IB2 Hazardous substances and other chemicals - assessment of risk

Element IB2 Hazardous substances and other chemicals -

assessment of risk
Learning outcomes.

On completion of this element, candidates should be able to:

 Outline the factors to consider when assessing risks from chemicals which are hazardous to
health.
 Explain elimination of risk or control measures for chemicals which are hazardous to health
 Explain the specific requirements for asbestos.

Relevant Standards

 Health & Safety Executive, Workplace Exposure Limits, EH40/2005, HSE Books, 2005. ISBN:
0717629775
 American Conference of Governmental Industrial Hygienists, Documentation of the Threshold
Limit Values and Biological Exposure Indices, 7 th Edition, (ACGIH), 2001. ISBN
9781882417438
 International Labour Office, Safety in the Use of Chemicals at Work, an ILO Code of Practice,
ILO, 1993. ISBN: 9221080064

Section 6: Operational control measures

 International Labour Office, Ambient Factors in the Workplace, an ILO Code of Practice, ILO,
2001. ISBN 922111628

Minimum hours of tuition: 5 hours.

1.0 Exposure limits for airborne contaminants

Introduction - Amendments to COSHH Regulations in 2005

The amendments to the Control of Substances Hazardous to Health Regulations 2002 came into
force in early 2005. There are a number of changes; however, we will briefly refer to the pre-changes
should you be looking at any old NEBOSH examination papers throughout your studies.

Occupational Exposure Limits (OELs).

Prior to the amendments, there were two types of Occupational Exposure Limit. These were:

 The Occupational Exposure Standard (OES) - A target level of exposure which was deemed
to be safe for the majority of the population.
 The Maximum Exposure Limit (MEL) - An absolute maximum level of exposure which it was
illegal to exceed.
Following the Amendments, OESs and MELs have now been replaced by the Workplace Exposure
Limit (WEL). These limits were approved by the Health & Safety Commission and are therefore legal
standards.
What are workplace exposure limits?

Definition:

'the maximum concentration of an airborne substance, averaged over a reference period*, to which
employees may be exposed by inhalation'

* Two reference periods are used - 8 hours and 15 minutes - discussed later.

Workplace Exposure Limits (WELs) are Occupational Exposure Limits (OELs) set under Regulation
7 of COSHH 2002 (amended).

The averaged reference period (the time-weighted average or TWA) may be over two time periods -
the long-term exposure limit (LTEL) over eight hours, and the short-term exposure limit (STEL) over
15 minutes. In this respect, there has been no change from the old system.

The units used to express WELs are also the same as under the old system: parts per million (ppm)
and milligrams per cubic metre (mg/m3, or mg m-3).

WELs are listed in the HSE publication EH40/2005: Workplace Exposure Limit, which is updated
annually. EH40 also provides detailed guidance on the use of WELs.

Significantly, the amended Regulation 7 of COSHH now clearly states that control of exposure to
hazardous substances will only be treated as adequate if the appropriate WEL is not exceeded.
Thus it can be viewed as a maximum or ceiling which must not be exceeded on a time-weighted
average basis.

Also significantly, the amended Regulation 7 clearly states that control of exposure to hazardous
substances will only be treated as adequate if the "principles of good practice" for control have been
applied. We shall look at these principles later.

The two tests for adequacy of control outlined above apply in the case of exposure of employees to
any substance hazardous to health.

However, in certain situations, a stricter level of control is required by the amended Regulation 7 of
COSHH. Where the hazardous substance is either carcinogenic or mutagenic (i.e. carries the risk
phrases R45, R46, R49 or is listed in Schedule 1 of COSHH), or is capable of causing occupational
asthma (i.e. carries the risk phrases R42, R42/43 or is listed in Section C of HSE publication:
Asthmagen: Critical Assessments of the Evidence for Agents Implicated in Occupational Asthma)
then control will only be deemed adequate if exposure is reduced to as low a level as is reasonably
practicable.

So for most substances assigned a WEL, employers can achieve adequate control by applying the
"principles of good practice" and by ensuring that the WEL is not exceeded.
For carcinogens, mutagens and sensitising agents capable of causing occupational asthma,
employers must ensure that the control measures in place reduce employee exposure as far below
the WEL as is reasonably practicable. Thus, for these latter substances, a higher degree of control is
required by law and can be enforced. For these substances, it is not enough just to be below the
WEL. Workplace exposure must be below the WEL and further reduced below the WEL, to the
greatest extent reasonably practicable.

The list of WELs for use under the COSHH (Amended) Regulations 2004, and published in
EH40/2005 can be accessed via this link:

Table 1: List of approved workplace exposure limits [50kb] kohlapur road 5316 ,kamla

1.1 Occupational Exposure Limits (OELs)

In unit B2, we have been concerned with setting out the basic principles and methodologies of
toxicology and epidemiology. Now we must utilise the knowledge gained from both types of study,
and consider how the data obtained can be used to identify and reduce the likelihood of occupational
ill-health through the development of occupational exposure standards.

The principal application of toxicological and epidemiological data is to identify the possibility of work
related ill-health and to establish appropriate exposure limits aimed at preventing its occurrence.

We begin this study unit by considering some of the problems in interpreting toxicological data which
may have relevance to its application in standard setting.

We then move on to examine in some detail the way that occupational exposure limits are set and
the function of toxicological and other data in establishing these limits. This includes the role of
WATCH and ACTS, and the criteria that these committees use in agreeing occupational exposure
limits. We end the study unit by looking at the way that specific occupational exposure limits are
applied in particular circumstances.

PROBLEMS IN INTERPRETING TOXICOLOGICAL DATA.

In Unit B2, we reviewed the principles and methods of toxicological investigation, mainly from the
point of view of collecting information. However, having acquired toxicological data, its application
requires a certain degree of interpretation and the following issues need to be taken into
consideration during this interpretation process:

Relation of materials in use in the workplace to substances for which toxicological data is available.

Proprietary substances in use in the workplace may be complex formulations that do not correspond
exactly to substances for which data exists.

Knowledge of chemical structures and properties may be limited, compositions may vary from batch
to batch, chemicals in mixtures may react or degrade, or contamination may occur.
In addition, animal exposure data may not correspond to the exposure routes and patterns found in
the workplace. So how well does the available toxicological information correspond to the workplace
situation?

Type of effect (stochastic or non-stochastic) of the substance in question.

Non-stochastic effects are those where the severity of the effect varies with the exposure level,
enabling a threshold level to be determined which can be used to establish exposure limits.

In contrast, stochastic effects are those where the probability of effect depends on the degree of
exposure (or dose) making exposure limits much more difficult to define. So is there a 'safe'
threshold limit for the substance in question?

Interpretation of carcinogen, mutagen and reproductive data.

Interpretation of this type of data is based both on the source of the data (animal or human) and the
quality of the data (type and number of studies). The International Agency for Research on Cancer
(IARC) uses three different classifications, depending on the source of the data:

(1) 'Carcinogenic to humans' based on human data.

(2) 'Probably carcinogenic to humans' based on good animal evidence.

(3) 'Possibly carcinogenic to humans' based on less good evidence.

However, we have already noted the problems associated with the extrapolation of animal
carcinogenicity studies being applied to man, and therefore the limitations on the usefulness of
categories (2) and (3).

So what weight can we put on assertions that substances are 'probably' or 'possibly' carcinogens?

Sensitisers.

Sensitisation is a complex process involving the immunological system, with not all individuals being
susceptible. Evidence of effect only occurs in pre-susceptible individuals who have already been
sensitised from an earlier exposure. Thus measures of exposure which provoke a response in
sensitised individuals may be much lower than those inducing a sensitised state and different
NOAELs (No Observed Adverse Effect Levels) may be necessary depending on the immune status
of the individual exposed.

NOAELs : No observed adverse effect level.

Setting occupational exposure limits.

Despite the problems outlined above in interpreting toxicological data in order to prevent
occupational ill-health occurring as a result of exposure to workplace agents, we need to be able to
establish limits for exposure. Certain methodologies are therefore used to arrive at limits which are
practically useful in the workplace, but also take into account the inherent uncertainty in the available
toxicological data.
ACTS and WATCH.

ACTS: advisory Committee on toxic substances

WATCH : Working group on the assessment of toxic chemicals

WELs are set on the recommendation of the Advisory Committee on Toxic Substances (ACTS),
following assessment by the Working Group on the Assessment of Toxic Chemicals (WATCH) of the
toxicological, occupational hygiene and analytical data.

Each substance is first reviewed by WATCH, which considers whether an OES is appropriate and, if
so, what value should be recommended to ACTS. Setting an OES is the first option to be
considered, based on scientific judgement of the available data, and we shall consider the criteria
necessary for this below.

If, however, WATCH decides that an OES (either short-term or long-term limit) cannot be established
nd a WEL is appropriate, the decision as to what level the WEL is to be set at is passed to ACTS,
since this involves socio-economic judgements (balancing risk to health against the cost and effort of
reducing exposure).

Recommendations for WELs are made by ACTS to the Health and Safety Executive (HSE).
Following public consultation, new OESs are added to EH40 (Occupational Exposure Limits) which
is then submitted to the HSE for approval.

New WELs require approval by the Secretary of State before listing in Schedule 1 of COSHH

1.2 Criteria for setting WELs and what they represent in terms of
health protection
WELs are set on the recommendation of the Advisory Committee on Toxic Substances (ACTS).
However, before this takes place, there has to be an assessment carried out of toxicological,
epidemiological and other relevant data.

The first step in deriving a WEL involves an assessment of the toxicology of the substance in order
to identify the potential for adverse health effects, and to understand the dose-response relationship.

The primary purpose of this stage in the process is to identify the No Observed Adverse Effect Level
(NOAEL); this is the point on the dose-effect curve below which no adverse health effect is
observed, but above which some adverse effect is observed.

Many hazardous substances will have such a 'threshold' level, but not all. For example, carcinogens
may not have a discoverable threshold level below which there is no possibility of cancer occurring.

If a NOAEL is identified, then this value is used as a starting point for determining the highest level of
exposure at which no adverse health effects are predicted to occur in an occupational context.

In other words, an estimate is made of the highest level of exposure that a worker could be exposed
to on a daily basis for their entire working life without experiencing ill-health effects.
Since much of the toxicological data is derived from animal studies, this estimate is made with built-
in safety factors.

The final step in the process is to determine the actual levels of exposure that are being achieved in
the workplace. If these actual exposure levels are below the level identified by ACTS, or if ACTS
believes that achieving a lower level is reasonably practicable, then ACTS will set the WEL at this
level.

In other words, ACTS determines a NOAEL and from this derives an estimated level at which
occupational exposure will not cause health effects over a working life. ACTS then sets the WEL at
this estimated level on the basis that it is reasonably practicable for workplace exposure to be kept
below this level.

However, for some substances the process outlined above is not applicable. For certain substances
it is not possible to set a NOAEL; this might be because a NOAEL does not exist, or because no
scientifically accepted method exists for determining the NOAEL, or because the scientific data are
of poor quality and do not allow an NOAEL to be set with a degree of confidence.

For other substances, a NOAEL can be determined, but ACTS considers that it would not be
reasonably practicable to control exposure down to this level in those industries using the substance.

In these cases, ACTS will set a WEL at a level commensurate with good occupational hygiene
practice. In setting this level, ACTS will consider the severity of likely health effects, and the costs
and efficacy of the possible control solutions.

Wherever possible, the WEL is not set at a level where there is positive evidence of adverse effects
on human health.

The degree of uncertainty surrounding occupational health risks will vary from substance to
substance, depending on the amount of safety testing and the nature of the information available.

In some cases, there is likely to be considerable confidence that the WEL will protect health fully,
while in other cases some residual uncertainties are likely to remain.

Also, the WEL needs to cover substances such as genotoxic carcinogens for which current scientific
thinking suggests it is not possible to identify a threshold level of exposure below which there would
be no risk.

A system in which there is a single type of OEL that has to apply to all types of substance means
that the WEL cannot be portrayed as representing a complete guarantee of health protection for all
workers.

SCOEL : Scientific Committee on occupational exposure limit.

This approach is consistent with the advice in the Scientific Committee on Occupational Exposure
Limits’ (SCOEL) key document on Methodology for the Derivation of Occupational Exposure Limits,
which states that “It should however be emphasised, that it is always prudent to reduce exposure as
far below OELs as can be reasonably achieved, in order to provide the greatest degree of health
protection. This is particularly true for OELs which are not ‘health-based’”.
Research commissioned by HSE found that the problems of understanding and use of OELs in the
UK identified in the HSC’s Discussion Document are borne out by experience in other EU countries.

The study concluded that the continental European experiences analysed either supported a single
limit or a two-tier system combining good practice with special arrangements for carcinogens.

1.3 Good practice advice

The good practice advice will give practical guidance on controls needed for specific tasks and
chemicals. It will:

 take account of the risk to employees' health; this will involve consideration of the nature and
severity of the hazard posed by the chemical and the potential for exposure;
 take account of the work process in which it is being used or generated; and
 be designed to keep exposures below any relevant WEL.

Good practice advice will be available from HSE for many substances including those assigned a
WEL. This will be either substance-specific advice, or generic advice, i.e. advice related to particular
hazard/risk combinations rather than a specific substance.

Following good practice advice published by HSE or advice prepared by others (e.g. trade unions,
industry, suppliers and consultants) and endorsed by HSE as representing good practice, will not be
compulsory.

Employers will be free to follow guidance from any source, providing it is equally effective in ensuring
compliance with the legal duty.

The good practice advice produced or endorsed by HSE will be designed to keep exposures below
any relevant WEL, and will be subject to peer review and consultation with stakeholders. It will, in the
vast majority of cases, bring exposure below the WEL.

However, while it is impossible to guarantee that generic advice will be suitable for every
substance/task combination, it is expected that in the vast majority of circumstances, it will result in
adequate control.

If an employer has concerns they should seek specialist advice. Thus the generic advice will make
clear that it is to help employers comply with the requirements of the COSHH (Amendment)
Regulations 2005.

The advice will cover all the points in the principles of good practice for the control of exposure to
substances hazardous to health, and take account of risks from skin contact and ingestion as well as
inhalation. So it will include information on design, degree of containment, maintenance, training,
supervision and housekeeping.

Good practice advice will remind readers of the need to consider other COSHH duties, and the need
to comply with legislation relating to safety risks (e.g. fire and explosion) and environmental
legislation. While not attempting to provide advice on these regulations, the aim will be to give advice
which does not conflict with duties under them.
See also http://www.hse.gov.uk/aboutus/hsc/iacs/acts/

Question: With respect to workplace exposure limits for airborne hazardous substance:

(a) In relation to time, identify the two types of workplace exposure limits.

Question: Outline the limitation of workplace exposure limits

1.4 Calculation methods

Calculation of exposure with regard to the specified reference periods

This section reproduces the approved methods for the calculation of exposure in relation to the 8-
hour, short-term and one-year reference periods.

These methods are legally binding because they have been approved by the Health and Safety
Commission (from 2008, the unified Health and Safety Executive).

Part 1 The 8-hour reference period

The term ‘8-hour reference period’ relates to the procedure whereby the occupational exposures in
any 24-hour period are treated as equivalent to a single uniform exposure for 8 hours (the 8-hour
time-weighted average (TWA) exposure).
The 8-hour TWA may be represented mathematically by:

C1T1+C2T2+…CnTn 8

where C1 is the occupational exposure and T1 is the associated exposure time in hours in any 24-
hour period.

Example 1
The operator works for 7 hours 20 minutes on a process in which he is exposed to a substance
hazardous to health. The average exposure during that period is measured as 0.12 mg.m -3.

The 8-hour TWA =

7 h 20 min (7.33 h) at 0.12 mg.m-3
40 min (0.67 h) at 0 mg.m-3

That is
(0.12 x 7.33) + (0 x 0.67)
8

= 0.11 mg.m-3

Example 2
The operator works for eight hours on a process in which he is exposed to a substance hazardous to
health. The average exposure during that period is measured as

0.15 mg.m-3.
The 8-hour TWA =
(0.15 x 8)
8

= 0.15 mg.m-3

Example 3
Working periods may be split into several sessions for the purpose of sampling to take account of
rest and meal breaks etc. This is illustrated by the following example:

Exposure (mg.m-3) Duration of

Working period sampling
0800-1030 0.32 2.5
1045-1245 0.07 2
1330-1530 0.2 2
1545-1715 0.1 1.5

Exposure is assumed to be zero during the periods 10:30 to 10:45, 12:45 to 13:30 and 15:30 to
15:45.

The 8-hour TWA =

(0.32 x 2.5) + (0.07 x 2) + (0.20 x 2) + (0.10 x 1.5) + (0 x 1.25)

8

0.80 + 0.14 + 0.40 + 0.15 + 0

8

= 0.19 mg.m-3

Example 4
An operator works for eight hours during the night shift on a process in which he is intermittently
exposed to a substance hazardous to health.

The operator’s work pattern during the working period should be known and the best available data
relating to each period of exposure should be applied in calculating the 8-hour TWA.

These should be based on direct measurement, estimates based on data already available or
reasonable assumptions.

Task Exposure (mg.m-3)

Working period
2200 to 2400 Helping in workshop 0.1 (known to be exposure of full-
time group in workshop)
2400 to 0100 Cleaning elsewhere in 0 (assumed)
factory
0100 to 0400 Working in canteen 0 (assumed)
0400 to 0600 Cleaning up after 0.21 measured
breakdown in workshop

The 8-hour TWA =

(0.10 x 2) + (0.21 x 2) + (0 x 4)
8

= 0.078 mg.m-3

Example 5
The operator works a 12-hour shift each day for five days, and then has seven days’ rest. The
exposure limits are based on an 8-hour reference period in each 24 hours in which an exposure
occurs; the seven days’ rest makes no difference. While at work, the operator is exposed to 4 mg.m -
3.

The 8-hour TWA=

(4 x 12)
8

= 6 mg.m-3

The short-term reference period.

Exposure should be recorded as the average over the specified short-term reference period,
normally 15 minutes, and should be determined by sampling over that period.

For short emissions of less than the reference period, which still may have the potential to cause
harm, appropriate action should be taken to ensure that a ‘suitable and sufficient’ risk assessment is
carried out to avoid any risk to health from such exposures.

22 2083

Continue

An airborne contaminant has an Occupational Exposure Limit (OEL) of 15ppm, 8-hour

time-weighted average (TWA). Engineering controls have been introduced but the airborne
concentration of the contaminant in a workshop has been measured at 190ppm, 8-hour TWA.

