup. Hyg. 33:
79–84.
Dale LS, Chapman JF, Buchanan SJ, Lavrencic SA (1999). Mechanisms for trace element
partitioning in australian coals, Project 4.2, Final Report to CRC for black Coal Utilisation,
Australian Black Coal Utilisation Research Limited 2002.
Dale L (2009). Monograph on trace elements in coal. ACARP Project C17003, End of Grant Report.
Prepared for the Australian Coal Association Research Program, 132pp.
Davies JM (1980). Stomach cancer mortality in Worksop and other Nottinghamshire mining town.
Br. J. Can. 41: 438–445.
Davies-Colley R and Smith D (2001). Turbidity, suspended sediment, and water clarity: a review. J.
Am. Water Res. Assoc. 37: 1085–1102.
Davis EC and Boegly WJJ (1981). Coal pile leachate quality. J. Environ. Engin. Div. 107: 399–417.
Donaldson K, Brown GM, Brown DM, Robertson MD, Slight J, Cowie H, Jones AD, Bolton RE, Davis
JM (1990). Contrasting bronchoalveolar leukocyte responses in rats inhaling coal mine dust,
quartz, or titanium dioxide: effects of coal rank, airborne mass concentration, and cessation of
exposure. Environ. Res. 52: 62–76.
Donbak L, Rencuzogullari E, Yavuz A, Topaktas M. (2005). The genotoxic risk of underground coal
miners from Turkey. Mutat. Res. 588: 82–87.
Dong D, Xu G, Sun Y, Hu P (1995). Lung cancer among workers exposed to silica dust in Chinese
refractory plants. Scand. J. Work Environ. Health 21: 69–72.
Duarte CM (1991). Seagrass depth limits. Aq. Botany 40: 363–377.
Emerson SE and Zedler JB (1978). Recolonization of intertidal algae: an experimental study. Mar.
Biol. 44: 315–324.
84 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Fendinger NJ, Radway JC, Tuttle JH, Means JC (1989). Characterization of organic material leached
from coal by simulated rainfall. Environ. Sci. Technol. 23: 170–177.
Fernandez-Navarro P, Garcia-Perez J, Ramis R, Boldo E, Lopez-Abente G (2012). Proximity to
mining industry and cancer mortality. Sci. Total Environ. 435–436: 66–73.
Finkelman RB (1994). Modes of occurrence of potentially hazardous trace elements in coal: levels
of confidence, Fuel Processing Technol. 39: 21-34.
Finkelman RB (1995). Modes of occurrence of environmentally-sensitive trace elements in coal,
Chapter 3, pp 24-50. In: Swaine DJ, Goodarzi F (Eds), Environmental aspects of trace elements
in coal. Kluwer, Dordrecht, The Netherlands, 312 pp.
Francis W (1961). Coal – its formation and composition. London: Edward Arnold.
Gerhart DZ, Richter JE, Curran SJ, Robertson TE (1980). Algal bioassays with leachates and
distillates from western coal. Duluth, US. US-EPA Report No. EPA-600/3-79-093.
Gerhart EH, Liukkonen RJ, Carlson RM, Stokes GN, Lukasewycz MT, Oyler AR (1981). Histological
effects and bioaccumulation potential of coal particulate-bound phenanthrene in the fathead
minnow Pimephales promelas. Environ. Pollut. Ser. A 25: 165–180.
Gluskoter HJ, Ruch RR, Miller WG, Cahill RA, Dreher GB, Kuhn JK (1977). Trace elements in coal:
occurrence and distribution. Illinois State Geological Survey, Circular No. 499.
Goldberg P, Leclerc A, Luce D, Morcet JF, Brugère J (1997). Laryngeal and hypopharyngeal cancer
and occupation: results of a case control-study. Occup. Environ. Med. 54: 477–482.
Golka K, Bandel T, Schlaefke S, Reich SE, Reckwitz T et al. (1998). Urothelial cancer of the bladder
in an area of former coal, iron, and steel industries in Germany: a case-control study. Int. J.
Occup. Environ. Health 4: 79–84.
Gonzalez CA, Sanz M, Marcos G, Pita S, Brullet E, Vida F, Agudo A, Hsieh CC (1991). Occupation and
gastric cancer in Spain. Scand. J. Work Environ. Health 17: 240–247.
Green FH, Boyd RL, Danner-Rabovsky J, Fisher MJ, Moorman WJ, Ong TM, Tucker J, Vallyathan V,
Whong WZ, Zoldak J et al. (1983). Inhalation studies of diesel exhaust and coal dust in rats.
Scand. J. Work Environ. Health 9: 181–188.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 85
Gu Z-W, Whong W-Z, Wallace WE, Ong T-M (1992). Induction of micronuclei in BALB/c-3T3 cells by
selected chemicals and complex mixtures. Mutat. Res. 279: 217–222.
