This OC provides details of the health effects of diesel engine exhaust emissions (DEEEs), gives a summary of the findings from the DEEEs Technical Development Survey (TDS), updates the position regarding the WATCH review of these substances and advises inspectors on control of exposure.
1 There is limited evidence that an increased risk of cancer is attributable to exposure to the particulates found in DEEEs.
2 HSC/E requested a TDS to obtain more information on workplace exposure to and control of DEEEs; to inform the WATCH/ACTS work programme; and to produce future guidance. The TDS report has now been completed and circulated throughout HSE. It is entitled Exposure to diesel engine exhaust emissions in the workplace and can be found in file 292.
3 Although sustained exposure to DEEEs over many years may produce cancer, there is insufficient evidence overall for DEEEs to be regarded as "a carcinogenic substance" under COSHH.
4 Diesel engine exhaust emissions contain a complex mixture of gaseous and particulate substances. The latter arise from the incomplete combustion of fuel in a limited oxygen supply. The major components by mass are gases, particularly carbon dioxide, carbon monoxide and nitrogen oxides. Diesel engines produce a greater quantity of particulate matter than petrol engines. The diesel particulates are less than 1m in diameter and are easily inhaled into the lower respiratory tract. Hundreds of organic compounds have been identified in the particulate phase many of which are potentially carcinogenic polycyclic aromatic hydrocarbons (PAHs).
5 The quality and composition of DEEEs vary depending on the fuel used, the type of engine and whether the engine has been regularly maintained and tuned. Examination of samples has shown that the elemental carbon fraction varies from 60% to 80% and the soluble organic fraction from 15% to 40% of the particulate content. These components can be taken as useful indicators of exposure to diesel fume.
6 Details of the effect of DEEEs with regard to environmental contamination are given in Appendix 1.
7 There is consistent, although limited, epidemiological evidence of a small increase in the relative risk of lung cancer in certain occupations where there has been sustained exposure to DEEEs for more than 20 years. This evidence does not, however, satisfy the commonly- recognised criteria for establishing a definite causal relationship between this exposure and cancer. There is no convincing evidence of a carcinogenic risk in relation to shorter durations of exposure and it follows from this that there is no perceptible risk to the general population.
8 There is strong epidemiological evidence of an association between urban particulate atmospheric pollution, measured at PM10level (particulate matter less than 10m in diameter), and small increases in overall morbidity and mortality. Indications are that these mainly occur amongst the elderly and people with pre-existing respiratory illness. The contribution of DEEEs to these effects is uncertain. There is no evidence to suggest that these findings are of concern for occupationally-exposed groups.
9 Exposure to DEEEs also causes irritation of the eyes and the respiratory system.
10 Appendix 2 gives further details of health effects.
11 The TDS was carried out in 1994/95. The objectives of the survey were to:
(1) obtain quantitative information on workplace exposure to DEEEs; and
(2) assess the range of measures used to control exposure to the DEEEs.
The survey involved the collection of data from sites where diesel-powered vehicles were used and where there was likely to be an accumulation of DEEEs. Diesel exhaust emissions are also generated from stationary power sources which may be used during maintenance work for example.
12 Forty sites were visited during the TDS. These were categorised into 7 workplace groupings, based on overall work activities, which are as follows:
(1) ambulance depots;
(2) ro-ro ferries;
(3) railway repairs;
(4) bus garage and/or repairs;
(5) vehicle testing;
(6) fork-lift trucks;
(7) toll booths, set-down areas, tunnel repair sites.
However, placing the various sites into these groups was a pragmatic approach to categorising the data and it cannot be assumed that each site will fall neatly into any one of them.
13 Within each grouping, personal samples were taken from those employees likely to be exposed to DEEEs such as bus drivers, toll-booth attendants, car mechanics, and ro-ro ferry cargo workers. Static samples were also taken. Sampling periods for both categories were from 6-8 hours.
14 The TDS sampled for respirable dust, carbon monoxide, carbon dioxide, nitrogen dioxide and aldehydes. Both personal and static samples were taken for each substance, except aldehydes where static samples only were taken.
15 All except one of the concentrations for the gaseous components were below the relevant 8-hour TWA occupational exposure standards (OESs), the exception being a personal exposure to CO2of 8000 ppm (OES 5000ppm). This occurred in a vehicle testing station and is thought to be an anomaly due to contamination.