The occupational hygienist has selected a piece of respiratory protective equipment (RPE)
with an assigned protection factor (APF) of 20, which is to be worn temporarily by all workers
in the contaminated area.

(a) Using the data above outline how the hygienist could have calculated the APF and
whether the hygienist made an appropriate selection.

(b) Outline other factors that should be taken into account when selecting appropriate RPE.

(c) When RPE is used it may not provide the level of protection stated by the manufacturer.

2.1 Chemical agents - Assessing risks

What COSHH requires.

To comply with COSHH, you need to follow these eight steps:

Step 1 Assess the risks

Assess the risks to health from hazardous substances used in or created by your workplace
activities.

Step 2 Decide what precautions are needed

You must not carry out work which could expose your employees to hazardous substances without
first considering the risks and the necessary precautions, and what else you need to do to comply
with COSHH.

Step 3 Prevent or adequately control exposure

You must prevent your employees being exposed to hazardous substances. Where preventing
exposure is not reasonably practicable, then you must adequately control it. The advice in this
leaflet, and in the other guidance to which it refers, will help you to make correct assessments and to
put the appropriate controls into place

Step 4 Ensure that control measures are used and maintained

Ensure that control measures are used and maintained properly, and that safety procedures are
followed.

Step 5 Monitor the exposure

Monitor the exposure of employees to hazardous substances, if necessary.

Step 6 Carry out appropriate health surveillance

Carry out appropriate health surveillance where your assessment has shown this is necessary, or
where COSHH sets specific requirements.

Step 7 Prepare plans and procedures to deal with accidents, incidents and emergencies
Prepare plans and procedures to deal with accidents, incidents and emergencies involving
hazardous substances, where necessary

Step 8 Ensure employees are properly informed, trained and supervised

You should provide your employees with suitable and sufficient information, instruction and training.

What is a chemical hazard and risk assessment?

Many of the substances that we encounter in our work, not only in laboratories but also in offices and
other not so likely places, can cause ill-health or fire and even explosion. The properties that cause
these effects are called hazards. In some activities we do not start with a hazardous substance but
one is produced from the process as a fume or residue.

In most cases, the harm is not caused by the substance alone but by an unsafe condition arising
from:

 the way a substance is used or produced; or

 incorrect storage. In many instances, the substances must be released in some way for an
unsafe condition to arise:
 as a gas, vapour, fume, dust, aerosol;
 from a liquid spill.

Unsafe conditions include:

 an atmosphere contaminated with gas, dust, vapour, fume, aerosol;

 oxygen deficiency;
 spills or splashes of liquids;
 mixing of incompatible substances;
 overheating, excess pressure, exposure to source of ignition.

An unsafe condition may cause:

 personal exposure by inhalation or eye or skin contact;

  asphyxiation;
 spills or splashes of liquids;
 violent reaction and/or release of further hazardous substances;
 ignition or detonation leading to fire or explosion.

The likelihood that an unsafe condition will actually arise is called the risk. In order to determine
whether an unsafe condition may arise and what to do about it, we need information about both the
substances and the processes involving them. That is, we need to do a chemical hazard and risk
assessment of the activity.

Chemical hazard and risk assessment involves:

 identifying the substances used or produced or released in an activity;

 gathering information about the hazards, the harmful or adverse effects of the substances;
 considering whether and how harm or adverse effects could actually arise from the way the
substances are used or produced, the risk to health and safety;
 identifying the people whose health and safety may be endangered;
 considering what methods of prevention or control and any other measures are needed;
 identifying the need for monitoring:
 performance of control measures;
 workplace conditions;
 personal exposure;
 health;
 determining the management of foreseeable emergencies;
 identifying the information, training and instruction needs of those who may be affected.

In addition to these general principles, there will also be the need to consider what else may need to
be done to satisfy specific requirements of relevant health and safety law.
In some instances, explicit legal requirements will apply to parts of this process. For example, fume
cupboards must be thoroughly checked every 14 months and undergo simple checks every week; a
health record must be maintained for anyone whose work involves a carcinogen.

The purpose of a chemical hazard and risk assessment is therefore to provide the information and
evaluations necessary to allow decisions to be made about the measures needed to ensure no
personal harm or adverse effects will arise from activities involving hazardous substances.

What it is not.

A chemical hazard and risk assessment is not:

 a list of the hazards of a substance;

 a collection of substance safety data sheets.

Scope and Application.

The requirement for risk assessment applies to all work activities, catering, cleaning, maintenance,
research, teaching, etc. that use, or that may produce or release, hazardous substances. However,
separate arrangements apply for substances that are hazardous solely because of radiation or
biological hazards.
2.1.1 Assessment Strategy - Generic Assessment
This is not a bureaucratic exercise. In many instances, the assessment may have been largely or
even wholly completed at enterprise level. In such cases, all that is required is to confirm local
arrangements conform to enterprise Policy.

For example, Hazardous Substances Policy specifies the requirements for the storage of highly
flammable solvents. Hazardous Substances Policy is developed from hazard and risk assessment.
The assessment does not need to be repeated for a particular storage if the enterprise's
requirements are fully met and this is stated in the local arrangements.

This is known as generic assessment. There are many examples of generic assessment. Following
a generic assessment is the easiest option, provided that local conditions do not invalidate it.

Guidance.

THE SUBSTANCES.

What is involved?

All the substances used or produced by an activity must be identified. Percentage compositions will
be required for mixtures.

It will be necessary to know what form the substance(s) will be in: gas, vapour, liquid, fume, dust,
mist, aerosol or solid. The form of a substance may change during an activity because of the effect
of temperature. For example, the flux used in soldering electronic components becomes liquid and
therefore volatile, and also fumes during the soldering process.

Physical and chemical properties.

Physical and chemical properties are very relevant to hazard and risk. Especially important to risk
are physical properties such as boiling point, vapour pressure, evaporation rate and particle size
which influence the mobility of a substance.

In addition to the hazardous properties mentioned below, stability and incompatibility or reactivity
with other substances are important chemical properties.

All of this information should be available in suppliers' catalogues and on suppliers' Material Safety
Data Sheets. Information about substances produced during or from an activity may be available
from other standard reference sources.

Is it hazardous?

A substance is hazardous if it is:

 listed under the labelling regulations or has properties similar to listed substances;
 listed in the COSHH regulations;
 assigned a Workplace Exposure Limit;
  a dust of any kind;
 any other substance, such as an asphyxiant, that because of its properties or the way in
which it is used or is present can cause a risk to health and safety.

The statutory labelling that appears on containers is very useful for identifying the hazards of a
substance.

Symbol Hazard Description of hazard

(Physicochemical)
E explosive Chemicals that explode.
O oxidising Chemicals that react exothermically with other
chemicals.
F+ highly Chemicals that may catch fire in contact with air,
flammable only need brief contact with an ignition source, have
a very low flash point or evolve highly flammable
gases in contact with water.
F extremely Chemicals that have an extremely low flash point
flammable and boiling point and gases that catch fire in contact
with air.
(Health)
T+ very toxic Chemicals that at very low levels cause damage to
health.
T toxic Chemicals that at low levels cause damage to
health.
T category 1 Chemicals that may cause cancer or increase its
carcinogens incidence.
T category 2
carcinogens
Xn category 3
carcinogens
T category 1 Chemicals that induce heritable genetic defects or
mutagens increase their incidence.
T category 2
mutagens
Xn category 3
mutagens
T category 1 Chemicals that produce or increase the incidence of
reproductive non-heritable effects in progeny and/or an
toxins impairment in reproductive functions or capacity.
T category 2
reproductive
toxins
Xn category 3
reproductive
toxins
 Xn harmful Chemicals that may cause damage to health.
C corrosive Chemicals that may destroy living tissue on contact.
Xi irritant Chemicals that may cause inflammation to the skin
or other mucous membranes.
(Environmental)
N dangerous for Chemicals that may present an immediate or
the delayed danger to one or more components of the
environment environment

Additionally, labelling will display explicit risk phrases such as:

 Spontaneously flammable in air.

 Contact with water liberates extremely flammable gases.
 Causes severe burns.
 May cause cancer.

The statutory hazard classifications of substances are included in various Hazardous Substances
Databases. This information may also be found in suppliers' catalogues and on suppliers' Material
Safety Data Sheets.

Where the classification of a substance is not known or is in doubt, refer to the CHIP Regulations
Approved Classification and Labelling Guide.

In the COSHH Regulations, certain substances that cause cancer, heritable genetic damage or
asthma are identified as particularly hazardous.

Dust, even if not a toxic substance, may still be harmful to health if inhaled in excessive quantity.
Dust, even if not a flammable or combustible substance may form an explosive atmosphere. In both
cases, particle size is important. The particle size for respirable dust is defined in BS EN 481 1993.
The range for explosive atmospheres may be many times greater, up to about 400 micrometres.

Asphyxiants are gases which, even if inert, present a risk to health if present in sufficient amount to
significantly reduce the proportion of oxygen to other gases in the air.

Harmful and adverse health effects.

Toxicity and other health effects data will be needed to determine what amount of substance would
harm health, whether the risk is acute or chronic or both and whether it is additive:

 acute, from a single contact causing serious effects or death, either immediate or delayed;
 chronic, from repeated contacts, even at low level, causing harmful effects or even death;
 whether both short-term or long-term effects could occur;
 Additive either from mixed or from consecutive contacts to different substances.

Some health effects are considered serious at all levels of contact because of the nature or
irreversibility of the consequences:
  mutagenic, capable of changing the genetic material that determines the heritable
characteristics of living cells; carcinogenic, can cause uncontrolled cell growth to give rise to a
cancer;
 reproductive, may impair fertility or cause developmental damage before conception, during
pregnancy or after birth;
 allergenic, can cause hypersensitive condition.

Reactivity and Instability.

Will the substance readily set on fire or explode, or produce a flammable mixture with air? Data such
as FLASH POINT, EXPLOSIVE LIMITS, AUTOIGNITION TEMPERATURE, SELF-ACCELERATING
DECOMPOSITION TEMPERATURE will be needed. Is the substance sensitive to heat or shock?
Are any of the substances incompatible or react with air or water?

The Activity.

The risk of harmful or adverse effects usually arises from the activity, that is, the way in which
substances are used or produced. Thus the assessment must consider what happens during an
activity.

Important features include:

 how much substance is used;

 are two or more substances mixed;
 procedures used, such as pouring, mixing, spraying, abrading, etc;
 experimental conditions such as temperature, pressure;
 containment or otherwise of the equipment, that is, the ability of the equipment to prevent a
release of the substance.

The assessment must also consider:

 any potential for change in the activity that would alter the risk;
 What could go wrong?

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2.2 Risk Assessment

The likelihood that an unsafe condition will actually arise is called the risk.

Unsafe conditions include:

 excessive personal exposure to a substance, sufficient to cause harm to health;

Contact with a substance can be brought about in a variety of ways and circumstances:

 working with it directly so as to touch it or to inhale it after discharge to air;

  the inadvertent unintentional mixing of incompatible substances that produces a harmful
product (e.g., the release of chlorine gas from the mixing of hypochlorite with an acid);
 being near to where it is handled, transported, used, worked upon, collected, packed, stored,
disposed of, discharged or given off etc.;
 entering an enclosed space where it might be present;
 disturbing deposits of the substance on surfaces (e.g., during cleaning or maintenance) and
making the substance airborne;
failure of controls;
 wearing previously contaminated clothing or protective equipment;
coming into contact with contaminated surfaces;
 having a substance passed on from someone else, e.g., from another person's contaminated
clothing or from personal contact.
 creation of an explosive atmosphere;
 exposure of a flammable substance or explosive atmosphere to a source of ignition;
 mixing a substance with one with which it is violently incompatible;
 exposure of an unstable substance to shock, heat or flame;
 loss of control arising from a mishap or equipment malfunction.

Criteria For Determining Excessive Personal Exposure.

Harm to health can only arise if there is exposure to a substance, that is, contact with it that could
lead to its absorption into the body. Is the substance likely to be present in a form in which it could
be:

 inhaled;
 swallowed (either directly, or by settling on food, or from putting contaminated fingers to the
mouth);
 absorbed through the skin or eyes (either directly, or from contact with contaminated surfaces
or clothing);
 in contact with skin or eyes;
 injected into the body by high pressure, equipment or contaminated sharp objects.

Exposure is judged excessive if the level exceeds a set standard, such as the Health and Safety
Executive's Workplace Exposure Limit for airborne substances, or oxygen deficiency in the case of
inert gases. Exposure may also be judged excessive according to the severity of the effect, such as
destruction of tissue by a "corrosive" substance.

Especially in research where small amounts of novel or little-known substances may be used, there
may be no official classification or standard applied to particular substances. In these cases, data
from the literature or supplier should be used in conjunction with the official criteria for hazard
classification to determine appropriate in-house standards.

Exposures to airborne substances.

Exposure to contaminated atmospheres will need to be controlled so as not to exceed the Workplace
Exposure Limit (WEL). However, where a substance causes cancer, heritable genetic damage or
asthma, then the requirement is to control exposure to a level as far below the limit as is practicable.
To predict whether the WEL is likely to be exceeded during an activity, it is necessary to estimate the
scale of evaporation or release of substance into the air and the resulting airborne concentration.

Alternatively, compare the amount that may become airborne with the amount needed to produce
the WEL.

For example, 0.67 cm3 of chloroform evaporated into 100 m3 of air will produce the WEL vapour in
air concentration of 2 ppm. In some cases, there is also a risk from skin absorption.

Oxygen deficiency.

Oxygen deficiency may arise when inert gases such as nitrogen and helium displace atmospheric
oxygen. The normal concentration of oxygen in air is 20.9%, and should not be allowed to fall below
18%. The release of about 17% of the room volume of an inert gas will lower the oxygen
concentration to 18%.

Exposures to substances absorbed through the skin.

Any exposure to hazardous substances that can be absorbed through the skin is excessive and
should be prevented. Such substances include those assigned the skin (sk) notation in EH40, and
those labelled with the specific risk phrases.

Exposures judged excessive by severity of effect.

The emphasis will be on preventing exposure. The classes of hazard to which this category applies
are:

 corrosive;
 carcinogenic;
 mutagenic;
 allergenic;
 toxic to reproduction.

Criteria for excessive risk of fire or explosion.

As with excessive personal exposures, there is scope for assessment by comparison with an
appropriate standard, and also by severity of effect.

Flammable/explosive atmospheres and flammable substances.

Three components are usually needed to cause fire and/or explosion:

 a flammable gas or vapour or a dust;

 oxygen;
 a source of ignition.

Controlling any one of these components should control the risk. In the case of gases, vapours and
dusts, it is usual to control the release of the substance because many flammable substances are
also harmful to health. The limits for the control of flammable/explosive concentrations in air are at
percentage levels, thousands of times higher than WELs.

Where it is possible for an explosive atmosphere to form the DSEAR regulations require the place to
be classified "hazardous" or "non-hazardous" according to whether this may occur in such quantities
as to require special precautions.

Some solid substances readily catch fire on brief contact with a source of ignition. Here the
emphasis would be on control of contact with air and the source of ignition.

Certain very unstable substances can catch fire/explode in the absence of an external source of
oxygen or ignition energy. This may be as a result of auto-oxidation as can happen with cellulose
nitrate. The decomposition of acetylene can continue in the absence of oxygen.

Unstable substances.

Some substances explode on brief contact with heat or flame or are sensitive to pressure change.
Here the emphasis will be on controlling the condition that invokes the instability.

Incompatible substances.

Some substances react violently with air or water. Some combinations of substances are
incompatible.

Frequency or Duration of Unsafe Condition.

The frequency and duration of an unsafe condition are also important considerations in the
evaluation of risk and the actions required for control.

Some adverse effects may be time-dependent, and may not occur if the duration of the dangerous
condition is too short.

Some adverse effects from brief exposure are less serious, such as simple reversible irritation that is
not likely to cause long-term harm. The same applies to exposure that is infrequent.

2.3 People who may be at risk from the work activity

Risks to health and safety from a work activity involving hazardous substances may endanger not
only the person performing the activity, but also colleagues working nearby, and a variety of other
people who may be in the vicinity at some time or other.

The risk assessment must identify the people who are performing the activity, and also assess the
extent to which any others from the following categories may be at risk:

 research staff;
 technical staff;
 students;
 supervisors;
  office staff;
 maintenance and cleaning staff;
 security staff;
 contractors, including service engineers;
 visitors;
 persons living or working nearby;
 persons using public footpaths on company property;
 emergency service personnel.

Also, certain groups of people could suffer more than others, e.g., pregnant women and nursing
mothers.

Conclusions about risk.

Possible conclusions are:

 an unsafe condition is not likely under any circumstances - no further action required unless
there are specific statutory measures for substance/activity (e.g. health record for work with
carcinogens);
 an unsafe condition is not likely during normal operation, but could arise from potential
changes in the activity - define potential changes and specify criteria for review of
assessment;
 an unsafe condition is not likely during normal operation, but could arise from mishap or
equipment malfunction - assess emergency measures;
 an unsafe condition is likely during normal operation - assess and specify measures for
prevention/control of risk.

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2.4 Prevention and control of risk

If exposure cannot be prevented, preferably by avoiding, so far as is reasonably practicable, the use
of a hazardous substance by substituting a substance or process which eliminates or reduces the
risks to health, then employers must adequately control exposure.

To achieve this, apply protection measures appropriate to the activity and consistent with the
assessment in the priority order specified by COSHH. That order is:

 first, a high level of inherent safety by careful design, selection and use of appropriate work
processes, systems and engineering controls, and use of suitable work equipment and
materials, e.g. use systems and processes which reduce to the minimum required for the
work the amount of hazardous substance used or produced, or equipment which totally
encloses the process;
 second, control exposure at source, e.g. by including adequate ventilation systems and
appropriate organisational measures such as reducing to a minimum the number of
employees exposed, and the level and duration of their exposure;
 and lastly, use personal protective equipment in addition to the previous measures where
adequate control cannot be achieved by them alone.
The protection measures to be put in place should be determined by:

 the extent of the risk of ill-health to employees resulting from their exposure to any hazardous
substance; and
 the scope for reducing the risk to a minimum.

COSHH permits protection measures to be proportionate to the risk the exposure poses. Therefore,
the measures should be appropriate to the work activity and consistent with the findings of the
assessment.