Guénel P, Breum NO, Lynge E (1989a). Exposure to silica dust in the Danish stone industry. Scand. J.
Work Environ. Health 15: 147–153.
Guénel P, Hojberg G, Lynge E (1989b). Cancer incidence among Danish stone workers. Scand. J.
Work Environ. Health 15: 265–270.
Hahon N, Booth JA, Green F, Lewis TR (1985). Influenza virus infection in mice after exposure to
coal dust and diesel engine emissions. Environ. Res. 37: 4460.
Hendryx M, Fedorko E, Anesetti-Rothermel A (2010). A geographical information system-based
analysis of cancer mortality and population exposure to coal mining activities in West Virginia,
United States of America. Geospat. Health 4: 243–256.
Hendryx M, O’Donnell K, Horn K (2008). Lung cancer mortality is elevated in coal-mining areas of
Appalachia. Lung Cancer 62: 1–7.
Hendryx M, Wolfe L, Luo J, Webb B (2012). Self-reported cancer rates in two rural areas of West
Virginia with and without mountaintop coal mining. J. Community Health 37: 320–327.
Heppleston AG (1988). Prevalence and pathogenesis of pneumoconiosis in coal workers.
Environ.Health Persp. 78: 159-170.
Herbert DWM, Richards JM (1963). The growth and survival of fish in some suspensions of solids of
industrial origin. Int. J. Air Water Pollut. 7: 297–302.
Hessel PA, Gamble JF, Gee JB et al. (2000). Silica, silicosis, and lung cancer: a response to a recent
working group report. J. Occup. Environ. Med. 42: 704–720.
Hillaby BA (1981). The effects of coal dust on ventilation and oxygen consumption in the
Dungeness crab, Cancer magister. Can. Tech. Rep. Fish. Aq. Sci. 1033: 1–18.
Holte B, Dahle S, Gulliksen B, Naes K (1996). Some macrofaunal effects of local pollution and
glacier-induced sedimentation, with indicative chemical analysis, in the sediments of two
Arctic fjords. Polar Biology 16: 549–557.
86 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Hosgood HD 3rd, Chapman RS, Wei H, He X, Tian L et al. (2012). Coal mining is associated with lung
cancer risk in Xuanwei, China. Am. J. Ind. Med. 55: 5–10.
Huang X, Li W, Attfield MD, Nadas A, Frenkel K, Finkelman RB (2005). Mapping and prediction of
coal workers’ pneumoconiosis with bioavailable iron content in the bituminous coals. Environ.
Health Perspect. 113: 964–968.
Huggins FE (2002). Overview of analytical methods for inorganic constituents in coal. Int.Coal Geol.
50, 169-214.
Hughes GM (1975). Coughing in the rainbow trout (Salmo gairdneri) and the influence of pollutants.
Revue Suisse de Zoologie 82: 47–64.
Hurley JF, Burns J, Copland L, Dodgson J, Jacobsen M (1982). Coal workers’ with simple
pneumoconiosis with exposure to dust at 10 British coalmines. Br. J. Ind. Med. 39: 120–127.
Hurley JF, Copland L, Dodgson J, Jacobsen M (1979). Simple pneumoconiosis and exposure to
respirable dust: relationships from twenty-five years’ research at ten British coal mines. IOM
Report No. TM/79/13. UDC 616.24-003.6. Edinburgh: Institute of Occupational Medicine.
Hyslop BT, Davies MS (1998). Evidence for abrasion and enhanced growth of Ulva lactuca L. in the
presence of colliery waste particles. Environ. Pollut. 101: 117–121.
Hyslop BT, Davies MS (1999). The effect of colliery waste in the feeding of the lugworm Arenicola
marina. J. Sea Res. 42: 147–155.
Hyslop BT, Davies MS, Arthur W, Gazey NJ, Holroyd S (1997). Effects of colliery waste on littoral
communities in north-east England. Environ. Pollut. 96: 383–400.
IARC (International Agency for Research on Cancer) (2006). Report of the Advisory Group to
Review the Amended Preamble to the IARC Monographs. IARC Int. Rep. No. 06/001.
IARC (International Agency for Research on Cancer) (2012). Silica dust, crystalline, in the form of
quartz or cristobalite. A review of human carcinogens: arsenic, metals, fibres and dusts. Lyon,
France: International Agency for Research on Cancer: 356–405.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 87
IARC (International Agency for Research on Cancer) Working Group on the Evaluation of
Carcinogenic Risks to Humans (1997). Silica, some silicates, coal dust and para-aramid fibrils.
IARC Monogr. Eval. Carcinog. Risks Hum. 68: 1–475.
Jacobsen M (1979). Effect of further dust exposure among men with early and more advanced
signs of simple pneumoconiosis. IOM Report No. TM/79/16. EUR.P25. UDC 622.872.