16 Where there was relatively high personal exposure to CO, this could be attributed to petrol engine vehicles, which emit greater concentrations of this gas than diesel engines. This could be a problem when sampling at toll booths where the majority of vehicles using bridges and tunnels are petrol driven.
17 All levels of formaldehyde were well below the maximum exposure limit (MEL) and those of acetaldehyde (which has no occupational exposure limit (OEL)) were of a similar order.
18 Both personal and static samples were analysed for respirable dust, elemental carbon (EC), organic carbon (OC) and total carbon (EC and OC combined). Statistical analyses show a wide spread in exposure patterns reflecting the different work practices, job categories and control methods. The geometric mean for all personal exposures to respirable dust was 0.193 mg/m3and ranged from nothing detected to 1.356 mg/m3(compare to the (pre-1996) COSHH "substantial" concentration for respirable dust of 5 mg/m3).
19 Mean personal and background concentrations of respirable dust, EC and OC were consistently high in premises where fork lift trucks were used, recording the highest levels for each of these amongst all categories of premises. Vehicle testing sites and toll booths/tunnels were generally at the lower end of the exposure range for all components.
20 Elemental carbon can be used as a marker of exposure to DEEEs where diesel engines are the only likely source of this component in the workplace (petrol engines produce only trace quantities). For personal exposures to EC, approximately 75% of the results were below 0.070 mg/m3and a result in excess of 0.200 mg/m3for EC would indicate 'high' exposure.
21 Measures used to control exposure to DEEEs in the workplace varied between premises, and included a combination of engineering controls, work practices (eg regular engine maintenance, turning the engine off when not in use) and job rotation.
22 The main types of engineering controls suitable for motor vehicle repair (MVR) and vehicle testing are engine exhaust filters and local tailpipe exhaust ventilation. However, while the former can be found at specialist test facilities, they are not normally found in average MOT testing and MVR premises.
23 Bus depots and railway locomotive depots tend to use a combination of general ventilation, local exhaust ventilation and roof extraction, but many use general ventilation only. A major drawback to such control is that much make-up air is provided by open doorways, which in winter tend to be shut to conserve heat thus causing DEEEs to accumulate.
24 In warehouses where fork-lift trucks are used, improved general ventilation as well as regular servicing are the 2 most important control measures. Proper management of delivery vehicles would also assist control.
25 Respiratory protective equipment was used to control exposure at only 2 sites.
26 The survey indicated that poor working practices, poorly-maintained engines and inefficient, poorly-maintained ventilation contribute to high exposure.
27 High exposure to gases, in particular CO2(over 1000 ppm 8-hour TWA) may indicate faulty, poorly-maintained or inadequately-designed control systems.
28 It is not possible to establish how far controlling exposure to the individual gaseous components to below their OELs will control the carcinogenic risk. However, reducing levels of these components at the workplace should reduce exposure to DEEEs in general and thereby the carcinogenic risk.
29 There is no marker of exposure to diesel exhaust as a whole. Elemental carbon is only produced in trace amounts by petrol engines, but constitutes a significant quantity of the diesel particulate mass. With some exceptions (coal mines, manufacture/use of carbon black) the diesel engine is likely to be the only significant source of EC in the workplace. This would indicate that EC may be a useful marker of exposure to DEEEs in the workplace, but only where the particulate component is the main concern.
30 HSE does not consider that the current evidence on the carcinogenicity of DEEEs is strong enough to satisfy the criteria according to which substances are classified as category 1 or 2 carcinogens under CHIP. However, the available data are such that the possibility of DEEEs possessing carcinogenic properties relevant to human health cannot be discounted.
31 HSE was unable to propose an OES to WATCH (February 1997), because there were insufficient data to establish a clear, reliable threshold for all potential health effects.
32 HSE also felt that it was inappropriate to propose an MEL due to the uncertainty of available data for all health effects.
33 Uncertainty over the most appropriate marker to indicate exposure to DEEEs presents a problem in seeking to establish any type of OEL.
34 WATCH agreed that:
(1) it was inappropriate to attempt to set either an MEL or an OES at the present time on the basis of current evidence;
(2) HSE should give further consideration to setting an OEL, as more evidence on other health effects, particularly irritancy, becomes available;
(3) specific guidance should be produced on DEEE exposure and control strategy, and include information on irritancy effects;
(4) while information on environmental PM10levels should be acknowledged it should not influence decisions on control of occupational exposure.