This means that the greater the level of risk determined by the assessment, the greater should be
the effort in terms of the time, cost and trouble taken to avert the risk.

In practice, the assessment may result in identification of a number of suitable and appropriate
protection measures that would achieve adequate control of exposure.

In those circumstances, implement the control measures that will work best to protect the health of
employees without imposing a disproportionate effort to the risk arising from the work.

COSHH essentials: Easy steps to control chemicals. The step-by-step guidance in COSHH
essentials can be used to identify the appropriate controls for a range of hazardous substances/task
combinations.

Case study.

A company which manufactures lacquers buys liquid citox in drums. They transfer it from the drum,
in a 50 to 100 litre batch process, to a reactor containing resins, where it gets mixed to make
lacquers. They do this twice a day, for a period of two hours for each batch.

Using the Internet version of COSHH essentials (www.coshh-essentials.org.uk), they click 'Go' to
start an assessment, enter the process name 'lacquer making' and tick 'transferring and mixing' as
the tasks.

They choose the option that they are using one substance, type citox and confirm that this is a liquid.

The next stage determines to which hazard group the chemical belongs (one of A-E, with E being
the most hazardous, and group S for substances that can cause harm as a result of skin contact).

The supplier's safety data sheet (section 15) shows that citox has the risk phrase R21/22-36/37/38 -
harmful in contact with skin and if swallowed, and irritating to the eyes, respiratory system and skin.

After ticking these combinations and 'Go', the software decides the chemical belongs to hazard
groups C and S.

For liquids, they then need to know how volatile the chemical is. For the first task of transferring, this
is at room temperature (taken to be 25°C) and the safety data sheet gives its boiling point as 134°C.
So they enter this and proceed to consider how much they are using. For each batch, the company
adds litres of citox to the reactor, so they click 'medium quantity' followed by the time they spend on
the transferring task.
At this point, the assessment on transferring citox is completed and they get a summary of their
inputs. Unless they wish to change anything, they can then view the advice offered.

Based on a medium amount of a group C chemical with medium volatility, COSHH essentials
allocates the right control approach as 'Containment'.

It lists seven control guidance sheets as downloadable PDF files: the general control guidance sheet
300; four specific sheets on transferring (of which they decide 306 is most relevant); and, because
citox is also hazard group S, two sheets with advice on protecting employees' skin and eyes, and
selecting and using personal protective equipment.

They also download a summary of the assessment as a record, and this reminds them of other
actions they may need to take.

They then do a similar assessment on the second task of mixing citox at 50°C. The key new control
guidance sheet from this is 318 about mixing liquids.

As a result of sheet 306 about drum emptying, they realise that their current system of controlling
exposure when transferring citox from the drums to the reactor needs updating. They use the advice
to purchase a suitable drum pump. This is installed, and the firm trains its staff on how and why to
use the pump. The firm also improves storage facilities and buys suitable personal protective
equipment to protect workers' skin.

Both COSHH and DSEAR specify the measures required, and in order of preference.

Prevention.

The law places the emphasis on prevention. Elimination of a risk is the most effective form of
prevention.

Elimination of risk may be by:

 not performing the activity;

 a change in the way the work is done;
 substituting a less hazardous substance; or
 removing one of the risk factors, e.g. source of ignition.

Control.

Both COSHH and DSEAR are explicit or clear about methods of control and the order of preference
in which they should be considered. Some controls are inherently more effective than others. Choice
should be of the most effective and reliable controls that minimize the escape and spread of
substances.

The most effective and reliable is eliminating the substance. If a substance is not used, it cannot be
a risk to health and safety. Especially for more dangerous substances, an assessment should
include a brief statement of why it could not be eliminated.
Amounts of substances and release rates should be restricted, and residual risk must be
controlled at source by appropriate engineering measures. Examples include a totally
enclosed system so that the substance is not released, or local exhaust ventilation to contain
or capture the substance, before it is released to air.

Local exhaust ventilation performance varies according to type and individual specification. The
assessment will need to identify the specification needed to control risk to an acceptable level.
However, a COSHH principle of good practice is that control measures should be proportionate to
the risk.

If potential exposure is 100 times the WEL, then the performance of control measures will need to be
much greater than if the potential exposure were only twice the WEL. However, if a particular
measure is more convenient or acceptable, it does not matter if it reduces exposure more than is
strictly necessary.

However, where there is potential exposure to a carcinogen or mutagen, and it is not reasonably
practicable to prevent it, additional measures required by COSHH include:

 total enclosure;
 Designation of areas that may be contaminated.

All the requirements of DSEAR Regulation 7 must be fulfilled for an area classified "hazardous".

Further Measures.

Information, instruction and training will always be needed. Do the basic arrangements need to be
supplemented because of specific features of the activity or control measures?

Personal protective equipment may also be needed in addition to all other control measures if the
combination of all control measures fails to achieve adequate control of exposure.

The performance of personal protective equipment varies according to type and individual
specification. For example, no single glove material will give protection against all substances.

The assessment will need to identify the specification needed to give adequate protection, and
whether personal fitting is required.

Personal fit testing of tight-fitting respirator face pieces is a specific requirement for compliance with
COSHH. The performance of such respirators depends on a good contact between the wearer's face
and the face seal of the mask.

2.5 Monitoring
Performance of Control Measures.

Are special arrangements needed for checking the performance of controls? COSHH requires that
controls are kept in efficient working order, good repair and clean and that they are visually checked
at least once a week. Engineering controls and respiratory protective equipment have to be
examined and, where appropriate, tested at suitable intervals. The assessment will need to indicate
whether the standard checking procedures will be adequate, if they are not, they need to specify
what extra needs to be done.

Workplace Conditions.

Monitoring workplace conditions might be necessary if there is a risk of a dangerous condition

arising unexpectedly. Examples include toxic, explosive or oxygen-deficient atmospheres. How will
this be done? By installing sensors linked to alarms? Will any interlocking of sensors and control
measures be needed?

Personal Exposure.

If the work will cause people to be exposed to a substance, and either it is not known whether the
exposure will be excessive or exposure is expected to be close to the limit, personal monitoring may
be required. Personal monitoring may also be necessary if exposure could occur unexpectedly from
a failed control. The type and frequency of monitoring should be specified. However, personal
exposure monitoring may not be necessary if, for example, workplace monitoring gives advance
warning of potentially unacceptable personal exposure.

Health.

Some form of health surveillance is mandatory for specified activities or work with certain substances
and if it is believed likely that exposure may give rise to observable health effects.

Relevant examples of substances for which health surveillance is required:

 Substances of recognised systemic toxicity (e.g. carcinogens, substances labelled "may

cause cancer" or "may cause cancer by inhalation" or heavy metals such as lead, cadmium).
 Substances labelled "May cause sensitisation by inhalation" and other substances known to
cause occupational asthma.
 Substances labelled "May cause sensitisation by skin contact" and other substances known to
cause severe dermatitis.
 Soldering using rosin flux.

Emergency measures.

What could foreseeably go wrong?

 Equipment failure or malfunction.

 Spills and leaks.

Other loss of control.

What hazards and risk would arise from foreseeable emergencies?

 Fire/explosion.
  Contamination of the workplace.
 Personal exposure to hazardous substances.
 Contamination of water courses/sewers.

What arrangements will be needed to:

 stop the incident and bring the hazards under control;

 protect people;
 provide first aid to people exposed to hazardous substances;
 decontaminate/clean up/return to normal;
 contact emergency responders.

In particular, are special arrangements indicated, such as the need for hydrofluoric acid burns gel, or
not using water on a fire involving water-reactive substances?

Recording the assessment.

The significant findings of the assessment should be recorded when the assessment is made, or as
soon as is practicable afterwards.
In some circumstances, not all the findings will have been determined at the same time. Some may
be awaiting further information before they can be resolved, and it will not be possible to record
these until then, e.g. where there is a pilot operation which runs for a period before being assessed
completely, or where air monitoring results are awaited.

In these circumstances, complete or update the record of the significant findings as information
becomes available.

Review of the assessment.

The need for review is indicated if there is any reason to suppose that the original assessment is no
longer valid, or if any of the circumstances of the work should change significantly.

For example, if there are any significant changes in:

 the scale of the activity, quantities of substances involved;

 the substances;
 the equipment;
 control measures.

It is also necessary to be alert for the need of review if, for example:

 ill health related to work is reported;

 there are fire or explosion incidents;
 there is new evidence about the hazards of the substances;
 monitoring or health surveillance results show any loss of control;
 new or improved techniques of control become feasible.

Hazardous Substances Policy specifies that risk assessments are reviewed at least annually to
ensure that they remain relevant.
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Continue

2.6 Appendix
COSHH Requirements, Regulation 7 Prevention or Control of Exposure to Substances
Hazardous to Health.

Exposure to substances hazardous to health must be prevented or, where this is not reasonably
practicable, adequately controlled using protection measures including, in order of priority:

1. the design and use of appropriate work processes, systems and engineering controls and the
provision and use of suitable work equipment and materials;

2. the control of exposure at source, including local exhaust ventilation and work procedures; and

3. as a last resort, where adequate control cannot be achieved by other means, in addition to the
above, personal protective equipment.

The measures referred to above to include:

 safe handling, storage and transport, including waste;

 suitable maintenance procedures;
 reducing, to the minimum number of employees exposed;
 restricting level and duration of exposure, and quantity of substances;
 control of the working environment, including appropriate general ventilation;
 appropriate hygiene measures, including adequate washing facilities.

Control of exposure will only be regarded as adequate if:

 the principles of good practice set out in Schedule 2 to the regulations are applied;
 any workplace exposure limit is not exceeded;
 for carcinogens, mutagens and asthmagens, exposure is to as low a level as is reasonably
practicable.

Principles of Good Practice for the Control of Exposure to Substances Hazardous to Health
(COSHH Schedule 2).

(a) Design and operate processes and activities to minimise emission, release and spread of
substances hazardous to health.

(b) Take into account all relevant routes of exposure - inhalation, skin absorption and ingestion -
when developing control measures.

(c) Control exposure by measures that are proportionate to the health risk
(d) Choose the most effective and reliable control options which minimise the escape and spread of
substances hazardous to health.

(e) Where adequate control of exposure cannot be achieved by other means, provide, in
combination with other control measures, suitable personal protective equipment.

(f) Check and review regularly all elements of control measures for their continuing effectiveness.

(g) Inform and train all employees on the hazards and risks from the substances with which they
work, and the use of control measures developed to minimise the risks.

( h ) Ensure that the introduction of control measures does not increase the overall risk to health and
safety.
DSEAR Requirements, Regulation 6 Elimination or Reduction of Risks.

Risk must be either eliminated or reduced SFARP.

Preference should be given to risk reduction by substitution. Otherwise, use controls including, in
order of priority:

1. the reduction of quantities to a minimum;

2. avoidance or minimising of release;

3. control of the release at source;

4. prevention of the formation of an explosive atmosphere, including the application of appropriate

ventilation;

5. any release which may give rise to risk is suitably collected, safely contained, removed to a safe
place, or otherwise rendered safe, as appropriate;

6. avoidance of

(i) ignition sources, including electrostatic discharges, and

(ii) adverse conditions that could cause harmful effects;

7. segregation of incompatible dangerous substances;

and mitigate effects of fire/explosion or dangerous substances, including these measures:

 reduction to a minimum number of employees exposed;

 the avoidance of the propagation of fires or explosions;
 explosion pressure relief arrangements;
 explosion suppression equipment;
 equipment able to withstand the pressure likely to be produced by an explosion;
 suitable personal protective equipment;
  arrange for the safe handling, storage and transport of dangerous substances including
waste;
 risk reduction conditions must be maintained;

Use the following general measures:

Workplace and Work Procedures.

Workplace designed, constructed and maintained so as to reduce risk.

Designing, constructing, assembling, installing, providing and using suitable work processes so as to
reduce risk.
Maintaining work processes in an efficient state, in efficient working order and in good repair.

Ensuring that equipment and protective systems meet the following requirements:
i) where power failure can give rise to additional risk, independent supply needed for equipment and
protective systems;

ii) manual override operated by employees competent to do so;

iii) on operation of emergency shutdown, accumulated energy must be dissipated or isolated as

quickly and as safely as possible;

iv) necessary measures must be taken to prevent confusion between connecting devices.

Organisational Measures.

appropriate systems of work including the issuing of written instructions for the carrying out of the
work; and a system of permits to work, where the work is carried out in hazardous places or involves
hazardous activities.

DSEAR Requirements, Regulation 7 Places where Explosive Atmospheres May Occur

 Classify places where an explosive atmosphere may occur into hazardous or non-hazardous,
and hazardous places into zones in accordance with Schedule 2.
 Equipment in hazard zones must conform to Schedule 3.
 Hazard zones must be signed.


 Before a place is used for first time, the explosion safety must be verified by a person
competent in explosion protection.
 Work clothing used in hazard zones must not give rise to electrostatic discharges.

2.7 Factors which affect hazard/risk to the individual

Factors which affect hazard/risk to the individual include:

 solubility in body fluids;

  synergy;
 individual susceptibilities (e.g. atopic persons, women of child bearing capacity);
 age;
 sensitisation;
 and morphology.

We will now look at the above in more detail.

Solubility in Body Fluids.

In the previous study unit, we encountered a number of examples where the harmful effect of an
agent depends on its particular chemical properties and its ability to interact with absorbing areas of
the body.

Examples include:

 ammonia gas which can dissolve in moist areas of the respiratory tract (and there are many
other examples of soluble gases which can cause harm by this route);
 toxic metals which are only soluble in water at a particular pH which determines where in the
gastrointestinal tract dissolution and absorption can take place; and
 organic chemicals which are not water soluble but will dissolve in fats or lipids in the body,
and consequently accumulate in target organs which are susceptible, (e.g. chlorinated
hydrocarbons).

Consequently, the particular physical form of the substance (gas, liquid, solid) and its chemical
properties (water soluble, organic liquid soluble in lipids/fats, soluble in acid or alkaline solutions)
gives us an indication of the way in which the material may interact with the body, and hence its
potential for harm.

Synergy.

Chemical agents are able to exert a harmful effect on the body if exposure to the substance in
isolation occurs.

However, if exposure to a combination of agents occurs, it is possible, in some cases, for one or
other of the agents to enhance the harmful effect of the other.

This is called synergy and means that the effect of the combination of agents on the body is greater
than the sum of the individual effects.

The most common example of this is the effect of exposure to asbestos fibres on smokers. Tobacco
smoke is known to contain carcinogenic substances, and it is possible to estimate the likelihood of a
smoker contracting lung cancer. Asbestos fibres are also a recognised carcinogen, and
epidemiological data gives us the probability of an asbestos worker developing lung cancer following
exposure to asbestos dust.

However, if epidemiological data for asbestos workers who smoke is studied, it is found that the
likelihood of these individuals contracting lung cancer is much higher than that expected from
exposure to each agent individually.
As a result of this, in assessing the risk from exposure to a range of chemical agents, it is necessary
to consider any synergic effects that may enhance the harmful effect of one or more of the
substances.

Individual Susceptibility.

It is not only the particular properties of the chemical agent in question that determines the risk to the
worker; an equally important consideration is the individual susceptibility, and this can depend on a
number of factors:

Pregnancy or women who have recently given birth.

CHIP 4 provides a number of risk phrases which are of particular significance to pregnant women:

R40: possible risk of irreversible effects.

R45: may cause cancer.
R46: may cause heritable genetic damage.
R61: may cause harm to the unborn child.
R63: possible risk of harm to the unborn child.
R64: may cause harm to breastfed babies.

Examples of chemicals which can have an adverse effect on pregnant women include:

 Organic mercury (slows growth and affects development of the central nervous system)
 Carbon monoxide (crosses the placenta and affects the foetus)
 Lead (can cause miscarriage, stillbirth and infertility)

Younger or older workers.

Younger workers are vulnerable to chemicals which affect the reproductive system (e.g.
insecticides/pesticides), and older workers may have pre-existing medical conditions (e.g. respiratory
or skin problems) that increase the risk from certain substances.

Lifestyle.

Personal habits can contribute to the vulnerability to harm from exposure to certain chemicals.

The effects of some chemicals will be increased where the person is a smoker, drinker or drug user.
We have already referred to the synergistic effect of exposure to asbestos fibres in smokers.
Respiratory and lung disorders arising from smoking will compound the effects of exposure to
airborne contaminants.

Excessive alcohol consumption leading to liver damage will reduce the body’s ability to metabolise
toxic chemicals. Dietary intake will affect the rate of absorption of certain occupational chemicals.

In practice, these factors should be addressed through the occupational health screening and health
surveillance programmes that should support the use of chemical agents in the workplace.
2.8 Exposure Time
We are already familiar with the concept of dose, i.e. level of exposure combined with duration of
exposure, and therefore the significance of exposure time.

The basic concept is that any “assault” on the body by a harmful agent is immediately countered by
the body’s natural defences. Study Unit B1 has considered various defence mechanisms that the
body employs. However, these defence mechanisms take time to respond.

If a low-level exposure occurs over a short finite time and then stops, the body has time to recover.

(If I suffer an acute exposure to ammonia gas, for example, at the STEL OES (3 times the LTEL
OES) for a short period, my lungs have time to clear the contaminant and recover from the incident,
and I should suffer no ill-effects.)

If a higher level exposure occurs over a short finite time and then stops, a greater degree of damage
is done and the body will take much longer to repair the damage. However, recovery will take place
since exposure has now ceased.

(If I suffer an acute exposure to ammonia gas, for example, at a much higher concentration than the
STEL OES, my lungs will suffer short-term damage (corrosion, irritation), but recovery will
commence as soon as exposure ceases, although it may take me some time to fully recover from
the damage done to the respiratory tract.)

If a higher level exposure occurs over a longer period of time, damage continues, which eventually
overwhelms the body’s defences. The level and duration of the exposure is such that recovery is not
possible because the body’s defences are not able to cope with the continued assault, and there is
no break from exposure to allow the body to recover.

(If I suffer chronic exposure to ammonia gas, for example, at a much higher concentration than the
STEL OES, my lungs will suffer continual damage from the corrosive and irritant effects, and the
respiratory defences will not be able to cope.)

We encountered the concepts of exposure time and dose when we examined hygiene standards in
unit B2, and you will remember that reduced time exposure is a possible control option for harmful
agents. However, it is important to be aware of the significance of likely duration of exposure when
assessing risk.