Edinburgh: Institute of Occupational Medicine.
Jenkins WD, Christian WJ, Mueller G, Robbins KT (2013). Population cancer risks associated with
coal mining: a systematic review. PLoS ONE 8(8): 1-12.
Jöckel KH, Ahrens W, Jahn I, Pohlabeln H, Bolm-Audorff U (1998). Occupational risk factors for lung
cancer: a case-control study in West Germany. Int. J. Epidemiol. 27: 549–560.
Johnson LJ, Frid CLJ (1995). The recovery of benthic communities along the County Durham coast
after cessation of colliery spoil dumping. Mar. Pollut. Bull. 30: 215–220
Joy GJ, Colinet JF, Landen DD (2012). Coal workers’ pneumoconiosis prevalence disparity between
Australia and the United States. Min. Eng. 64: 65–71.
Karagianes MT, Palmer RF, Busch RH (1981). Effects of inhaled diesel emissions and coal dust in
rats. Am.Ind.Hyg. Assoc. 42: 382-391
Kendrick GA (1991). Recruitment of coralline crusts and filamentous turf algae in the Galapagos
archipelago: effect of simulated scour, erosion and accretion. J. Exp. Mar. Biol. Ecol. 147: 47–
63.
Kleineidam S, Schüth C, Grathwohl P (2002). Solubility-normalised combined pore-filling-
partitioning sorption isotherms for organic pollutants. Environ. Sci. Technol. 36: 4689–4697.
Kolling A, Ernst H, Rittinghausen S, Heinrich U (2011). Relationship of pulmonary toxicity and
carcinogenicity of fine and ultrafine granular dusts in a rat bioassay. Inhal. Toxicol. 23: 544–
554.
Krishna G, Nath J, Soler L, Ong T (1987). ln vivo induction of sister chromatid exchanges in mice by
nitrosated coat dust extract. Environ. Res. 42: 106–113.
88 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Kuempel ED, Attfield MD, Vallyathan V, Lapp NL, Hale JM, Smith RJ, Castranova V (2003).
Pulmonary inflammation and crystalline silica in respirable coal mine dust: dose-response. J.
Biosci. 28: 61–69.
Kuempel ED, Stayner LT, Attfield MD, Buncher CR (1995). Exposure-response analysis of mortality
among coal miners in the United States. Am. J. Ind. Med. 28: 167–184.
Kurppa K, Gudbergsson H, Hannunkari J, Koskinen H, Hernberg S, Koskela RS, Ahlman K (1986).
Lung cancer among silicotics in Finland. ln: Goldsmith DF, Winn DM, Shy CM, eds., Silica,
silicosis, and cancer. Controversy in occupational medicine, New York: Praeger, 311–319.
Kvitko K, Bandinelli E, Henriques JA, Heuser VD, Rohr P, da Silva FR, Schneider NB, Fernandes S,
Ancines C, da Silva J (2012). Susceptibility to DNA damage in workers occupationally exposed
to pesticides, to tannery chemicals and to coal dust during mining. Genet. Mol. Biol. 35: 1060–
1068.
Lacasse Y, Martin S, Gagne D, Lakhal L (2009). Dose-response meta-analysis of silica and lung
cancer. Cancer Causes Control 20: 925–933.
Laney AS and Attfield MD (2009). Quartz exposure can cause pneumoconiosis in coal workers. J.
Occup. Environ. Med. 51: 867.
Laney AS, Petsonk EL, Attfield MD (2010). Pneumoconiosis among underground bituminous coal
miners in the United States: is silicosis becoming more frequent? Occup. Environ. Med. 67:
652–656.
Leite JC and Schüler-Faccini L (2001). [Congenital defects in a coal mining region]. Rev Saude
Publica 35: 136–141.
León G, Pérez LE, Linares JC, Hartmann A, Quintana M (2007). Genotoxic effects in wild rodents
(Rattus rattus and Mus musculus) in an open coal mining area. Mutat .Res. 15: 42–49.
León-Mejía G, Espitia-Pérez L, Hoyos-Giraldo LS, Da Silva J, Hartmann A, Henriques JA, Quintana M.
(2011). Assessment of DNA damage in coal open-cast mining workers using the cytokinesis-
blocked micronucleus test and the comet assay. Sci. Total Environ. 409: 686–691.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 89
Lewis TR, Green FHY, Moorman WJ, Anne JE, Burg JR, Lynch DW (1986) A chronic inhalation study
of diesel engine emissions and coal dust, alone and combined. Dev.Toxicol.Environ.Sci. 13 :
361-380
Liao Y, Wang J, Wu J, Driskell L, Wang W, Zhang T, Xue G, Zheng X (2010). Spatial analysis of neural
tube defects in a rural coal mining area. Int. J. Environ. Health Res. 20: 439–450.