2.9 Exposure to chemical agents in the workplace

So far in this study unit, we have examined the broad categories of harm under which chemical
agents are classified and considered some of the factors that affect the risk to health arising from
exposure to these types of substances.

Now we look at the range of typical substances that might be encountered in an occupational setting
and study, in more detail, their specific harmful effects.

However, to begin with, let us quickly review the types of substances that we are likely to come
across in the workplace before examining typical examples along with occupations that present
exposure risk.

We have already seen how chemical health hazards may be divided into the following categories:

 Toxic, including carcinogenic.

 Corrosive and irritant.
 Dermatitic.

In addition, we have noted that chemical hazards can be classified according to their physical state
as liquids, dusts, fumes, mists, vapours or gases.

Liquids.

It has been estimated that two-thirds of all industrial injuries from chemicals are skin injuries caused
by direct bodily contact with liquid acids and alkalis, due to the corrosive effect of these substances.

Dusts.

Dusts consist of solid particles, and are created by such operations as grinding or sieving of solid
materials, controlled detonations and various drying processes.

Dusts can, in the event of constant exposure, cause serious lung damage in the form of
pneumoconiosis. General poisoning can result from the inhalation of toxic dusts (e.g. lead).

Fumes.

Fumes are finely particulate solids which are created by condensation from a vapour, very often after
a metal has been converted to the molten state. The metallic fumes are usually the oxide of the
metal, and produce highly toxic fumes.

Lead, cadmium, zinc, copper and magnesium are particularly hazardous and inhalation of these
fumes can give rise to an illness known as 'metal fume fever'. Complete removal from the exposure
sees full recovery within a matter of days.

Mists.

Mists consist of finely suspended droplets formed by condensation from a gas, or the atomising of a
liquid, or from aerosols.

Mists are created by many industrial processes, such as chromium plating or the charging of lead
acid batteries, and serious hazards can arise. The mists are caused by chemical reaction.

Vapours/Gases.

Vapour is the gaseous form of a solid or a liquid. Rise in temperature causes the vaporisation.

Examples of vapours are petroleum and solvent vapours.

Mercury is a particularly hazardous chemical, as we will see later, since it can vaporise at room
temperature and create a toxic atmosphere. Poisoning has been caused by the inhalation of mercury
in a laboratory where mercury has been spilled, with rapid vaporisation.

Gas is a formless chemical which occupies the area in which it is enclosed. Its form can be changed
by the combined effect of increased pressure and decreased temperature.

There are many toxic gases used in industry, such as chlorine, hydrogen sulphide, etc. Many are
nasal and respiratory tract irritants. This irritant factor can give rise to immediate evacuation (e.g.
sneezing) before too much harm is done to the tissues lining the respiratory passages.

Liquids, particulates, gases and various aerosols are all physical states, which are liable to create
hazards in terms of corrosion or toxicity.

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2.10 ACGIH - American Conference of Governmental Industrial

Hygienists, Inc.
The American Conference of Governmental Industrial Hygienists (ACGIH), is an organisation open
to all practitioners in industrial hygiene, occupational health, environmental health or safety. Their
web site is http://www.acgih.org/.

ACGIH publishes over 400 titles in occupational and environmental health and safety. They are most
famous for their Threshold Limit Values publication which lists the TLVs for over 700 chemical
substances and physical agents, as well as 50 Biological Exposure Indices (BEI) for selected
chemicals.

There was considerable controversy concerning the regulatory implications of TLVs, and the ACGIH
was sued by a manufacturer's association in December 2000. See the links below for more
information. ACGIH's press release on the TLV lawsuit settlement.

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3.0 Toxic Hazards

Chemicals may be considered in the following toxic groups:

Respiratory Irritants.
Chemical irritants have an instant effect on the airway (the respiratory tract and the lung tissues) and
can cause immediate and long-term damage. The effect of an irritant may appear immediately after
exposure, or there may be a delayed reaction.

Examples Producing an Immediate Effect

Halogens and halogenated compounds, bromine, chlorine and fluorine; hydrogen fluoride and
hydrochloric acid; ammonia vapours.

Exposure to these chemical gases or vapours to any great degree can produce serious damage.

However, the irritant effect is such that a very mild unprotected exposure causes immediate
discomfort and hasty withdrawal from the vicinity.

Severe exposure may result in pulmonary oedema - the tissues of the air passages become
'waterlogged' and swollen, preventing air exchange.

Examples Showing Delayed Action

Certain metallic compounds, e.g. nickel carbonyl or tetracarbonylnickel (0); iron carbonyl; nitrous
fumes (particularly hazardous); certain phosphorus compounds.

The inhalation of these chemicals can induce dizziness, nausea and vomiting and considerable
difficulty in breathing at an early stage. Removal to fresh air can remove the symptoms, and the
apparent recovery of the patient follows.

The delayed action occurs some 12 hours or more later, when the patient becomes breathless,
shows signs of cyanosis and complains of chest pains, indicating pulmonary oedema.

3.1 Chemical Asphyxiants

Here, there is a physiological effect on the blood and body tissue.

Haemoglobin is the pigment in the red blood cells which, in the form oxyhaemoglobin, conveys
oxygen to the tissues where the oxygen is released for respiration.

Certain substances combine with the haemoglobin and prevent its function as oxygen carrier, which
causes tissue asphyxia.

Examples are:

 Carbon monoxide, a very dangerous asphyxiant, which forms carboxyhaemoglobin. The

inhalation of carbon monoxide is lethal.
 Nitro- and amino-compounds react with haemoglobin to form methaemoglobin; this compound
is similar to oxyhaemoglobin but is more stable. Absorption of toxic concentrations of aniline
results in a bluish tint to the lips, due to the conversion of the haemoglobin to
methaemoglobin.
  Nitrobenzene exposure can cause chronic poisoning, inducing cyanosis, fast irregular
breathing, convulsions and coma.
 Cyanides are extremely toxic and dangerous, and full precautions in their use are essential.

Many compounds can be absorbed through the skin and this may, in fact, present a greater hazard
than inhalation. Chlorinated solvents are an example.

3.2 Haemolytic Poisons

Haemolysis is the destruction of the red cells of the blood, resulting in excretion of the broken-down
red blood cells and a loss of their function.

The most common example of haemolytic poisoning in industry is arsine.

Symptoms develop some time after exposure and consist of weakness, nausea, abdominal pain,
headache and drowsiness. Hospital treatment is required.

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3.3 Narcotics
Narcotics are organic substances, some of which have an irritating effect on the lungs; others have
little or no effect.

They are absorbed into the bloodstream with anaesthetic effect.

Chronic poisoning may result from continuing exposure.

Narcotics fall into four main groups:

 Those having an anaesthetic action.

 Those which injure the liver, heart and kidneys.
 Those which injure the blood-forming system.
 Those which injure the central nervous system.

The narcotic effects of the chemicals used in an industry should be carefully reviewed.

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3.4 Nervous System Poisons

Compounds which affect the central nervous system are hydrogen sulphide, phenols and cresols
and nicotine.
There can be corrosive action in some cases, and acute poisoning which results in faintness,
collapse and coma.

Liver and kidney damage may result, also oedema of the lungs.

3.5 Metallic Poisons

Many metals and their compounds are cell poisons. They destroy living matter with which they come
into contact. Typical examples are arsenic and mercury.

Mercury vapour can rise to toxic concentrations very quickly - it can also be absorbed through the
skin.

Mercurial poisoning can affect the gastrointestinal tract and can cause nervous and muscular
changes.

3.6 Carcinogens
Experimental work on animals has identified many substances shown to cause malignant tumours.
In addition, there is a range of substances which have been proved to induce cancer in humans from
occupational exposure in industry.

The more important chemical carcinogens are:

Halogenated compounds.

 vinyl chloride (angiosarcoma of blood vessels in the liver)

 tetrachloromethane (rat liver cancer)

Nitro-compounds.

 4-nitrobiphenyl (prohibited by COSHH)

 chrysoidine (an azo dye)

Aromatic amines.

 2-napthylamine (bladder cancer)

 benzidine or biphenyl-4, 4´-diamine (bladder cancer)

Polycyclic aromatic hydrocarbons.

 mineral cutting oils (scrotal cancer)

 benzo(a)pyrene or 1,2-benzpyrene (soots, tars, vehicle exhausts)
 Natural carcinogens - aflatoxin B1 (animal carcinogen)

Inorganic carcinogens.

 nickel, chromium, arsenic compounds (occupational lung cancer)

  asbestos (lung cancer and mesothelioma)
 Benzene (leukaemia)

4.0 Examples of Toxic Hazards

Lead.

Elemental lead is one of the heavy metals, having a relatively high density of 11.34 kg m-3 (most
other metal densities are below 9 kg m-3).
It is not a reactive metal, especially under average conditions. Being fairly soft and having a low
melting temperature of 600°C, as well as being a relatively easy metal to extract from its principal
ore, lead sulphide, lead has provided mankind with a useful material of construction since early
times. Some lead figures are believed to have been made as early as 3800 BCE and lead beads
have been found at Catalhuyuk in Turkey, dating back to 6400 BCE. The use of lead in plumbing
systems was well established by the time of the Roman Empire; the Latin name for lead, plumbum
nigrum, literally 'black soft metal' has given the English language the word 'plumber'.

Lead compounds have been, and are still being, used as raw materials in manufacturing processes,
and as a material of construction.

They can be roughly categorised into inorganic lead, e.g. lead oxide in lead/acid batteries, lead
chromate (chrome yellow) red lead (Pb2O4) used for pigments (although its use is being reduced
and banned by some countries), and organic lead, e.g. petrol antiknock agent, lead tetraethyl
(Pb(C2H5)4), another product which will eventually be discontinued.

Mode of Entry.

Lead metal in its massive solid state has virtually no ability to be absorbed into the body by any of
the three normal modes of entry.
As a fume or very finely divided dust, lead inhalation becomes a serious risk as a potential mode of
entry. In this form, however, lead metal will almost certainly have been changed to lead oxide, so the
absorption reactions will not be truly representative of lead metal itself. Absorption by skin contact or
via the gastrointestinal tract has no occupational risk.

For inorganic lead compounds, inhalation of dusts generally poses the most serious situation.
Absorption by skin contact and ingestion is limited.
For organic lead compounds, inhalation and skin contact form the main occupational mode of entry
for absorption into the body. Ingestion poses only a minor risk. The best example of an organic lead
compound is lead tetraethyl. It is highly volatile at normal temperature and passes easily through the
skin following skin contact.

When lead compounds are absorbed into the body, the inorganic compounds produce different
symptoms from the organo-lead compounds.

An important point to note about the entry of the element lead into the metabolism of the body by
occupationally-induced situations is that lead is also a ubiquitous substance in the natural world. The
element enters into our bodies in small but regular doses from the food we eat and the water we
drink.
As lead has no known beneficial effect in the metabolic process, it is not required and so any
additional absorption of the element lead resulting from occupation is an added body burden.

Target Organs.

The target organs associated with lead intoxication are:

 Central nervous system.

 Gastrointestinal tract.
 Blood and blood-forming organs.
 Exterior (straightening) muscles of the wrist or foot.
 The gums.

Lead becomes incorporated in bone structure where it accumulates, giving it a site where it can
become a cumulative toxin.

Effects and Symptoms.

Intoxication by inorganic lead compounds leads to general symptoms related to the gastrointestinal
tract, the nervous system and the blood.

Acute intoxication, resulting in general from inhalation of high concentrations of lead fume or dust,
produces nausea, vomiting and headaches. This is often followed by constipation and severe
intermittent colic. During the attack of colic, the victim becomes very pale, feels cold and may sweat
freely. If the brain becomes affected, then dullness, restlessness, tremor convulsion or coma may
develop.
When exposure has occurred over long periods and chronic intoxication takes place, other clinical
symptoms develop. The classical symptoms are headaches, anaemia, palsy (muscle weakness), the
appearance of a blue line on the gums and, very rarely, encephalopathy (changes in the nerve
output of the brain).

(i) The headache is related to adverse effects on brain activity.

(ii) Anaemia results from the interference by leaded metabolic substance in the synthesis of
haemoglobin.

(iii) Palsy results from the paralysis of the motor neurones that control muscles. The particular
muscles concerned are those liable to fatigue due to occupational activity. “Wrist drop” was a
characteristic symptom where the conditions had been allowed to proceed untreated. “Foot drop”
has also been recorded. With better hygiene control, these conditions hopefully belong to
occupational disease history.

The famous blue line on the gums associated with lead intoxication results from soluble lead
compounds being precipitated from the general circulation as lead sulphide in the gum region below
the lower front teeth. The sulphide is a black compound but appears blue in the gum tissue.

The condition results from the reaction of lead ions with sulphide ions generated by micro-organisms
in gum tissue. The blue line is not a direct measure of lead intoxication, only an indication of the
absorption of lead into the body’s metabolism.
The depth of colour produced is, however, an indication of the duration and severity of the exposure
to which the victim has been subjected.

The incorporation of lead into the body metabolism causes certain biochemical abnormalities to
occur. These effects are related to the impairment of haemoglobin synthesis. The particular effects
are outside the requirements of this course, but you should note they are used in the diagnosis of
lead intoxication.

One point of note is that the presence of lead can cause a breakdown of haemoglobin structure. It
can therefore be classified as a weak haemolitic toxin.

The concentration of lead compounds in the blood as a measure of lead intoxication must be used
with extreme caution. Lead is stored in the body from natural and possibly occupational input; the
blood lead level generally indicates the state of the balance between the body and the leaded bone
store.

However, it has been shown that the balance can be upset and, under certain circumstances,
massive amounts of lead can be discharged into general circulation from the bone store. A raised
body temperature can cause this situation to occur.

Absorption of lead tetraethyl, or tetraethyl lead (TEL), as it is more accurately described, is a very
hazardous situation. The material is highly toxic in low atmospheric concentrations, and inhalation of
the vapour can have fatal consequences.

Its absorption into the body mainly affects the central nervous system. It produces restlessness, a
raised level of excitement and talkativeness, muscular twitching and possible delusions, acute and
violent mania. These conditions are accompanied by a fall in body temperature and a drop in normal
blood pressure.

Where the level of intoxication is lower, headaches, vertigo, fatigue, a sense of physical weakness,
and insomnia with disturbing dreams are classic symptoms.

Encephalopathy is also associated with absorption of organic lead compounds.

In all cases, the severity of the effects of lead in the body depends upon the difference between the
level of absorption and that of excretion. The ratio of these two factors goes a long way to
determining whether certain individuals are affected or not by the lead in their body.

Occupations and Persons at Risk.

The following list covers commonly occurring situations:

 Lead smelting.
 Lead chemical manufacture.
 Lead/acid battery manufacture.
 Shipyards.
 Petrol manufacture and handling.
 Plumbers.
 Painters.
  Welders.

Control measures are covered within B4 as well as within the Control of Lead at Work Regulations
2002

4.1 Mercury
Elemental mercury is another member of the heavy metal group, with a density greater than lead.

It is unique in that it is a liquid at normal temperatures and pressures, a property used to advantage
in the electrical industry where liquid contacts are required, or for measuring equipment such as
thermometers or barometers.

It is a relatively un-reactive metal, quite easily extracted from its main sulphide ores. For this reason,
mercury, like lead, has been known for a considerable time. Its toxic potential was recognised by the
Romans.

Mercury is able to form inorganic compounds, e.g. mercuric chloride (HgCl2) (corrosive sublimate),
mercurous chloride (Hg2Cl2) (calomel), and organic compounds, e.g. diethyl mercury or methyl
mercury hydroxide.

Mode of Entry.

Elemental mercury liquid is not absorbed by the gastrointestinal tract or through the skin in normal
circumstances. Absorption of mercury metal vapour does occur readily following inhalation into the
lungs. There is vague evidence that the vapour is absorbed into the body following skin contact.
Liquid mercury does readily form mercury vapour in considerable concentrations at room
temperatures, but the ability to vaporise is almost completely prevented by the formation of a dust or
moisture layer over the free surface of the liquid.

It is for this reason that many schools or electrical workshops have mercury vapour-free
atmospheres, but have small lakes of mercury metal under benches or the floor.

The situation changes dramatically if the temperature is raised above normal ambient levels, and
vaporisation then becomes vigorous and potentially very hazardous.

When mercury liquid is used with surfaces open to the atmosphere, a layer of water should be used
to make a safety seal.

Target Organs.

The two main target organs for mercurial intoxication are the brain and kidneys. An acute response
following inhalation of fumes or gases containing elemental mercury produces irritation with a
delayed cough and chest pains; often this proceeds to acute pneumonia. The eyes are also affected
by absorbed mercury vapour.

Chronic Effects and Diagnosis.

The vapour from mercury metal is absorbed into the blood following inhalation and becomes
deposited mainly in the brain. The metal molecules become involved in metabolic reactions which
result in injury to the central nervous system (CNS).
Inorganic compounds of mercury can also affect the CNS but, in general, kidney damage occurs.
The excretion of protein in the urine is an indication of this condition.
Exposure to mercury vapour can result in a brownish discolouration developing in the lens of the
eyes. The condition does not appear to interfere with vision and it can occur without other symptoms
of mercurial intoxication.

The initial signs of mercurial intoxication include general symptoms such as headaches and a
gradually developing sallow colour. Irritability and aggressiveness develop, as do tremors in the
hands, which have a marked effect on the ability to write. The tremors also occur on the eyelids, lips
and tongue. The tremor condition is aggravated by alcoholism. Gingivitis occurs, and in severe
cases this results in teeth being lost. Gums become very sore and swollen, bleed easily and may
ulcerate.

The marked effects on the personality resulting from damage to the CNS can become extreme. The
expression 'Mad as a hatter' referred to an occupational condition resulting from the use of hot acid
solutions of mercuric nitrate in treating rabbit furs to produce felt for hats.

In extreme cases of chronic mercurial intoxication, loss of memory, hallucinations and considerable
loss of intellectual capacity occurs.

Where organic mercury compounds have been absorbed into the body, the nervous condition
(tremor and reduced visual field) is more pronounced than the psychotic condition (erethism).

Where kidney damage has occurred, apart from excretion of protein, loss of albumin may result as
well. This can upset the normal fluid balance causing a more generalised kidney failure. When the
victim is removed from exposure, complete recovery from the adverse condition usually occurs.

One particular effect from mercury fulminate is the development of dermatitis. Swelling and itching of
the affected area are the primary symptoms. This is followed by local oedema and pus-forming
pimples. If the powder becomes lodged in skin folds or cracks, painful necrotic ulcers may develop.
Inhalation of the dust causes extreme irritation of the eyes, nose and throat.