Liu H, Tang Z, Weng D, Yang Y, Tian L, Duan Z, Chen J (2009). Prevalence characteristics and
prediction of coal workers' pneumoconiosis in the Tiefa Colliery in China. Ind. Health 47: 369–
375.
Liu Y, Steenland K, Rong Y et al. (2013). Exposure-response analysis and risk assessment for lung
cancer in relationship to silica exposure: a 44-year cohort study of 34,018 workers. Am. J.
Epidemiol. 178: 1424–1433.
Lloyd OL, Ireland E, Tyrrell H, Williams F (1986). Respiratory cancer in a Scottish industrial
community: a retrospective case-control study. J. Soc. Occup. Med. 36: 2–8.
Longstaff BJ, Dennison WC (1999). Seagrass survival during pulsed turbidity events: the effects of
light deprivation on the seagrasses Halophila pinifolia and Halophila ovalis. Aq. Bot. 65: 105–
121.
Maclaren WM and Soutar CA (1985). Progressive massive fibrosis and simple pneumoconiosis in
ex-miners. Br. J. Ind. Med. 42: 734–740.
MAK (2002). Coal mine dust. MAK Value Documentation, the MAK Collection for Occupational
Health and Safety, 108–156.
Martin JC, Daniel H, Le Bouffant L (1977) Short- and long-term experimental study of the toxicity
of coal-mine dust and of some of its constituents. ln: Walton WH (Ed.), Inhaled Particles IV
(Part 1), Oxford, Pergamon Press, pp. 361 -371
McCunney RJ, Morfeld P, Payne S (2009). What component of coal causes coal workers'
pneumoconiosis? J. Occup. Environ. Med. 51: 462–471.
McDonald JC, Burgess G, Turner S, Cheney NM (1997). Cohort mortality study of Staffordshire
pottery workers: lung cancer, radiographic changes, silica exposure and smoking habit
(abstract). ln: Cherry NM and Ogden TL, eds., Inhaled particles VIII, Occupational and
90 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
environmental implications for human health, revised final programme and abstracts, 26–30
August 1996, Robinson College, Cambridge, UK: Elsevier Science Ltd.
McDonald JC, Cherry N, Burgess G, McNamee R, Burgess G, Turner S (1995). Preliminary analysis of
proportional mortality in a cohort of British pottery workers exposed to crystalline silica.
Scand. J. Work Environ. Health 21: 63–65.
McLaughlin JK, Chen JQ, Dosemeci M, Chen RA, Rexing SH, Wu Z, Hearl F, McCawley MA, Blot WJ
(1992). A nested case-control study of lung cancer among silica exposed workers in China. Br.
J. Ind. Med. 49: 167–171.
McLintock JS, Rae S, Jacobson M (1971). The attack rate of progressive massive fibrosis in British
coalminers. In: Walton WH, ed. Inhaled particles III. Vol. II. Old Woking, Surrey, England: Unwin
Brothers Limited, 933–950.
Meijers JM, Swaen GM, Slangen JJ, van Vliet C (1988). Lung cancer among Dutch coal miners: a
case-control study. Am. J. Ind. Med. 14: 597–604.
Meijers JMM, Swaen GMH, Slangen JJM, van Vliet K, Sturmans F (1991). Long-term mortality in
miners with coal workers' pneumoconiosis in the Netherlands: a pilot study. Am. J. Ind. Med. 19:
43–50.
MEPC (Marine Environment Protection Committee) 62/24, Annex 13, Resolution MEPC.201(62),
adopted on 15 July 2011, Amendments to the Annex of the Protocol of 1978 Relating to the
International Convention for the Prevention of Pollution from Ships, 1973 (Revised MARPOL
Annex V).
MEPC (Marine Environment Protection Committee) 63/23/Add.1, Annex 24, Resolution
MEPC.219(63), adopted on 2 March 2012, 2012 Guidelines for the implementation of
MARPOL Annex V.
Merlo F, Costantini M, Reggiardo G, Ceppi M, Puntoni R (1991). Lung cancer risk among refractory
brick workers exposed to crystalline silica: a retrospective cohort study. Epidemiology 2: 299–
305.
Miller BG and Jacobsen M (1985). Dust exposure, pneumoconiosis, and mortality of coalminers. Br.
J. Ind. Med. 42: 723–733.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 91
Miller BG and MacCalman L (2010). Cause-specific mortality in British coal workers and exposure
to respirable dust and quartz. Occup Environ Med. 67: 270–276.
Minowa M, Stone BJ, Blot WJ (1988). Geographic pattern of lung cancer in Japan and its
environmental correlations. Jpn. J. Cancer Res. 79: 1017–1023.