Occupations and Persons at Risk.

Risk from mercurial intoxication occurs in:

 Mining and processing of mercury ores.

 Manufacture of thermometers, barometers and electrical switchgear.
 The use of mercury amalgams in dentistry and water-gliding.
 Manufacture and use of mercury compounds, e.g. inorganic salts used in antifouling paints, or
fur felt treatments.
 Organo-mercury compounds used as fungicides in seed dressing, e.g. ethyl or diethyl
mercury.
 Manufacture of detonators using mercury fulminate.

4.2 Benzene
Benzene has a molecular formula C6H6 and its structural formula provides the basic structure for
aromatic chemicals (Figure 4.1).

Figure 4.1 Molecular structure of Benzene

Benzene is a colourless, sweet-smelling, volatile liquid with a boiling temperature of 80°C. It is very
harmful and is absorbed into the body following inhalation and/or skin contact.

Acute Effects.

Inhalation of the vapour in high concentration causes headaches and dizziness, and can act as a
stimulant.

These symptoms will soon be overtaken by narcosis which can progress to coma and death. The
vapour also causes considerable irritation to the eyes and mucous membranes of the nose, nasal
cavities and the mouth.

Chronic Effects.

Absorption of low concentration of benzene into the body over a long period of time results in severe
anaemia. This results from the impairment of the blood-forming metabolism in the bone marrow. The
condition can progress to aplastic anaemia as the terminal phase. It is now generally accepted that
leukaemia, the blood cancer, can result from absorption of benzene into the body over long periods
of time.

The homologues of benzene, toluene and the xylenes, produce the same acute chronic effects as
benzene, but their toxic action is very much less than benzene.

It is believed that as alkyl groups are added to the benzene ring structure, the carcinogenic risk
declines markedly.

One word of caution: you should be aware that the homologues of benzene invariably contain small
amounts of benzene as an impurity. This could lead to an enhanced toxic potential due to the
presence of these trace quantities.

4.3 Phenol
Phenol has a molecular formula C6H5OH and a structure related to benzene which is shown in
Figure 4.2.

Figure 4.2

Acute Effects.

The main effect following a high level of absorption occurs within the central nervous system.
Collapse and coma follow rapidly after the body has been in contact with phenol solutions. Death
often results following contact. Periods of between 30 minutes and several hours before death
occurs have been recorded, depending upon concentration of the liquid and the area of body
affected.

In high concentrations, phenol solution can cause death if the body area contaminated exceeds 15-
20%.

Where death is delayed or the absorption is not fatal, extensive damage occurs in the kidneys, liver,
pancreas and spleen. A pulmonary oedema could also occur following inhalation.

Chronic Effects.

Exposure to phenol, and absorption over long periods, especially of vapours or fumes, cause
digestive disturbances, e.g. vomiting, excessive salivation or diarrhoea. Nervous disorders, e.g.
headache, dizziness and mental disturbances can also occur. Dermatitis often follows contact with
the skin. Liver and kidney failure following long exposure have been recorded as causes of death.

4.4 Coal Tar Pitch Volatiles

These are the vapours and fumes which are evolved from a liquid residue formed when coal is
heated and decomposed in the absence of air.

Coal tar pitch is the complex liquid mixture of mainly organic aromatic substances and ammoniacal
liquors which remain after coal gas has been produced from coal. In more recent times, coke ovens
and patent fuels manufacture provide equivalent hazardous conditions.

Toxic Hazards.
The general presence of coal tar pitch volatiles is considered as a potential carcinogenic or co-
carcinogenic risk to humans.

The level of concentration should be well below the working limit for possible 'simple toxic'
concentrations of many substances contained within the vapours.

Associated Substances.

The following list comprises the better-known compounds derived from coal tar pitch:

 Benzene.
 Toluene.
 Xylenes.
 Napthalene.
 Phenanthrene.
 Anthracene.
 Crude tar bases (Pyridine 0.1).
 Crude tar acids (phenols, cresols, xylenols).

From the reactions during the decomposition of coal, aromatic polycyclic hydrocarbons will be
produced. It is very likely that these contribute to the carcinogenic potential of the coal tar pitch
volatiles.

4.5 Aliphatics
Aliphatic halogen compounds are used extensively as solvents and reagents for manufacturing
processes.

Apart from their ability to cause dermatitis, and especially the particular condition termed 'chloracne'
from compounds containing chlorine, they can cause carcinogenic responses in animals as well as
in humans, e.g. vinyl chloride (see later). They can cause acute narcotic responses in high
concentrations; they can be addictive, and can cause liver failure.

Target Organs.

Aliphatic organic compounds have a high affinity for fats, waxes and greases, hence their use as
solvents. When they are absorbed into the body, they will concentrate in areas of high body fat. The
two main target organs are the brain and the liver.

In the brain, they interfere with the central nervous system which results in a narcotic response.

In the liver, they cause toxic metabolic processes which can eventually lead to necrosis (breakdown)
of liver tissue. As the liver is the main detoxification organ for harmful body substances, any failure
will result in rapid body damage, even premature death.

Examples.
Two classic examples of halogenated hydrocarbons which exemplify the above-stated problems are
trichloroethylene and tetrachloromethane (carbon tetrachloride).

Trichloroethylene (TCE).

This compound was officially listed as an animal carcinogen in July 1976 by the United States
National Cancer Institute, and therefore constitutes a potential risk to humans.

Since that time, research has not identified a definite link with human risk.

In the UK, the substance is still under review, but concern by the Health and Safety Executive may
be described as marginal.

The potential of TCE to trigger a narcotic response is accepted, and strict control over airborne
concentration should be maintained.

Where a gassing accident situation occurs, the result may be permanent brain damage or death. In
low concentration, the effects are mainly debilitating, i.e. headaches, drowsiness, fatigue and loss of
ability to concentrate.

The potential risk from TCE as a liver toxin generally results from low, and apparently harmless,
inhalation over many years. As a breakdown in the liver structure occurs, i.e. cirrhosis, liver functions
are impaired. Stomach pains, vomiting and jaundice are typical symptoms.

Tetrachloromethane (CTC).

CTC (carbon tetrachloride) is cited as a substance with a carcinogenic risk for humans.

There is, however, some doubt as to the direct ability of CTC to evoke a carcinogenic response on
its own. Many references to CTC list the substance as a co-carcinogen, i.e. it has the ability to assist
another compound to evoke a carcinogenic response.

CTC has the ability to cause narcosis in the same way as TCE and the symptoms are similar.

As well as affecting the brain (CNS) and the liver, CTC causes injury to the kidneys. There is
evidence to suggest that the kidneys are more vulnerable to attack than the liver.

CTC has been used in the past in portable fire extinguishers, a wax polish solvent and a general
degreasing agent. It is still used for certain chemical manufacturing processes, e.g. fluoroalkanes
used for aerosol propellants.

Other chlorinated hydrocarbons that may be encountered are 1,1-trichloroethane (genklene), sym-
tetrachloroethane, trichloromethane (chloroform), and tetrachloroethylene (perchloroethylene).

4.6 Isocyanates
Organic di-isocyanate compounds are used to make adhesives, synthetic rubber, polyurethane
paints and lacquers and quick-drying printing inks. Their most important application, however, is in
the manufacture of plastics, especially the flexible and rigid (poly) urethane foams.

A large number of di-isocyanates can be made, but only a few have important industrial applications:

(a) Hexamethylene di-isocyanate (HDI) was the first to be used, but this aliphatic isocyanate is very
volatile and was found to cause significant respiratory problems, following which it was withdrawn
from use in Great Britain when a suitable alternative was found.

(b) This was toluene di-isocyanate (TDI), an aromatic compound; but this, in turn, was eventually
found to be responsible for severe respiratory problems because of its irritant effect. However, TDI is
still widely used in the manufacture of flexible foams and paints; it presents a severe hazard to fire
fighters.

(c) A more recent introduction, with virtually no vapour hazard, is methane diphenyl isocyanate
(MDI).

Effects and Symptoms.

Of the commonly used isocyanates, both HDI and TDI act as irritants and allergens.

Irritant effects include rhinitis (inflammation of the mucous membrane of the nose), pharyngitis
(inflammation of the part of the throat immediately beyond the mouth), bronchitis, and, in cases of
excessive exposure, bronchiolitis obliterans.

In most cases, the symptoms and signs clear rapidly after the worker is removed from contact with
the isocyanate.

But in many of those who have shown a quick initial recovery, the symptoms have recurred, often
violently, after further contact with even very low concentrations of isocyanate (a condition known as
sensitisation).

Others are known to suffer from a chronic form of asthma, particularly in cold weather, and have to
depend on bronchodilator inhalations to ameliorate the symptoms.

Question How isocynate effect our boby system.

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4.7 Polycyclic Aromatic Hydrocarbons

Cancer of the skin is associated with processes where workers come in contact with substances
containing a group of chemicals called polycyclic aromatic hydrocarbons (PCH).

By their name, you should be able to deduce that they have within their structure benzene rings, that
they are joined or fused together, and that they only contain the atoms of carbon and hydrogen.
A well-known member of the series is benzo(a)pyrene (1,2-benzpyrene), the structure of which is
shown in Figure 4.3.

Figure 4.3

There are, however, many such compounds, and a large number have been listed as having
carcinogenic potential. They will always be found together in mixtures having a varying level of
concentration.

Recent evidence suggests that the carcinogenic potential of PCH is enhanced by a very small
concentration of extremely potent PCH containing atoms of sulphur in its structure.

Occupations or Processes at Risk.

The following is a list of processes or occupations where workers are at risk from PCH mixtures:

 Coke ovens.
 Patent fuel manufacture.
 Distillation of coal tar.
 Bitumen-felt production and uses (e.g. roofing).
 Automatic lathe worker.
 Lubrication of machinery.
 Petroleum workers.
 Road workers (laying tarmac).
 Underground telephone electricity linesmen (making waterproof pitch joints).

Secondary exposure can occur from petrol or diesel engine exhaust fumes and the burning of
carbonaceous materials, e.g. coal, oil or domestic refuse, especially on rubbish tips.

The types of materials commonly associated with these processes are coal tar, pitch, asphalt,
creosote and mineral oils.

Effects and Symptoms.

The substances mentioned are all skin irritants. You will remember that oils and greases can cause
non-infective dermatitis; the same is true for coal tar, pitch or creosote.

Following long periods of exposure, the irritant effect develops into more serious conditions where
benign and malignant growths may be formed.
The growths occur as small lumps with a wart-like appearance, hence the name 'tar wart'. In the
early stages of the growth, it is very likely to be of benign nature, but if it goes untreated, it will
eventually become malignant.

Where the wart-like growths develop after only short exposures, recovery from the condition is likely
to be complete, especially if exposure ceases.

Where the growths take a long time to develop, the progression to the malignant state is more likely.
Due to the latency period, the condition can develop long after exposure has ceased. With the
development of the malignant state, the wart becomes ulcerated.

Skin cancer is described as squamous celled carcinoma. This means that the disease is involved
with the cellular structure associated with the epithelium. In the skin, these cells are found in the
lower levels of the epidermis, between the dermis and the horny keratinised outer layer. This type of
skin cancer can occur all over the body, but is usually confined to the main regions of exposure.

Main Body Regions Associated with Skin Cancer.

The main regions where skin cancer develops are generally related to the type of occupation to
which the person belongs:

 For shale oil workers, the growth commonly occurs on the arms, but cancer of the scrotum
may also develop.
 For persons working in the cotton industry with mule spinners, cancer of the scrotum is the
usual site of the disease, as in the case of persons working on automatic lathes or involved
with lubricating machinery.

Where carbonaceous mixtures and their fumes are involved, the condition can develop over a wider
region, e.g. someone on a patent fuel plant could develop skin cancer on the eyelids, face, neck,
arms, thighs, scrotum or behind the ears.

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4.8 Mineral Oils

Cancer of the scrotum occurs mainly in workers who are exposed to mineral oils which, by the
nature of the process they operate, cause their clothes to become heavily contaminated over the
thigh region.

Wart-like lumps are produced, which develop into painful sores; if the condition is allowed to
develop, the lesion will spread and cause objectionable odours from the decaying flesh around the
ulcerated condition.

Without medical intervention, tumours will spread to the testicle, spermatic chord and into the
abdomen. For many, the condition has been fatal. During the time leading up to death, considerable
weight loss and pain can occur.
If early diagnosis of the condition is made, then, as with other skin cancers, recovery from the
condition becomes possible. Better still, the condition can be avoided if sufficient care is taken to
'design out' conditions that allow a worker to become saturated with oil.

When there is a possibility of oil contamination of the genital area, the workers must be made fully
aware of the potential risk, and be provided with special personal hygiene facilities, i.e. regular use of
clean working clothes and underwear, with special washing facilities.

To overcome possible reticence in reporting adverse genital conditions, compulsory medical

inspections must be adopted as a back-up service.

4.9 Asbestos
It is generally accepted that the type of asbestos classified as crocidolite (blue asbestos) is the
causative agent for mesothelioma. It belongs to a group of inorganic crystalline fibrous silicates
generally called asbestos.

Mesothelioma is the name given to malignant tumours that develop in the pleura and the
peritoneum. It is a very rare disease in normal circumstances. Where there has been exposure to
asbestos, however, the possibility of developing the disease is markedly increased.

Evidence from many studies indicates that not only are the workers directly involved with the
material at risk, but also those who work in the vicinity of its use.

The problem also affects the localities around the area where the material is used, and a high
incidence of the disease often occurs in areas 'down wind' from factories involved with asbestos
products. The families of asbestos workers are also at risk, as cases have been reported where
wives and children have succumbed to the disease.

The risk of mesothelioma from the other types of asbestos in general use, i.e. amosite (brown
asbestos) and chrysotile (white asbestos), is considerably reduced, but there is a risk.

Asbestos Types - Crocidolite( Blue) Chrysotile (White) Amosite (Brown)

The mode of entry into the body is generally by inhalation into the lungs. Mesothelioma of the pleura
occurs when the asbestos fibres have migrated through the lung structure into the pleura, where
they can remain undisturbed until they trigger off this sinister disease.
Mesothelioma of the peritoneum can result from fibres migrating through the gastrointestinal tract to
reside in the relative physiological calm of the peritoneum. The fibre may enter the gastrointestinal
tract by simple ingestion, but the mechanism most likely is the swallowing of fibres removed from the
respiratory system by the cilia escalator after inhalation.

Tumour development in the peritoneum sometimes occurs from tumours which began in the pleura.

Factors Involved in Tumour Formation.

The carcinogenic potential of asbestos substances is generally accepted as being related to the
physical size of the fibre and not its chemical composition.

The importance of size has been demonstrated experimentally on rats, where crocidolite fibres which
had been reduced to a non-fibrous dust did not evoke a carcinogenic response in the pleura,
compared with fibrous crocidolite which did evoke a response.

The evidence as to the precise size of fibre required to evoke the carcinogenic response is still
subject to considerable debate, although a general area of potential harm is agreed. Fibres having
diameters greater than 0.2 µm but less than 0.5 µm have been given in research literature. Fibre
lengths in excess of 10 µm or between the range 10 to 80 µm have been put forward.

The aspect ratio, i.e. the ratio of fibre length to diameter, has been quoted as 10:1 and 5:1.

The general standard for defining risk fibres are those which have a length greater than 5 µm and a
diameter less than 3 µm, with an aspect ratio of 3:1. There is still some doubt about the validity of
these dimensional characteristics in determining risk.

An important question arising from the relationship between the physical dimension of crocidolite
fibres and their ability to evoke a carcinogenic response is: 'Can other fibrous materials evoke the
same response?'

The answer is unfortunately 'yes'. Aluminium silicate fibres and glass-fibres of equivalent dimension
have induced pleural tumours in experimental animals.

The ability of crocidolite to migrate into the pleura and peritoneum and evoke a harmful response is
generally believed to be related to its ability to produce fine, straight fibres. They are able to break up
into the size range which can migrate fairly freely in body tissue and take with them their potential for
harm. When they cease their wandering and 'retire' to a quiet haven, they are then able to
concentrate their irritation in that particular area.

Amosite tends to produce less fine fibres than crocidolite; its potential for harm is therefore reduced.

Chrysotile forms curly fibres which tend to gather into bunches. These properties reduce its ability to
migrate through tissue, which considerably reduces its potential to evoke mesothelioma; but, if finely
milled, the curly fibres can be reduced to dimensions comparable with crocidolite fibres, so the
potential of white asbestos to evoke mesothelioma becomes dramatically increased. It is a point
which is not well publicised.
The exact mechanism by which the cell damage is caused is unknown. One tentative hypothesis
postulates that the potentially harmful size range of the fibres equates to that of viruses, but the
exact relationship has not been explained.

Symptoms:

Pleural Mesothelioma.

In the early stages of tumour growth, there is an increase in fluid around the lungs, which causes
breathlessness and a feeling of heaviness within the chest. It is often mistaken for a heart condition
or the ageing process.

As tumour growth rate increases, the lungs and structures in the thoracic cavity become more
compressed until the effects are fatal. Pain usually only develops in the final stages of the disease,
due to the effects upon the nerves in the walls of the thoracic cavity and in the spine. The pain level
is very difficult to control.

Peritoneal Mesothelioma.

The tumour development follows a similar course to that in the pleura. Initially, a general swelling of
the abdomen occurs which is often mistaken as 'middle-age' spread. As the tumour size increases,
normal movement of the intestine is impeded and constipation follows. Pain is sometimes
experienced when defecation takes place. Eventually, cramp pains cause the victim to seek medical
help.

In both cases, the medical diagnosis of the condition is of no value. The victim has, by this time, long
passed the point of no return. One glimmer of hope is that in a few cases, tumours have
spontaneously disappeared.

About six months after recognising there is something wrong with their bodies, the victims will
usually seek medical advice. Few live longer than about a year after consultation; many less.

It is not possible to define conditions or safety limits whereby this form of cancer can be prevented.
There is little or no hope of recovery if the condition develops.

The condition occurs fairly readily where there is exposure to blue asbestos. It is likely to arise from
brown asbestos and may possibly arise from white asbestos.

The latency period of mesothelioma is not well-defined. Values ranging from 5 to 60 years are
quoted; the average is about 25 years. Exposure times have been as low as two months.

Except for laggers and insulators whose exposure ranges over the working lifetime, i.e. 25-50 years,
the average exposure for victims in one epidemiological survey was about 10 years.

These facts are put forward as the basis of the argument that not only should blue asbestos be
banned from use, but the other forms as well. There are counter arguments of economics related to
employment in the asbestos industry, and the value of asbestos as an industrial and social material
of construction.
4.10 Vinyl Chloride
Occupationally, exposure to vinyl chloride is linked to angiosarcoma of the liver, the name given to
malignant tumours which form in the cells lining blood vessels. It is a very rare condition, which can
occur in any blood vessel, but as occupational diseases, only tumours of this type in the liver are of
any significance.

Vinyl chloride monomer (VCM) is a small unsaturated chlorinated ethene compound, CH2:CHCl
(chloroethyene) and is the basic monomer used for the production of polyvinylchloride polymers.

The main victims have all been exposed to high concentrations of the vapour when carrying out
cleaning operations in polymerisation vessels, but some workers were only concerned with other
manufacturing processes.

Entry into the body is believed to be by inhalation into the lungs, followed by absorption into the
blood. The absorbed vapours are then deposited in the liver where biochemical reactions involve the
material in liver metabolism. Experimental data on humans have found that very little of the VCM
inhaled is expired from the body.

There is no evidence of absorption into the body via skin contact.

Symptoms.

In its early stages, only minor liver function abnormalities are experienced. The condition is only
identified by exhaustive liver function tests. Liver enlargement can be detected and a high blood
pressure in the portal vein (portal hypertension) can occur. This can lead to leakage of fluid
(oedema) into the abdominal cavity. Serious bleeding into the gastrointestinal tract from ruptured
blood vessels has also occurred in some cases.

The tumours eventually invade the whole liver and the victim dies. Secondary growths resulting from
the original growth form widely as the disease progresses. There is no known cure.

Due to the relatively few deaths from the disease, no accurate latency period for the disease has
been established; from reported cases, an average of about 15 years can be calculated, although
the range is from 4 to 28 years.

Occupations at Risk.

The main victims of this disease are workers on the polymerisation plants using VCM. One case has
been reported of a worker involved in the production of VCM, and three cases involved workers
concerned with compounding and related processes.

There is no evidence that the polymerised material, polyvinylchloride (PVC), has any carcinogenic
potential, except where there may be residues of VCM in the material. No VCM has been detected in
PVC which has been decomposed.

Other Harmful Effects of Vinyl Chloride.

Having discussed the carcinogenic properties of vinyl chloride, it is appropriate to review the other
harmful effects produced by this material:

 Sclerotic skin changes: a marked hardening in the skin involving changes in the collagen
fibres.
 Osteoporosis: loss of calcium from the bones. It occurs in the bones of the fingers, hands and
wrists, but has also been reported in certain bones in the pelvic girdle.
 Reynaud’s Disease: a condition related to circulatory problems in the fingers. In this case, it is
not induced by vibration.
 Thrombocytopenia: a reduction in the number of thrombocytes in the blood, which reduces
the ability of blood to form clots; extensive bleeding occurs in open wounds and excessive
bruising is caused by relatively light knocks to the body.
 Fibrosis of the liver: mainly concerned with fibrotic changes in the portal vein.
 Impaired liver function: identified by abnormal results from blood and urine tests.
 Impaired lung function: associated with fibrotic changes in the delicate tissue sections of the
lung. It causes reduced efficiency in gaseous exchange.
 Narcosis: caused by inhalation of high concentrations of vinyl chloride. Fat-soluble
compounds have the characteristic action of depressing the central nervous system and
producing narcosis. The level of the effect is related to the extent that the substance dissolves
in brain tissue. Vinyl chloride vapour was once considered as a human anaesthetic.
Fortunately, there is no record of its general use.

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4.11 MbOCA (2,2 Dichloro-4,4 Methylene Dianiline)

MbOCA is used as a curing agent with isocyanate-containing polymers to make abrasion-resistant
urethane rubbers and moulded semi-rigid polyurethane foam articles with a hardened skin.

These materials are used in a wide range of products such as wheels, rollers, conveyor pulleys,
cable connectors and seals, anti-vibration mounts, etc.

It is manufactured in the UK by the reaction of formaldehyde with o-chloroaniline; some is also

imported. When pure, MbOCA is a colourless crystalline solid. The commercial grades are yellow-
brown and may contain small quantities of o-chloroaniline and polyamines. MbOCA and its salts are
classified as toxic, to be labelled with the risk phrases R45: 'May cause cancer' and R22: 'Harmful if
swallowed'.

Toxicity.

MbOCA has low acute toxicity when administered orally, but gives positive results in tests for
mutagenicity, so MbOCA or its metabolites may cause genetic damage in certain organisms.

In addition, long-term oral administration has been shown to produce an increase in the incidence of
tumours over those seen in controls. Also, long-term subcutaneous administration in rats resulted in
liver and lung tumours. As a consequence, MbOCA is regarded as an animal carcinogen.
There is not enough information available to assess the human toxicity of MbOCA following either
acute or repeated exposure. An epidemiological study of exposed workers did not reveal any
evidence of cancers attributable to MbOCA exposure. However, it could be argued that this study
was limited by lack of information on exposure levels and duration of exposure.

Carcinogenicity.

In view of the above comments, MbOCA is considered genotoxic and an animal carcinogen. The
mechanisms suggested for carcinogenicity seen in animal studies are related to metabolic processes
in the human liver; related substances, which are known human carcinogens, are believed to act by
similar metabolic pathways.

Consequently, MbOCA is regarded as carcinogenic to humans. A no-effect level has not been
established, and skin absorption may account for a significant proportion of uptake. Due to these
uncertainties, a Workplace Exposure Limit (WEL) has been set, with skin designated as the potential
absorption route.

This indicates the difficulty in interpreting toxicological data and extrapolating the findings to set
exposure standards for humans. The WEL set for MbOCA represents a compromise between
cautious interpretation of the available toxicological data and standards of exposure which industry
can realistically achieve.

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4.12 Corrosive and Irritant Hazards

The following are some of the corrosive and irritant substances which may be encountered in the
course of industrial processes:

Acids.

Sulphuric acid (H2SO4); hydrochloric acid (HCl); nitric acid (HNO3); phosphoric acid (H3PO4).

Alkalis.

Sodium hydroxide (caustic soda) (NaOH); potassium hydroxide (caustic potash) (KOH).

Gases, Vapours.

Tetrachloromethane (CCl4): gives off an irritant vapour, with corrosive and toxic effect.
Monochloroacetic acid (CH2Cl.COOH): a corrosive acid which can cause serious chemical burns
when it comes into contact with the skin or eyes, and also emits harmful vapours.
Chlorine: a greenish yellow gas with a choking, irritating smell; it is very poisonous, even if inhaled in
a very small quantity.
All corrosive chemicals can produce, under the correct conditions, damaging corrosive vapours.

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4.13 Occupations at Risk from Hazardous Substances

Occupation(s) Chemical Disease or effect
Brewery workers Carbon dioxide Asphyxia
Chemical laboratory Benzene Leukaemia
workers
Coin manufacture Nickel Dermatitis
Dye stuff manufacture Benzidine Bladder cancer
Electroplating workers Hydrogen cyanide Asphyxia
Fertiliser manufacturer Ammonia Irritant gas
Garage workers Carbon monoxide Asphyxia
Gardeners Paraquat (Weedol) Lung and kidney damage

Gas workers Benz(a) pyrene Cancer of the bronchus

Iron ore mining Radon Lung cancer
Lead workers (paint, pipes, Lead Lead poisoning (anaemia)
manufacture of petrol
additives)
Mercury workers Mercury Mercury poisoning (brain
(manufacture of mercury damage)
cells, treatment of furs,
dentists)
Nickel refining Nickel Lung cancer
Pesticide users DDT Nerve damage
Polystyrene manufacture Styrene Irritant (eye, nose,
respiratory tract)
Sewer workers Hydrogen sulphide Asphyxia
Shipbuilding, car brake Asbestos Lung cancer
shoe manufacture
Swimming pool workers Chlorine Irritant gas
Woodworkers Hardwoods Nasal cancer
5.0 Types of Injury and Preventative Measures
Injury through Contact with the Skin and Eyes.

The Skin.

The skin is extremely vulnerable, a simple fact not always appreciated by workmen who are required
to work in processes where corrosive chemicals are used, and protective clothing is required to be
worn. Two-thirds of all industrial injuries from chemicals are due to bodily contact with liquids causing
chemical burns.

Direct contact of corrosive liquids with the skin or eyes causes chemical reactions with the fatty
tissue of the skin, resulting in the evolution of heat and a breakdown of the various layers of skin.
This inflicts chemical burns of either first, second or third degree magnitude, depending on the
degree of penetration into the skin layers. Substantial third-degree burns can be very serious,
particularly if a large area of skin is affected by the chemical.

The immediate first aid treatment of any patient incurring chemical burns is to apply copious
quantities of water to the affected part, whether skin or eyes. If necessary and convenient, immerse
the patient in cold water to dilute and wash away the corrosive and reduce heat in the affected area.

Eyes.

Gases, vapours, mists or aerosols may contact the cornea of the eye, and the irritant or corrosive
may cause eye damage. The greatest source of injury, however, is liquid splashing into the eye.

The immediate first aid treatment is continued irrigation of the eye with cold water until medical aid is
available. The irrigation may continue for 15/20 minutes. Thorough cleansing is essential and speed
is vital.

Protective factors: everyone required to work in areas where corrosive chemicals are used must be
issued with suitable PVC gloves or gauntlets, eye shields and other items of protective clothing
considered necessary, as determined by the original protective clothing job assessment.

You will recall that the employer has a responsibility to supply, and the employee a duty to wear, the
prescribed protective clothing.

Injury through Inhalation.

The respiratory system is particularly vulnerable in corrosive and toxic atmospheres. Any chemical
carried in gas, vapour, dust, fumes or aerosol will, on being inhaled, contaminate the nose, throat
and mouth and further down the respiratory tract, depending on the extent of the exposure.

The 'walls' of the air sacs (alveoli) are penetrated with ease by most chemicals, which can then enter
the bloodstream with poisonous effect. Remember that the inhaling rate of an adult is about 20 times
each minute, and each inhalation takes in about ½ litre of air.
You can therefore calculate the air intake of a worker in one eight-hour shift, and consider how
harmful the effect of even weak concentrations of corrosive materials would be.

The extent to which gases, vapours and mists cause problems on inhalation depends upon their
solubility and irritant properties. The effect varies considerably between the various chemicals:

 Ammonia is highly soluble and irritant. The gas dissolves in the first moist tissues it contacts,
and produces intense irritation.
 Chlorine has low solubility, and is an irritant only on reaching the lower respiratory areas.
Thus, one or two deep breaths at high concentration can be very harmful.

Gases of low solubility generally may not produce any immediate corrosive or irritating effect and
may be absorbed without any apparent danger. As concentration and exposure times increase,
'chemical pneumonia' may develop. Typical examples of low solubility gases are phosgene (carbonyl
dichloride) and nitrogen oxides.

Protective factors include:

 Design of plant should aim at the elimination of possible leakage.

 Process control should aim at the elimination of vapours, fumes, mists and dusts.
 Adequate ventilation and scrubbing systems should be provided.
 Suitable respirators should be available in hazardous areas.

Injury through Ingestion.

Risk of injury by the accidental swallowing of chemicals is not usually considered serious in industrial
processing, but it is a definite hazard in laboratory operations where careless pipetting of chemicals
can be dangerous, due to the possibility of swallowing materials and inhaling vapours. Pipetting
should be done using a bulb aspirator or other mechanical means.

The main hazard of chemical ingestion comes from lack of personal hygiene, e.g. failing to wash the
hands before eating meals, smoking or drinking, or from airborne dusts getting into the mouth and
being swallowed.

In the case of ingestion, a much higher concentration of chemical is usually required than for injury
by inhalation. Ingested chemicals are absorbed in the digestive tract and pass through the liver,
where many deoxifying mechanisms operate.

Digestive disturbances and loss of appetite are early symptoms of chemical poisoning.

Protective factors include:

 Full attention must be given to ventilating systems.

 Breathing apparatus must be available.
 Safe working systems for pipetting of materials in the laboratory must be established.
 When working on experiments involving the use of toxic materials, the fume cupboard must
be correctly used.
 Strict attention must be paid to personal hygiene at all times to avoid contamination of the
mouth when eating.
  Injury through Contact with the Skin and Eyes

5.1 Injury through Absorption

As we have already seen, there can be an immediate and severe danger following skin contact with
chemical compounds such as chlorinated solvents, hydrocarbons, etc. This absorption into the body
system can result in serious internal organ damage.

The concentration of the chemical and the length of time it is on the skin are vital factors. Barrier
creams provide limited protection; but, once again, sensible hazard assessment and the issue of the
right protective equipment for the job are essential.

Protective factors: plant design and the elimination of hazards are the first prerequisites. Protective
clothing is the second line of defence.

Preventing Personal Injury by Chemicals.

In addition to the protective factors mentioned earlier, the risk of personal injury from chemicals may
be controlled as follows:

Handling of Chemicals:

 Safe working systems at receiving points for corrosive materials.

 Tank car reception of acids and alkalis to be kept under review.
 Adequate installation of emergency showers.
 Cautionary notices to be conspicuous.

Manual handling to be reduced to a minimum, but where it is necessary to receive chemical

corrosives in glass carboys (a glass bottle surrounded by protective packaging), care must be
exercised in off-loading and general handling of them. Assessment of protective clothing should
have full regard for the potential hazard of the glass carboy breaking with consequent serious
hazard. Fortunately, this method of delivery is being replaced by tank car, but it still exists -
particularly, where only small quantities are required.

Fumes.

Fumes and dusts should be removed by suitable ventilation.

Safe Entry into Vessels.

Adequate precautions must be taken and full control exercised where workmen are required to enter
closed vessels for the purpose of cleaning and maintenance of vessels which have contained
hazardous chemicals.
Permit-to-work systems are essential for this type of work, with the precautions clearly defined and
the relevant protective clothing and safety equipment clearly stipulated.

Adequate ventilation and the provision of a good air supply are high priorities.
Clothing.

A protective clothing entitlement must be assessed for all work where there is a danger of chemical
contamination, based on the principle and standards of the individual protective clothing entitlement.

Procedures.

Emergency procedures must be established, and emergency showers and eye washing facilities
made available.

Training.

This should be given:

 In relation to the nature of the materials being processed and the hazards involved, together
with preventative measures.
 In first aid requirements and procedures.

Permit-to-work Systems.

Must be instituted for work involving the breaking of pipe lines conveying corrosive materials. Valves
on mains should be painted a distinctive colour to ensure easy identification.

Sampling Arrangements.

Arrangements for corrosive materials should be closely investigated, and safe working systems
devised and implemented.

Storage Facilities.

Facilities for chemicals in packages, bags, etc, should be thoroughly checked to avoid the possibility
of moisturisation and cross-contamination of chemicals and potential chemical reaction.

Compressed Gas Cylinders.

These require very special care.

Spillages.

Require immediate treatment and cleaning up; contaminated articles should be carefully inspected
and, if necessary, discarded.

The hygienist and safety practitioner, when studying the chemical environment, will obviously give
some time to the assessment of these factors.

The original assessment will commence with an Initial Hazard Assessment of the chemicals being
used to determine the potential hazard of the materials being processed. This will indicate the type of
training to be given and the protective clothing required.
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5.2. Examples of Corrosives and Irritants

Chrome.

Air contaminated with chromic acid mist, or with dust from chromates or dichromates, is the principal
source of harmful exposure in industry.

(a) Chromium plating is carried out using an electrolyte containing about 50% chromic acid and,
during electrolysis, reddish-brown fumes of chromic acid are forced off in the form of mist by the
evolution of bubbles of hydrogen at the cathode.

(b) In anodising, a coating highly resistant to corrosion is formed on aluminium and its alloys through
the anodic oxidation of aluminium. Again, chromic acid is used as the solution in which anodising is
carried out, and the hydrogen liberated at the cathode carries significant quantities of chromic acid
mist into the atmosphere. It is this chromic acid, and any dissolved salts of chromium it contains, that
are responsible for the dermatitis, ulceration and even lung cancer.

Dermatitis and Chrome Ulcers.

Lesions of the skin due to chromium salts have been known since 1827 when it was found as
chrome holes on the fingers of bichromate workers in Glasgow.
It has since been established that both chromates and bichromates of sodium and potassium,
together with chromic acid, may cause either dermatitis or localised ulceration.

Exposure to these substances occurs in chromium plating, French polishing, calico printing,
photographic processing, litho-etching, chrome tanning and colour workers.

Typically, dermatitis develops on exposed parts of the body such as the hands, arms, chest or face.
Onset is often sudden, occurring sometimes after an exposure of several months and, in severe
cases, the face becomes intensely red and swollen, with the affected parts itching a great deal and
perhaps becoming painful. There is some evidence that fair-headed/skinned people are particularly
prone to chrome dermatitis, and their presence at chrome operations calls for particular care.

Chrome ulcers are thought to begin in abrasions in the skin and are most commonly found at the foot
of the finger-nail, the knuckle of the hand, or dorsum (top) of the foot. They are circular in shape, up
to one centimetre in diameter and look as if they are punched out, hence 'chrome hole'. Some
penetrate deeply, even to the bone and, although usually painless, they itch incessantly, especially
at night. In chromium plating and anodising, where chromic acid fumes are frequently present,
inhalation leads to perforation of the nasal septum. This effect has even been reported in people
spray painting anti-corrosive zinc chromate-based paints.

Cancer of the Lung.

The first reported case of cancer of the respiratory system in a chrome worker occurred in a 47-year
old man who had worked in the chromate industry in Scotland (1890).
Since then, it has been established that the incidence of lung cancer is about 3.6 times that of the
'normal' population, but with a latency period of about 25 years, this figure for risk may be an
underestimate.

Preventive Measures.

Prevention of chrome-related diseases depends primarily on the removal of the dust or mist at
source by suitable ventilation equipment; cleanliness, supported by regular medical supervision, and
covering cuts and abrasions with suitable dressings.

Where contact with the arms or hands is likely, then workers should be supplied with adequate
protective equipment, including gloves, aprons and boots; but great care needs to be taken to
ensure that solutions cannot run down the arms or legs and into the protective clothing, or severe
ulceration may result.

Good hygiene is particularly important, and should be encouraged by the provision of ample washing
facilities backed up with good care of the hands, using barrier creams and lanolin-based creams.