Moore PG (1977). Inorganic particulate suspensions in the sea and their effects on marine animals.
Oceanogr. Mar. Biol.: an Annual Review 15: 225–363.
Moore KA, Wetzel RL, Orth RJ (1977). Seasonal pulses of turbidity and their relations to eelgrass
(Zostera marina L) survival in an estuary. J.Exp.Mar.Biol.Ecol. 215: 115-134.
Morfeld P, Lampert K, Ziegler H, Stegmaier C, Dhom G (1997). Overall mortality and cancer
mortality of coal miners: attempts to adjust for healthy worker selection effects. Ann Occup
Hyg 41: 346–51.
Morfeld P (2010). Respirable crystalline silica: rationale for classification according to the CLP
Regulation and within the framework of the Globally Harmonised System (GHS) of
Classification and Labelling of Chemicals. Available via
www.crystallinesilica.eu/content/classification-and-labelling-rcs
Morgan WK, Burgess DB, Jacobson G, O'Brien RJ, Pendergrass EP, Reger RB, Shoub EP (1973). The
prevalence of coal workers' pneumoconiosis in US coal miners. Arch. Environ. Health 27: 221–
226.
Newcombe CP, Jensen JOT (1996). Channel suspended sediment and fisheries: a synthesis for
quantitative assessment of risk and impact. N. Am. J. Fish. Manage. 16: 639–727.
Newcombe CP, MacDonald DD (1991). Effects of suspended sediments on aquatic ecosystems. N.
Am. J. Fish. Manage.11: 72–82.
Nikula KJ, Avila KJ, Griffith WC, Mauderly JL (1997). Lung tissue responses and sites of particle
retention differ between rats and cynomolgus monkeys exposed chronically to diesel exhaust
and coal dust. Fundam. Appl. Toxicol. 37: 37–53.
NIOSH (National Institute for Occupational Safety and Health) (1995). Criteria for a recommended
standard: occupational exposure to coal mine dust. DHHS (NIOSH) Publication No. 95–106.
Washington, DC: National Institute for Occupational Safety and Health.
92 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
NIOSH (National Institute for Occupational Safety and Health) (2011). Current Intelligence Bulletin
64: Coal mine dust exposures and associated health outcomes – a review of information
published since 1995. DHHS (NIOSH) Publication Number 2011-172.
Norton MG (1985). Colliery-waste and fly-ash dumping off the northeastern coast of England. In:
Dueall et al., eds., Wastes in the ocean. Volume 4. Energy wastes in the Ocean. New York: John
Wiley & Sons, 423–448.
Oberdörster G (1995). Lung particle overload: implications for occupational exposures to particles.
Regul. Toxicol. Pharmacol. 21: 123–135.
OECD (2002). OECD Series on Testing and Assessment, Guidance Document on
Transformation/Dissolution of Metals and Metal Compounds in Aqueous Media. Organisation
for Economic Co-operation and Development, Paris, France. 19pp.
Ong T, Whong WZ, Xu J, Burchell B, Green FH, Lewis T (1985). Genotoxicity studies of rodents
exposed to coal dust and diesel emission particulates. Environ. Res. 37: 399–409.
Page SJ (2003). Comparison of coal mine dust size distributions and calibration standards for
crystalline silica analysis. AIHA J. 64: 30–39.
Page SJ and Organiscak JA (2000). Suggestion of a cause-and-effect relationship among coal rank,
airborne dust, and incidence of workers’ pneumoconiosis. AIHA J. 61: 785–787.
Paine MD, Chapman PM, Allard PJ, Murdoch MH, Minifie D (1996). Limited bioavailability of
sediment PAH near an aluminium smelter: contamination does not equal effects. Environ.
Toxicol. Chem. 15: 2003–2018.
Partanen T, Pukkala E, Vainio H, Kurppa K, Koskinen H (1994). lncreased incidence of lung and skin
cancer in Finnish silicotic patients. J. Occup. Med. 36: 616–622.
Pautzke CF (1937). Study on the effect of coal washings on steelhead and cutthroat trout. Trans.
Am. Fish. Soc. 67: 232–233.
Pearce BC, McBride J (1977). A preliminary study on the occurrence of coal dust in Roberts Bank
sediments and the effect of coal dust on selected fauna. FMS technical Report Series. PAC/T-
77-17 (cited in Hillaby, 1981).
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 93
Petsonk EL, Rose C, Cohen R. (2013). Coal mine dust lung disease. New lessons from old exposure.
Am. J. Respir. Crit. Care Med. 187: 1178–1185.
Pies C, Yang Y, Hofmann T (2007). Polycyclic aromatic hydrocarbon (PAH) distribution in bank and
alluvial soils of Mosel and Saar River. J. Soils Sediments 7: 216–222.