5.3 Ammonia (NH3)

Ammonia is a colourless gas with a pungent odour, readily soluble in water, with which it forms
ammonium hydroxide (NH4OH).

It is used as a refrigerant, in petrol refining, metallurgy, water purification, fertilisers, and in the
manufacture of many drugs and chemicals.

Ammonia Burns.

Burns, which may be severe and even fatal, may follow splashing of ammonia onto the skin.

If ammonia gets into the eyes, there is an immediate effect on the conjunctiva, causing severe pain.
Ulceration of the conjunctiva and cornea, scarring of the tissues and lenticular opacity may interfere
with vision, even causing blindness. Apparatus to irrigate the eyes with water must therefore be
installed wherever the hazard of splashing with ammonia exists, although goggles/face masks
should always be worn. Irrigation must be promptly applied and continued for at least an hour.

Effects and Symptoms.

One of the largest and best documented cases of ammonia poisoning occurred on 11th September,
1940 when 75 people were overcome in the cellars of the Wenlock Brewery, London, used as an air-
raid shelter. Debris from an explosion fell on the refrigeration plant, causing it to leak ammonia gas.

Those farthest from the leak were the least affected, with smarting of the eyes and mouth,
accompanied by pain on swallowing. All were hoarse and could hardly raise their voices above a
whisper, and there was a strong smell of ammonia on the breath. The lips, mouth and tongue were
reddened and raw; the conjunctiva and eye-lids were red and swollen.
The group with moderate exposure additionally complained of a feeling of tightness in the chest,
difficulty in swallowing, coughing and sometimes blood-stained sputum. Moist sounds were present
in the lungs, and several developed ulcers in the buccal mucosa and cornea. Some developed
oedema of the lungs (liquidity) within six hours and the overall fatality rate of this group was 22%.

Survivors rapidly recovered a semblance of normal health, although hoarseness only cleared up
over a number of weeks.

Preventate Measures.

 All equipment containing ammonia should be tested and inspected regularly, and any
necessary repairs effected immediately.
 Detectors should be fitted to operate at well below the occupational exposure limit (25 ppm
LTEL, 8-hour TWA; 35 ppm STEL, 15 minutes), with control valves placed outside the
building.
 Gas-masks/canister respirators must be provided and stored in a readily accessible locality.
 Employees must be instructed as to the dangers, and trained in how to avoid them.
 Every workman engaged in repair or maintenance work must carry a gas-mask in case of an
escape of gas.
 No work should be attempted on ammonia plant without initiating a permit-to-work.

Other Dangerous Gases.

Some other gases having a high hazard potential are:

 Sulphur dioxide (SO2)

 Sulphur trioxide (SO3)
 Nitrogen dioxide (NO2 and N2O4)
 Nitrous oxide (N2O)
 Nitric oxide (NO)
 Chlorine (Cl2)
 Phosgene (COCl2)
 5.4 Dermatitic Hazards
 Occupational Dermatitis.
 Occupational dermatitis is a non-infectious, inflammatory condition of the skin, which results
from external contact with chemical, biological or physical agents.
It is a prescribed disease under the Social Security (Industrial Injuries) (Prescribed Diseases)
Regulations 1985, as variously amended, with the exception of dermatitic conditions caused
by ionising particulate or electromagnetic radiation.
 The condition may, in some cases, cause only minor inconvenience, but it is also capable of
causing considerable handicap as well as being very unsightly.
 With the increase in the areas by which employees are covered under the HASWA, some
forms of dermatitic response are not producing the obvious reddening of the skin which has
been observed in the past. There is now a move to change the general description of the
condition to Occupational Dermatoses. This is only a name change, and does not affect the
general description of signs and symptoms.
 The importance of understanding the condition, its causes and prevention, become apparent
when you realise that estimates indicate that dermatitis accounts for about 70% of industrial
 disease. The cost to the national accident bill must therefore be considerable, running into
many millions of pounds per year.
 The skin provides the body’s main defence against external irritants, in particular the cornified
epithelium (the outermost layer of the epidermis) and glandular secretions, which provide a
greasy protective coating.
 The cornified epithelium, which consists mainly of keratinised dead cells, gives the skin
toughness and a high level of waterproofing. It has the ability to withstand fairly high acid
concentrations, but is attacked by high concentrations of alkali and alkaline sulphide solutions.
 Organic solvents are able to dissolve away the greasy secretion, so the natural protective
mechanism is reduced. Any breaks or reduction in the thickness of the cornified layer caused
by friction, heat or excessive sweating, will also reduce resistance to attack from external
irritants. The openings to the hair follicles and sebaceous glands provide another means of
access for irritants to enter the skin structure, especially for fat soluble substances.
 Inflammation resulting in oil folliculitis and chloracne start at these points of entry.
 Predisposition to Dermatitis.
 Analysis of people who suffer from dermatitis has revealed that predisposition to the disease
may be classified under a number of headings:
 Types of Skin.
 Oily skins tend to develop oil acne and folliculitis (septic hair follicles) in contact with grease
and oil, but tend to resist the effects of fat-soluble solvents. Where a person sweats
excessively, the outer skin layers become softened and less resistant to the effects of irritants.
 A secondary problem with sweating occurs when dry material adheres to the skin and reacts
with the water to produce higher irritant levels, e.g. lime or dry cement.
 Dry skin is susceptible to most irritant conditions.
 Racial Characteristics.
 Dark-skinned races appear less sensitive to external irritants than those of Caucasian origins.
 People of Mongolian origins generally have very dry skin, which is susceptible to pressure or
frictional abrasion.
 Age.
 Young people are more prone to dermatitis than older workers under the same working
conditions. Whether this is due to lack of care, or a younger and more sensitive skin, is
debatable.
 Workers in their late fifties and above are very prone to chronic dermatitis; this may be related
to the ageing process, which reduces the skin’s natural defences against external irritants.
 Gender.
 Females are, in general, more prone to dermatitis than males. This is related to the fact that
females have, on average, very dry skin. Also, due to the considerable variation in the
composition of their skin excretions, a variation in the skin’s natural defence mechanisms may
occur.
 A greater involvement with washing clothes, and a higher frequency of personal washing
compared with males, is also cited as a reason for susceptibility.
 Season of the Year.
 The incidence of dermatitis increases in hot weather as a result of an increase in sweating. It
also increases in cold weather in processes where there is a high use of water. Chapping of
the skin leads to inflammatory conditions.
 Natural High Level of Immune Response and Related Skin Conditions.
 People who suffer from the effects of an over-active immune response mechanism (i.e. who
suffer allergies) usually develop a skin structure that is very susceptible to dermatitis. This is
especially true for dermatitic substances, which can cause sensitisation dermatitis.
 Persons with asthma-related skin conditions should not be exposed to potential dermatitic
conditions.
 General Health.
 Where a person is unwell or undernourished, the natural skin protection will also be reduced.
The lowering of resistance will allow a dermatitic condition to develop much more quickly and
aggressively than in a person who is in good health.
 Personal Hygiene Standards.
 Personal hygiene standards are a contributory factor in whether or not a person is likely to
contract dermatitis. For those whose approach to washing is superficial, the risk must be
higher compared with those who are concerned with their personal cleanliness. There is, of
course, one very disquieting feature about this situation: “How was the operative so
contaminated that personal hygiene became a factor in the risk equation?”
 Clarification.
 Occupational dermatitis has been classified into two main forms:
 Contact Dermatitis.
 Contact dermatitis is a condition brought about by contact with substances (or conditions)
called primary cutaneous irritants.
 Dermatitis occurs at the site of contact, provided the irritants act for a sufficient time and in
sufficient concentration.
 Direct attack on the outer layers of the skin causes tissue destruction and/or degreasing,
allowing absorption into the “active” areas of the skin, where inflammatory conditions develop.
 An important point to note about dermatitis is that after removal of the operative from contact
with the irritant, recovery generally occurs.
 Further exposure to the irritant can be tolerated, provided extra precautions are taken to limit
contact and exposure.
 Contact dermatitis develops on the body where contact occurs. Main body areas are the
hands, arms, face and neck.
 Sensitisation Dermatitis.
 Sensitisation dermatitis is caused by substances called cutaneous sensitisers. These
substances do not always cause an inflammatory response on first contact, but may take a
week or more to develop.
 A more serious condition, immune (allergic) response, occurs in the metabolic reactions of the
skin structure and develops within hours of contact with the sensitising material.
 Recovery from the dermatitic condition occurs when contact with the offending material is
removed. However, in complete contrast to contact dermatitis, the sensitisation remains, so
that further contact with the substance evokes a severe dermatitic and immunological
response. Only a small concentration of the cutaneous sensitiser is required to cause the
recurring attack.
 In the chemical industry, operatives who have suffered this condition can react simply by
being “down wind” from the particular plant where the material is being manufactured.
Recurrent immune responses cause dermatitis to occur in areas of the body other than where
the initial condition developed.
 Immunological reaction may cause symptoms such as massive swelling around the eyes and
face, on the hands, arms and ankles.
 The consequences of contracting sensitisation dermatitis are obvious: the person must be
removed from any contact with the offending material.
 Another problem resulting from sensitisation is that the immune response may be stimulated
by materials other than the original cutaneous sensitiser. This condition is called cross-
sensitisation.
  Persons sensitised by teak wood have been reported as having violent reactions when
exposed to certain photographic developers. Penicillin can evoke an immune response after
sensitisation has occurred, from substances with a similar chemical structure.
 (Note: The description of occupational dermatitis as non-infective means the condition is not
transmitted from one person to another. It does not mean that bacterial infection cannot be
superimposed upon the condition, and sepsis might cause added complications.)
22 805

Continue


5.4.1 Examples of Dermatitic Hazards

The list of materials which can cause dermatitis is almost endless. In the occupational situation, you
must find out about the harmful effects of any substance that your workforce has to handle. For the
examination, some clear examples of materials which evoke a dermatitic response will suffice.

Examples of Primary Cutaneous Irritants.

 Greases.
 Mineral oils.
 Solvents, e.g. white spirit.
 Chlorinated hydrocarbons.
 Propanone (acetone).
 Strong alkali and acids.
 Cement.
 Physical agents: heat, cold, radiation, friction.

Examples of Cutaneous Sensitisers.

 Rubber additives.
 Nickel compounds.
 Hair dyes containing p-phenylenediamine.
 Methanol solutions (formalin).
 Wood dust: African (Iroko) teak.
 Resins used in plastic manufacture.

Many modern chemicals are able to evoke both irritant and sensitising responses. Compounds of
chromium and arsenic can cause dermatitis, which may progress further to give ulceration of the
affected areas.

Control of Potential Dermatitic Situations.

The main aim in the control of potential dermatic situations is the limitation of exposure to a level
where the risk is eliminated, or reduced to a practical minimum.

For dusts and vapours, total enclosure with mechanical handling and exhaust ventilation systems
provides a safe place strategy. The exhausted materials should be rendered safe, and not
indiscriminately vented into the atmosphere.
For liquids, pastes, or dustless solids, mechanical handling may be satisfactory.

When it is not possible to provide a safe place strategy, a safe person strategy must be adopted and
suitable protective equipment provided, e.g. gloves, impervious overalls with close-fitting collars and
cuffs, wellington boots; and, in certain circumstances, half-mask respirators. Barrier creams provide
very limited protection where primary irritants are encountered, and are useless against cutaneous
sensitisers.

Where protective equipment is supplied, management is mainly responsible for its use and should
provide adequate supervision and the necessary incentives for workers to use the equipment when
they are not supervised.

Personal hygiene should really only provide a 'back up' if a breakdown in safety control occurs; but,
in practice, it does provide a positive method of reducing the risk of contracting dermatitis.

Where there is a known risk from cutaneous sensitisers, 'patch testing' personnel before they are
exposed to potentially hazardous conditions is a commonly used practice. Patch testing involves
applying a small amount of various materials to the skin, often on the forearm, and checking to see
whether or not a positive reaction to the material occurs. Patch testing must only be carried out by a
professionally-trained person.

Problems resulting from occupational dermatitis should always be referred to a dermatologist with
adequate industrial experience in your particular industry.

5.5 Summary
In this study unit, we have considered the classification of chemical agents. This included the
Chemical (Hazard Information and Packaging for Supply) (Amendment) Regulations 2005, as
amended, the categories of danger and risk phrases and safety phrases.

The various factors which affect the risks to individuals:-

 concentration,
 solubility in body fluids,
 synergy,
 age and susceptibility of the individual,
 sensitisation,
 aerosol/particle size and morphology, and
 exposure time.

have all been discussed. This led on to consideration of exposure of the employee to chemical
agents in the workplace - to toxic, corrosive and irritant and dermatitic hazards. For each type of
hazard, we described exposure risks, effects and symptoms, protective factors and occupations at
risk, giving specific examples.

Class of Toxin Target Some Symptoms Example

Organ/System
damaged
 Hepatotoxins Liver Jaundice, liver Carbon tetrachloride
enlargement
Nephrotoxins Kidney oedema, Proteinuria Halogenated
hydrocarbons
Neurotoxins Nervous system Narcosis, Mercury and
behavioural changes compounds,
Chloroform, ether
Haematopoietic Blood or haemato- Cyanosis, loss of Carbon monoxide,
agents poietic system consciousness cyanides
Lung toxins Lungs Cough, difficulty Asbestos, siliceous
breathing dust
Reproductive toxins Reproductive organs, Sterility, birth Lead and
developing foetus defects, compounds
Cutaneous agents Skin Defatting, rashes, Ketones, chlorinated
irritation organic solvents
Eye toxins Eye Conjunctivitis, Acids, organic
corneal damage solvents

In relation to occupational dermatits

(a) Identify two causative agents.

(b) Describe the typical system of the condition.

(c) Outline specific measure designed to prevent the occurrence ofoccupational deramtits

6.0 Biological monitoring guidance values

The framework for the use of biological monitoring and the setting of Biological monitoring guidance
values (BMGVs).
* Health Guidance Values (HGVs) are set at a level at which there is no indication from the scientific
evidence available that the substance being monitored is likely to be injurious to health.

Values not greatly in excess of an HGV are unlikely to produce serious short or long-term effects on
health. However, regularly exceeding the HGV does indicate that control of exposure may not be
adequate. Under these circumstances, employers will need to look at current work practices to see
how they can be improved to reduce exposure.

** Benchmark Guidance Values (BGVs) are not health-based.

They are practicable, achievable levels set at the 90th percentile of available biological monitoring
results collected from a representative sample of workplaces with good occupational hygiene
practices.

If a result is greater than a BGV, it does not necessarily mean that ill-health will occur, but it does
indicate that control of exposure may not be adequate. Under these circumstances, employers will
need to look at current work practices to see how they can be improved to reduce exposure.

In the UK there were, until recently, two approaches to biological monitoring guidance values. (In
principle, this was analogous to the previous position of the two different types of OEL (MEL and
OES) before it became a single WEL).
You can see this difference if you compare the BMGV entries in EH40/2002 with those in
EH40/2005. One is called a ‘Health Guidance Value’ and is the level of a substance or its
metabolites in blood, or urine that is not associated with any adverse health effects. Usually, this is
the average value that may be found in blood or urine of workers exposed for 8h to the current
occupational exposure limit. This approach is similar to the ACGIH BEI and DFG EKA.

The second type of biological monitoring guidance value is called a ‘Benchmark Guidance Value’.
This type of value is proposed when there are not enough data to set a Health Guidance Value, or
where a Health Guidance Value would not be appropriate – for example for substances, like
hexavalent chromium, that can cause cancer.

The benchmark value is set based on a survey of workplaces that are considered to have good
control of exposure to the substance and it is the value found in 9 out of 10 samples in those
workplaces.

This type of guidance value gives no direct guide to the risk of ill-health; rather, it is a value that is
associated with good occupational hygiene practice and control of exposure.

In the UK, from 2005 the two approaches were grouped under one generic heading – Biological
Monitoring Guidance Values (BMGV).

22 808

6.1 Summary
The application of toxicological data requires interpretation; the following issues need to be
considered:

 relation of materials in use to substances for which toxicological data is available;

 type of effect (stochastic or non-stochastic) of the substance;
 interpretation of carcinogen, mutagen and reproductive data; and
 sensitisers.

WELs are set on the recommendation of the Advisory Committee on Toxic Substances (ACTS),
following assessment by the Working Group on the Assessment of Toxic Chemicals (WATCH) of the
toxicological, occupational hygiene and analytical data.

6.2 Workplace Exposure Limits - Further Information

The following tables, supplementary information and calculation methods have been extracted from
EH40/2005 which contains the list of workplace exposure limits for use with the Control of
Substances Hazardous to Health Regulations 2002 (as amended).

 Table 1: List of approved workplace exposure limits [50kb]

 Table 1: Supplementary information [35kb]
 Table 2: Biological Monitoring Guidance Values [10kb]
 Calculation methods [33kb]
Tools for helping select a control strategy for compliance with COSHH Regs

6.3 Asbestos
The ILO Code of Practice ‘Safety in the Use of Asbestos’, establishes a set of principles for the
control of asbestos. The practical recommendations contained within the code are intended for the
use of all those having responsibility for safety and health in the use of asbestos; the code does not
replace national laws or standards.

In essence, wherever possible, harmful

General Preventative Methods
substances should be replaced by substances that offer the same
technical advantages but which are harmless or less harmful. The
proposed alternative should be assessed to determine the health
hazards associated with its manufacture, handling, use,
transportation, storage and disposal.
Asbestos controls can be divided into two categories – ‘Engineering’ and ‘Procedural’ or
‘Administrative’ controls, the objective being to eliminate or reduce exposure to the lowest possible
level.

Engineering controls should include:

 M echanical handling ;
 Ventilation;
 R edesign of the process to eliminate, contain or collect asbestos dust emissions by such means as:
o process separation, automation or enclosure;
o bonding asbestos fibres with other materials to prevent dust generation;
o general ventilation of the working areas with clean air;
o local ventilation of processes, operations, equipment and tools for the prevention of dust
dissemination;
o use of wet methods where appropriate;
o separate workplaces for certain processes.

Above: Asbestos Stripping

Procedural controls and work practices should include:

o R equirements to use and maintain equipment, tools, LEV etc in accordance with instructions;
o D amping of asbestos products and materials before processing, handling, using, machining,
cleaning, stripping or removing;
o R egular cleaning of machinery and work areas by appropriate methods;
o P roper use of PPE .