Preen AR, Lee Long WJ, Coles RG (1995). Flood and cyclone related loss, and partial recovery, of
more than 1000 km2 of seagrass in Hervey Bay, Queensland, Australia. Aq. Bot. 52: 3–17.
Puntoni R, Goldsmith DF, Valerio F, Vercelli M, Bonassi S, Di Giorgio P, Ceppi M, Stagnaro E,
Filiberti R, Santi L, Merlo F (1988). A cohort study of workers employed in a refractory brick
plant. Tumori 74: 27–33.
Puntoni R, Vercelli M, Bonassi S, Valerio F, Di Giorgio F, Ceppi M, Stagnaro E, Filiberti R, Santi
L (1985). Prospective study of the mortality in workers exposed to silica. ln: Detsch EI,
Marcato A, eds., Silice, silicosi, e cancro (‘Silica, silicosis and cancer’), Padua: University
of Padua, 79–92.
Püttmann W (1988). Analysis of polycyclic aromatic hydrocarbons in solid sample material using a
desorption device coupled to a GC/MS system. Chromatography 26: 171–177.
Querol X, Juan R, Lopez-Soler A, Fernandez-Turiel J, Ruiz CR (1996). Mobility of trace elements
from coal and combustion wastes. Fuel 75: 821–838.
Radke M, Willsch H, Teichmuller M (1990). Generation and distribution of polycyclic aromatic
hydrocarbons in coals of low rank. Org. Geochem. 15: 539–563.
Reisner MTR (1971). Results of epidemiological studies of pneumoconiosis in West German coal
mines. In: Walton WH, ed., Inhaled particles III. Vol. II. Old Woking, Surrey, England: Unwin
Brothers Limited, 921–929.
Riley KW (2005). Investigation Report IR787R. Background information for website on trace
elements in coal. Report on ACARP Project C 12060, 57pp.
Rockette, RE (1977). Cause specific mortality of coal miners. J. Occup. Med. 19: 795–801.
Rohr P, Kvitko K, da Silva FR, Menezes AP, Porto C, Sarmento M, Decker N, Reyes JM, Allgayer Mda
C, Furtado TC, Salvador M, Branco C, da Silva J. (2013). Genetic and oxidative damage of
94 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
peripheral blood lymphocytes in workers with occupational exposure to coal. Mutat. Res. 758:
23–28.
Ross H, King EJ, Yoganathan M, Nagelschmidt G (1962). Inhalation experiments with coal dust
containing 5 percent, 10 percent and 20 percent quartz: tissue reactions in the lungs of rats.
Ann. Occup. Hyg. 5: 149–161.
Sartorelli P, Montomoli L, Sisinni AG, Bussani R, Cavallo D, Foà V (2001). Dermal exposure
assessment of polycyclic aromatic hydrocarbons: in vitro percutaneous penetration from coal
dust. Toxicol. Ind. Health 17: 17–21.
Schifflers E, Jamart J, Renard V (1987). Tobacco and occupation as risk factors in bladder cancer: a
case-control study in southern Belgium. Int. J. Cancer 39: 287–292.
Schins RPF, Schilderman P, Borm PJA (1995). Oxidative DNA-damage in peripheral blood
lymphocytes of coal workers. Int. Arch. Occup. Environ. Health 67: 153–157.
Scullion J, Edwards RW (1980). The effects of coal industry pollutants on the macroinvertebrate
fauna of a small river in the South Wales coalfield. Freshwater Biology 10: 141–162.
Seixas NS, Robins TG, Attfield MD, Moulton LH (1993). Longitudinal and cross sectional analyses
of exposure to coal mine dust and pulmonary function in new miners. Br. J. Ind. Med. 50: 929–
937.
Shaw DG, Wiggs JN (1980). Hydrocarbons in the intertidal environment of Kachemak Bay, Alaska.
Mar. Pollut. Bull. 11: 297–300.
Shelton RGJ (1973). Some effects of dumped solid wastes on marine life and fisheries. In: Goldberg
DD, ed., North Sea science. NATO North Sea Conference, Aviemore, Scotland. Cambridge, US:
MIT Press, 415–436.
Shennan DH, Washington JS, Thomas DJ, Dick JA, Kaplan YS, Bennett JG (1981). Factors
predisposing to the development of progressive massive fibrosis in coal miners. Br. J. Ind. Med.
38: 321–326.
Sim PG (1977). Concentrations of some trace elements in New Zealand coals. N. Zea. Dep. Scientif.
Indus. Res. (DSIR) Bull. 218: 132–137.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 95
Solid Energy New Zealand Ltd (2002). Specifications of typical New Zealand semi-soft, Stockton
coking coal and Stockton high.
Soong R, Berrow ML (1979). Mineral matter in some New Zealand coals: Part 2 Major and trace
elements in some New Zealand coal ashes. N. Zea. J. Sci. 22: 229–233.
Soutar CA and Hurley JF (1986). Relation between dust exposure and lung function in miners and
ex-miners. Br. J. Ind. Med. 43: 307–320.
Soutar CA, Hurley JF, Miller BG, Cowie HA, Buchanan D (2004). Dust concentrations and respiratory
risks in coalminers: key risk estimates from the British Pneumoconiosis Field Research. Occup.
Environ. Med. 61: 477– 481.
⇧rám RJ, Holá N, Kote⌃ovec F, Vávra R (1985). Chromosomal abnormalities in soft coal open-cast
mining workers. Mutat. Res. 144: 271–275.
Stamm SC, Zhong BZ, Whong WZ, Ong T (1994). Mutagenicity of coal-dust and smokeless-tobacco
extracts in Salmonella typhimurium strains with differing levels of 0-acetyltransferase
activities. Mutat. Res. 321: 253–264.
Steenland K and Brown D (1995). Mortality study of gold miners exposed to silica and non-
asbestiform amphibole mineral: an update with 14 more years of follow-up. Am. J. Ind. Med. 27:
217–229.
Steenland K and Ward E (2014). Silica: A lung carcinogen. CA Cancer J. Clin. 64(1) :63–9.
Steenland K, Mannetje A, Boffetta P, Stayner L, Attfield M, Chen J, Dosemeci M, DeKlerk N, Hnizdo
E, Koskela R, Checkoway H; International Agency for Research on Cancer (2001). Pooled
exposure-response analyses and risk assessment for lung cancer in 10 cohorts of silica-
exposed workers: an IARC multicentre study. Cancer Causes Control 12: 773–784.
Stout SA, and Emsbo-Mattingly S (2008). Concentration and character of PAHs and other
hydrocarbons in coals of varying rank – implications for environmental studies of soils and
sediments containing particulate coal. Org. Geochem. 39: 801–809.
Stout SA, Uhler AD, McCarthy KJ, Mattingly SE (2002). Chemical fingerprinting of hydrocarbons. In:
Murphy BL and Morrison RD, eds., Introduction to environmental forensics. Amsterdam,
Netherlands: Elsevier Academic Press, 137–260.
96 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Swaen GM, Aerdts CW, Slangen JJ (1987). Gastric cancer in coalminers: final report. Br. J. Ind. Med.
44: 777–779.
Swaen GM, Meijers JM, Slangen JJ (1995). Risk of gastric cancer in pneumoconiotic coal miners and
the effect of respiratory impairment. Occup. Environ. Med. 52: 606–610.
Swaine D, Goodarzi F (eds.) (1995). Environmental aspects of trace elements in coal. Dordrecht:
Kluwer.
Swaine DJ (1977). Trace elements in coal. In: Hemphill DD, ed., Symposium on Trace Substances in
Environmental Health-XI. Columbia, US: University of Missouri, 107–116.
Swaine DJ (1979). Colloquium on combustion of pulverised coal: effect of mineral matter. Stewart
IM, Wall TF (Eds.), University of Newcastle, NSW, Australia, pp 3-14.
Swanson GM, Lin CS, Burns PB (1993). Diversity in the association between occupation and lung
cancer among black and white men. Cancer Epidemiol. Biomarkers Prev. 2: 313–320.
Taylor GH, Teichmüller M, Davis A, Diessel CFK, Littke R, Robert P (1998). Organic petrology.
Berlin-Stuttgart: Gebrüder Borntraeger, Germany.
Terrados J, Duarte CM, Fortes MD, Borum J, Agawin NSR, Bach S, Thamanya U, Kamp-Nielsen L,
Kenworthy WJ, Geertz-Hansen O, Vermaat J (1998). Changes in community structure and
biomass of seagrass communities along gradients of siltation in SE Asia. Estuar. Coast. Shelf
Sci. 46: 757–768.
Tomaskova H, Jirak Z, Splichalova A, Urban P (2012). Cancer incidence in Czech black coal miners in
association with coalworkers’ pneumoconiosis. Int. J. Occup. Med. Environ. Health 25: 137–
144.
Tor M, Oztürk M, Altın R, Cimrin AH (2010). Working conditions and pneumoconiosis in Turkish coal
miners between 1985 and 2004: a report from Zonguldak coal basin, Turkey. Tuberk Toraks.
58: 252–260.
Tucker JO and Ong T (1985). Induction of sister chromatid exchanges by coal dust and tobacco
snuff extracts in human peripheral lymphocytes. Environ. Mutag. 7: 313–324.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 97
Tucker JO, Whong WZ, Xu J, Ong T (1984). Genotoxic activity of nitrosated coal dust extact in
mammalian systems. Environ. Res. 35: 171–179.