The employer should establish, implement and regularly review a general control programme
to reduce workers’ exposure to asbestos dust. This should be made available to inspectors
and/or workers’ representatives upon request, should take account of the specific features of
the workplace and include at least the following:

o A description of each operation, the processes and machinery used, the materials handled, the
control devices, the number of exposed workers, the job responsibilities of each worker, the
operating procedures and the maintenance practices;
o A description of the specific means for controlling exposure to asbestos dust;
o E ngineering plans, safety data sheets, study reports or other relevant technical information;
o A ir monitoring data on the efficiency of control measures;
o A description of the work practices or administrative controls needed; and
o A detailed schedule for implementation of the control programme.

In large enterprises it may be appropriate for specified departments, branches or persons to

be given special duties in the implementation of the control programme, particularly in
connection with the:

o D esign of new buildings, equipment, processes and materials;

 o P urchase of materials, products, machinery or equipment;
o C ontracts for the supply and maintenance of ventilation systems and other engineering
controls;
o I nformation and training given to the workers; and
o P urchase and maintenance of PPE and the provision of ins tructions in regard to its use.

Principles of Design and Installation

The code of practice (chapter 5.4.1) recommends that materials, processes and equipment
should be designed such that the exposure of workers to asbestos dust is eliminated or
reduced to the lowest practicable level. The following principles and controls associated with
design and installation are also referred to:

o Manufacturers of machinery, equipment and materials are to provide information on the nature
and level of asbestos dust emissions as well as the means of control;
o Workrooms are to be designed, built and maintained so as to:
 separate the hazardous operations from the remainder of the premises;
 limit surfaces on which asbestos dust and waste may accumulate;
 facilitate the cleaning of floors, walls, ceilings and machinery; and
 facilitate the collection of asbestos dust which may escape in the event of an incident.
o Use of automatic processes or remote control systems to avoid direct handling of asbestos or
materials containing asbestos;
o Where practicable, total enclos ur e of the process;
o Use of internal exhaust ventilation to create negative pressure inside the enclosure;
o Where practicable, building materials such as boards, sheets and plates should be so
designed, prefabricated and packed in the factory that no further cutting, drilling or other
machining is needed by the user;
o Measurements of asbestos dust emission and of the exposure of workers to asbestos dust
should be made as soon as the machinery and equipment have been installed in order to
establish that the standard required by the competent authority in those respects has been
achieved.

Local Exhaust Ventilation

Where total enclosure of the dust-producing process is not practicable, local exhaust
ventilation (LEV) equipment should be provided and maintained. This should be located as
close as possible to the source of dust emission by the use of captor hoods, booths or
enclosures and should be designed to collect and remove all dust-laden air.

LEV (or other effective methods) should be used for operations such as feeding, conveying,
crushing, milling, screening, mixing or bagging of asbestos materials; for carding, spinning,
weaving, sewing and cutting of asbestos textiles, and for cutting, punching, drilling, sawing,
grinding or machining of asbestos cement and friction materials.

The LEV system will need to be designed by a competent specialist. The nature and quantity
of dust emission should be taken into consideration when:

o Designing enclosures;
o Selecting equipment for air movement, ducting and dust filtration;
o Calculating air flow rates and capture velocities; and
 o Choosing m onitoring instruments .

LEV function should be checked and tested periodically using techniques such as smoke
tests or air flow measurements or by comparing the static pressure readings in the system
with the readings recorded at the same points upon commissioning.

Where asbestos dust is collected by the filtration equipment, it should be removed carefully
under controlled conditions.

General ventilation

Where appropriate in conjunction with LEV, the entire work area should be supplied with
clean air to replace the air as it is exhausted and to reduce airborne asbestos concentrations.
There should be a sufficient number of air changes per hour and exhausted air should be
efficiently filtered and not recirculated back to the working environment, except when:

o the airborne asbestos concentration is substantially less than the exposure level and does not
add to the exposure;
o the filtration and ventilation system is regularly checked and maintained;
o the air quality is monitored by adequate instruments;
o the process has been approved by the competent authority according to national practice.

Personal Protection

Respiratory equipment

Above: Protective Clothing and RPE

Use of Respiratory Protective Equipment (RPE) should be regarded only as a temporary or

emergency measure and not as an alternative to technical control. RPE should be available in
the workplace and should be provided free of charge for workers where levels of airborne
asbestos fibre exceed or are liable to exceed the exposure limits.
Workers should be informed when concentrations of airborne asbestos fibre exceed or are
liable to exceed the exposure limits, at which point they should use the equipment provided.

Workers who are required to wear RPE should be fully instructed in its use. Instruction should
cover the:

o R easons for the use of the equipment and the importance of using it conscientiously;
o C ircumstances in which it should be used and how these circumstances should be recognised
;
o M anner in which the equipment operates;
o C orrect method of use and of checking the fit;
o M ethod of checking for correct operation;
o N eed for regular servicing.

The employer should ensure adequate supervision and should arrange for the equipment to
be maintained.

When selecting RPE it is important to remember that only those types of RPE which have
been tested and approved by the competent authorities should be worn. Types of RPE
include:

o A ir-purifying respirators of the negative pressure (half face mask) type;

o P ositive pressure respiratory equipment;
o D irect air-line breathing apparatus.

For hygiene reasons, each specific item of RPE should be used only by the worker to whom it
was supplied. It should be regularly cleaned and serviced by appropriately trained operators
before reissue. Records should be kept of all cleaning, servicing and training.

RPE should be stored in a suitable container when not in use.

Protective clothing

In cases where personal clothing may become contaminated with asbestos dust, the
employer should provide appropriate work clothing. If there is a need to use RPE, then special
protective clothing, which should completely cover all work clothing, should also be provided
and worn.

When re-usable protective or work clothing is provided, separate locker rooms should be
available so that contaminated clothing can be stored separately from personal clothing to
prevent cross-contamination.

The routine for removal of contaminated work clothing will include:

o Removing dust by vacuuming work clothing at the entrance to the locker room in which such
clothing is removed and stored;
o Removal of a respirator only after de-dusting;
o Provision of s hower or washroom facilities and should be sited between the conta minated and
clean locker rooms.
Personal clothing should be removed, stored or put on only in the clean locker room.

The employer should arrange for the laundering of protective clothing. Laundering in people’s
homes is strictly prohibited. Laundering should take place under controlled conditions so as to
prevent release of fibres into the atmosphere.

Cleaning of Premises and Plant

Above: Vacuuming Asbestos

Employers need to ensure that the work premises are maintained in a clean state and are free
of asbestos waste. This includes all machinery, plant and equipment, which should be kept
free from dust, together with all external surfaces of exhaust ventilation equipment and all
internal surfaces of the building, including floors and walls.

Cleaning should be carried out as far as practicable by vacuum-cleaning equipment or by

some other means (e.g. wet techniques) in such a way that asbestos dust neither escapes
nor is discharged into the air of the workplace.

Where cleaning by a dustless method is impracticable, PPE and RPE should be worn.

Floor surfaces should be kept in good repair and cracked or broken surfaces should be
repaired.

Walls should, so far as is practicable, be smooth so as to facilitate ease of cleaning by

vacuum cleaner or wet methods. They should be cleaned at least annually.

Machinery and equipment should be cleaned at the end of each shift and the interval between
cleaning should never exceed one week. When cleaning machinery, any LEV with which it is
fitted should be in operation. Parts of the machine that may be inaccessible to the vacuum
cleaner should be cleaned out with oiled brushes where practicable and vacuum equipment
should be used to take up the material so removed.

Overhead structures of new buildings should be constructed with smooth surfaces and high
ledges should be avoided. Dust should be removed by vacuum cleaner, with extension hoses
being used as required, or by some other means that causes no secondary dust generation.
When overhead cleaning is taking place, equipment should be covered by plastic sheeting.
 Vacuum-cleaning equipment

Above: Vacuuming Asbestos with Extension Hose

Only vacuum equipment with a suitable high-efficiency filter should be used for collecting
asbestos dust and waste. Vacuum equipment should be designed to prevent dust escaping
from the equipment.

Collections bags within the vacuum-cleaning units should be disposable. Collected material
should be disposed of in accordance with the provisions of the ILO Code of Practice.

Packaging, Transport and Storage

Above: Bagged Asbestos Waste

Asbestos fibre should always be packed in impermeable bags. Plastic material used for bags
should incorporate an ultra-violet inhibitor to protect the bags from sunlight so as to prevent
deterioration. Bags should be closed by either heat-sealing or stitching and should be clearly
labelled.

Packaging for transport should eliminate the handling of individual bags as far as is practicable and
should minimise damage to bags which could result in spillage.

The following general principles should be applied when transporting asbestos:

o Where practicable, loads should be stacked on pallets and carried in closed vehicles or
containers;
 o Use a fork lift truck or similar method to load and unload so as to prevent the handling of single
bags and reduce the risk of damaging bags;
o Hooks and other sharp equipment should not be used on bags or unit loads;
o Loads carried in containers should be stacked so as to reduce the risk of damage to bags from
the wooden pallets;
o Vehicles should be properly cleaned by use of a vacuum cleaner or wet method after they have
been unloaded;
o Where the wrapping of a bag is damaged and spillage of asbestos is likely, suitable PPE and
RPE should be provided and worn;
o Suitable adhesive tape should be available for the repair of damaged loads and damage
should be repaired immediately .

Warehousing

o Before final storage, all units should be carefully inspected for cleanliness and for damage .
Damaged bags should be repaired immediately ;
o All bags should be stacked on pallets;
o Loose asbestos or other debris should be cleaned as soon as possible by vacuum equipment
or by some other means that causes no secondary dust generation;
o Workers should be provided with RPE and PPE;
o Final storage should be in a warehouse. If outside storage cannot be avoided, units should be
protected by tarpaulins, black plastic sheeting or other suitable covering .

The Disposal of Asbestos Waste

Above: Asbestos Waste Awaiting Disposal

As a general principle, the generation of asbestos waste should be minimised by the adoption
of the most effective production techniques. Arrangements should be in place for the
collection of various forms of asbestos waste, including dust, loose fibres, swarf, floor
sweepings, insulation, broken pieces of asbestos-containing materials and wet waste or
slurry.

Dust

The following principles should be employed when collecting asbestos dust:

 o Bagging of outlets from dust collection hoppers should be designed to make bag-changing
easy and to minimise dust leakage;
o Bag-changing should be carried out only by competent persons;
o Bags should be made of translucent material wherever practicable so that the dust level can be
seen and overfilling can be avoided;
o Water-soluble paper sacks should not be used where any risk exists of deterioration by wetting
before final disposal;
o When filled, the bags should be sealed to prevent the escape of dust during subsequent
handling;
o Plastic bags should be twisted tightly and folded over and the neck should be secured in the
folded position by a wire tie, adhesive tape etc;
o Paper sacks should be folded over twice and stapled along the folded edge;
o Suitable protective clothing and respirators should be worn when bags on a dust collector are
changed.

Loose fibre, swarf, floor sweepings

The following principles should be employed when collecting this type of asbestos waste:

o Loose fibre handled by fixed extraction systems should, wherever practicable, be returned to
the production process;
o Swarf accumulating around and under machinery should be cleaned by suitable vacuum
cleaners;
o Loose materials collected by other means should be placed in impermeable bags and the bags
should be sealed.

Waste materials from fixing or removing insulation

The following principles should be employed when collecting this type of asbestos waste:

o Floors should be covered with plastic sheeting which can be folded to form sealed containers;
o Machines should be designed to enable the automatic removal of offcuts and for their collection
in disposable receptacles which can be sealed and removed. Where automatic removal and
collection is not practicable, suitable receptacles which can be closed should be provided;
o There should be enough receptacles to prevent overfilling;
o R eceptacles should be sited to minimise asbestos dust emissions in use;
o Material should be placed in the receptacles in a controlled manner;
o If asbestos dust emissions from the receptacle occur during use, a dust-extraction hood should
be provided to prevent the escape of asbestos dust into the workplace;
o Where offcuts and rejects need to be broken down before disposal, this should be done
mechanically under suitable exhaust ventilation, wherever practicable. If this is not practicable,
the work should be performed in a separate area so that asbestos dust cannot escape to other
work areas;
o If appropriate, the material should be wetted in order to minimise asbestos dust emission and
workers engaged in this task should wear suitable protective clothing and respirators.
Offcuts, broken pieces and rejects of high-density materials

Above: Bagging Asbestos Waste

Hard waste, such as bonded asbestos, asbestos cement, jointings and bitumastic rubber
residues, should be stored in such a manner as to ensure that it will not be abraded or
crushed while awaiting disposal.

Sacks or bags which have contained asbestos

Sacks or bags which have contained loose asbestos fibres should be disposed of by grinding,
melting or bagging. Grinding or melting should be carried out under closed conditions
adjacent to the bag-opening station. Where bagging is employed, the used sacks or bags
should be collected under strict dust control conditions in impermeable containers, such as
unused plastic bags and such containers should be closed and sealed.

Wet Waste: Asbestos Sludge or Slurry

This should preferably be recycled or loaded into specially designed carriers or other
containers in such a way as to ensure that no spillage, which may subsequently dry out
occurs.

Identification and isolation of waste

All asbestos waste awaiting disposal should be adequately identified by markings on the bag
or receptacle. It should be stored in such a way that it is not exposed to damage likely to
cause spillage and should not be mixed with other waste for which there are no special
disposal requirements. Where practicable, a special area should be set aside for its storage.
Transport of waste

Above: Waste Asbestos Being Placed in Sealed Container

Asbestos waste, whether loose or in sealed containers, should be transported to the disposal
point in such a way that no asbestos dust is emitted into the air during transport. In the event
of accidental spillage (for example, as the result of a road accident), action appropriate to the
extent of the spillage should be taken immediately. Written instructions on the action to be
taken in the event of accidental spillage should be issued to drivers of vehicles carrying
asbestos waste.

Disposal of waste

Disposal sites should be both suitable and acceptable for the purpose. They should have
vehicular access to the working face, or to a hole or trench dug to receive the asbestos waste.
Waste should be deposited at the foot of the working face of the landfill site or at the bottom of
an excavation dug for it. When deposited, all waste other than high-density waste should be
covered to an acceptable depth (for example 20-25 cm (8-10 in)) as soon as possible. No
asbestos waste should be left uncovered at the end of a working day. Final covering of
asbestos waste should be to a minimum depth of 2 metres (6 ft 6 in).

Workers occupied in the collection, transport or disposal of asbestos waste, who may be at
risk of exposure to airborne asbestos, should be provided with suitable protective clothing and
respiratory equipment. Where vehicles and reusable receptacles and covers have been in
contact with asbestos waste, they should be cleaned after use by means of a vacuum cleaner
or by an alternative dustless method.

Supervision

Where an undertaking disposes of its own asbestos waste, written instructions should be
issued to the workers concerned. Periodic checks should be made to ensure that the
necessary safety precautions are being followed. If a waste disposal contractor is employed,
the relevant sections of the ILO Code should be incorporated in the contract, which should
state that the contractor is responsible for ensuring that safety measures are observed at the
disposal site. It will be necessary for periodic checks to be made to ensure that the contractor
is observing the code.
Supervision of the health of workers

Workers whose jobs involve exposure to asbestos dust should be provided with health
supervision, which should be free of charge. Workers should have the following rights:

o C onfidentiality of personal and medical information;

o F ull and detailed explanations of the purposes and results of the supervision;
o T he right to refuse invasive medical procedures which infringe the integrity of their bodies.

A medical examination of the worker potentially exposed to asbestos dust should take place
upon recruitment or prior to assignment to a place of work involving exposure to asbestos
dust. Further medical examinations will take place periodically throughout employment and on
cessation of employment.

The objectives of the pre-assignment medical examination should be to:

o D etermine any condition which would be a contraindication to occupational exposure to

asbestos dust;
o E stablish baseline records for the future supervision of the health of workers;
o E ducate and advise workers about the risks associated with exposure to asbestos dust

The objectives of the periodic medical examination should be to:

o D etect the earliest signs of asbestos-related disease;

o D etect any significant change in health status relative to the baseline examination;
o C ontinue to educate and advise workers about health risks and to ensure that appropriate
preventive measures are being taken to minimise risk.

Workers should be informed of the results of their medical examination. They should also be
informed if, in the occupational physician's opinion, they are suffering from an asbestos-
related disease and copies of their medical records should be made available to the worker
or, upon the request of the worker, to his physician.

Information, Labelling, Education and Training

Cigarette smoking interacting with asbestos is a risk factor for those who work with asbestos.
Therefore, specific information regarding the importance of cigarette smoking as a risk factor
in this disease and in causing other health effects should be provided to all groups concerned
with occupational exposure to asbestos dust.
Labelling of products and of risk areas

Above: Asbestos Signage

All asbestos-containing products should have an internationally recognised warning symbol

designating the product as asbestos-containing and warning the user that inhalation of
asbestos dust may cause serious damage to health.

Where practicable, asbestos-containing products should be accompanied by a safety data

sheet or other approved form, containing such information as:

o T he product designation;
o T he name and address of the manufacturer or supplier;
o T he chemical or widely recognised common name of all asbestos ingredients;
o T he approximate percentage by weight or volume which asbestos bears to the whole mixture;
o H ealth hazard data including dangerous properties of asbestos;
o P rocedures for the clean-up and disposal of leaked or spilled asbestos, including labelling and
disposal of containers retaining residues or contaminated materials;
o R equirements for PPE and RPE;
o A ny other general precautionary information on handling the product.

Clear signage should be used to show areas where asbestos dust may cause a hazard.

Education and training

All workers should, on employment and periodically, be provided with education and training
in regard to sources of asbestos dust exposure, potential health effects, risks associated with
asbestos dust exposure and smoking, and methods of prevention.

All categories of personnel involved in the prevention of the asbestos-related diseases, such
as managers, technicians, trade union representatives, labour inspectors, administrators,
safety and health personnel, etc. – should be given appropriate training.

Specialised training in sampling, in analytical methods and in engineering aspects of asbestos

dust exposure should be provided for occupational hygienists and for other occupational
safety and health workers.
 Occupational physicians and other occupational health personnel should have specialised
training in the health effects associated with asbestos dust exposure, chest radiography, the
technical aspects of carrying out and interpreting pulmonary function tests and the principles
of screening.

References:

http://www.ilo.org/wcmsp5/groups/public/@ed_protect/@protrav/@safework/documents/norm
ativeinstrument/wcms_107843.pdf , accessed on 4 June 2012

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