Ulker OC, Ustundag A, Duydu Y, Yucesoy B, Karakaya A (2008). Cytogenetic monitoring of coal
workers and patients with coal workers' pneumoconiosis in Turkey. Environ. Mol. Mutagen. 49:
232–237.
Une H, Esaki H, Osajima K, Ikui H, Kodama K et al. (1995). A prospective study on mortality among
Japanese coal miners. Ind. Health 33: 67–76.
Valkovic V (1983). Trace elements in coal, Vol 1. CRC Press, Florida, USA.
Vermaat J, Agawin NSR, Fortes MD, Uri JS, Duarte CM, Marbà N, Enriquez S, van Vierssen W (1996).
The capacity of seagrasses to survive increased turbidity and siltation: the significance of
growth form and light use. Ambio 25: 499–504.
Vestbo J, Hurd SS, Agustí AG, Jones PW, Vogelmeier C, Anzueto A, Barnes PJ, Fabbri LM, Martinez
FJ, Nishimura M, Stockley RA, Sin DD, Rodriguez-Roisin R (2013). Global strategy for the
diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD
executive summary. Am. J. Respir. Crit. Care Med. 187: 347–365.
Wade WA, Petsonk EL, Young B, Mogri I (2011). Severe occupational pneumoconiosis among West
Virginian coal miners: one hundred thirty-eight cases of progressive massive fibrosis
compensated between 2000 and 2009. Chest 139: 1458–1462.
Walton WH, Dodgson J, Hadden GG et al. (1977). The effect of quartz and other non-coal dusts in
CWP: Part I. Epidemiological studies. In: Walton WH, ed., Inhaled particles IV. Oxford:
Pergamon, 669–689.
Wang G, Kleineidam S, Grathwohl P (2007). Sorption/desorption reversibility of phenanthrene in
soils and carbonaceous materials. Environ. Sci. Technol. 41: 1186–1193.
Ward CR (1984). Coal geology and coal technology. Melbourne: Blackwell Scientific.
Weinberg GB, Kuller LH, Stehr PA (1985). A case-control study of stomach cancer in a coal mining
region of Pennsylvania. Cancer 56: 703–13.
98 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
Whong WZ, Long R, Ames RG, Ong TM (1983). Role of nitrosation in the mutagenic activity of coal
dust: a postulation for gastric carcinogenesis in coal miners. Environ. Res. 32: 298–304.
Wilber D, Clarke D (2001). Biological effects of suspended sediments: a review of suspended
sediment impacts on fish and shellfish with relation to dredging activities in estuaries. N. Am.
J. Fish. Manage. 21: 855–875.
Williams R, Harcup MF (1974). The fish populations of an industrial river in South Wales. J. Fish
Biol. 6: 395–414.
Willsch H, Radke M (1995). Distribution of polycyclic aromatic compounds in coals of high rank.
Polycyc. Aromat. Comp. 7: 231–251.
Woitowitz HJ, Armbruster L, Bauer HD et al. (1989). Uberprüfung des Grenzwertes für
quarzhaltigen Kohlengrubenstaub Zentralblatt für Arbeitsmedizin, Arbeitsschutz. Prophylaxe
und Ergonomie 39: 132–146.
Wu Z-L, Chen J-K, Ong T, Matthews, EJ, Whong W-Z (1990). Induction of morphological
transformation by coal-dust extract in BALB/3T3 A31-1-13 cell line. Mutat. Res. 242: 225–
230.
Yang Y, Cajthaml T, Hofmann T (2008). PAH desorption from river floodplain soils using
supercritical fluid extraction. Environ. Pollut. 156: 745–752.
Yi P, Zhiren Z, Gang X (1991). Experimental study of Syrian hamster embryo cell transformation
induced by chrysotile fibers and coal dusts in vitro. J. WCUMS 22: 399–402.
Zhang Q, Dai J, Ali A, Chen L, Huang X (2002). Roles of bioavailable iron and calcium in coal dust-
induced oxidative stress: possible implications in coal workers’ lung disease. Free Radic. Res.
36: 285–294.
Zhao ZB, Liu K, Xie W, Pan WP,Riley JT (2000). Soluble polycyclic aromatic hydrocarbons in raw
coals. J. Hazard. Mater. 73: 77–85.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 99
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
100 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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)
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 101
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
102 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 103
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
104 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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.
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 105
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
µg/L ( loading of 100 mg/L)
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
µg/L ( loading of 100 mg/L)
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.
106 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 107
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)
108 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
• 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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 109
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
110 Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards
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
Report 2. Analysis of Coal Composition, Ecotoxicity and Human Health Hazards 111
• 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.
www.worldcoal.org
twitter.com/worldcoal
www.worldcoal.org/extract
www.facebook.com/worldcoalassociation
www.youtube.com/worldcoal
For more information on the work of the World Coal Association, please visit:
www.worldcoal.org