35 As DEEEs cannot be classified as either category 1 or 2 carcinogens under CHIP or meet equivalent criteria, the particular provisions in COSHH for the control of carcinogens
(regs.7(3) and 7(9)) do not apply. However, DEEEs are considered by HSE to be "a substance hazardous to health" and are therefore subject to the general provisions of the COSHH Regulations. These require that exposure be prevented or, where this is not reasonably practicable, adequately controlled.
36 As all gaseous components are consistently below their limits, monitoring of these will not directly assist enforcement of standards of control. However, as indicated in para 27, the measurement of gases, particularly CO2, can be a useful indicator of the overall adequacy of control measures. This is easily carried out and will therefore often be a first useful step in any assessment of DEEE exposure.
37 Similarly, respirable dust will almost always be found to be below the COSHH 'substantial' concentration. It is, however, also easily measured and can give an initial pointer for particulate exposure, allowing comparison with results from the TDS, indicating whether levels are relatively high or low. Information on EC levels can enhance this comparison, but analysis of this is costly and further advice should be sought before proceeding with this course.
38 It should be noted that the emphasis on measuring particulates has been with a view to controlling the carcinogenic risk. If the focus switches to irritancy as the lead health effect, this may not continue to be the case. At the moment there is much uncertainty as to what a suitable indicator might be and more research is required, although aldehydes are one such possibility. Measurement of these (formaldehyde and acetaldehyde) will at least help to build up a database of exposure for these substances and thus contribute to any investigation into this aspect.
39 If the question of the carcinogenicity of exhausts is raised by employers or employees, advice can be given that HSE is aware of a link between exposure to diesel exhausts and cancer, but that the risk is very slight and as such, does not merit being regulated as a carcinogen under COSHH.
40 Individual gaseous components of DEEE do have exposure limits, but, as the TDS showed, these are generally found at low levels. In most situations, therefore, it is unlikely that control can be enforced using these OELs.
41 Although irritancy is a commonly-experienced health effect from exposure to DEEEs, it is uncertain which component is responsible for causing it and it may, in fact, result from a synergistic effect of more than one. It is not feasible, therefore, to control this health effect by reducing any particular component, so control of exposure to DEEEs as a whole should be pursued.
42 Inspectors should therefore encourage employers to develop specific policies on DEEEs as "a substance" in their own right, the primary aim of which should be the prevention and control of exposure under COSHH. The main elements in the policy should be identified in a suitable and sufficient risk assessment and should consider the following.
(1) Prevention - by considering alternative technologies or fuels. The most suitable will depend on particular circumstances and any assessment should weigh the health risks of DEEEs against the health and other risks posed by alternatives, eg flammability.
(2) The use of lower emission/more fuel-efficient engines where possible. This should include investigation of the use of "green diesel" and of catalyst technology. Use of particulate filters, where appropriate.
(3) Adopting a programme of proper engine maintenance.
(4) Proper engine/vehicle management, eg by reducing idling times and unnecessary revving of engines; by switching off engines during long waiting periods, eg fork-lift trucks waiting for pallets to be loaded.
(5) Effective mechanical ventilation employed in areas which have restricted or inhibited fume dispersion. Tailpipe exhausts should be considered for vehicle maintenance/testing activities.
(6) Job rotation.
(7) Adequate information, instruction and training given to staff on the health hazards associated with DEEEs and the use and maintenance of control measures.
RSG occupational hygienists will give further advice in specific instances.
43 COSHH extends these duties on the employer to protect the health of the public, so far as is reasonably practicable. This provides a link to the air quality standard proposed by the DoE (now part of the Department of Environment, Transport and the Regions), but inspectors should not use the latter as a surrogate OEL (see Appendix 1 for further details).
44 Where complaints arise about exposure to DEEEs, the Occupational Health and Environment Unit (OHEU) would be interested to hear details, particularly if they relate to the effects of irritancy.
45 OC 292/1 )
) -cancel and destroy.
OC 292/1, Supplement 1 )
24 October 1997
Carbon: carcinogens: diesel: extraction (exhaust) ventilation: internal combustion engine: lift trucks: motor vehicle repair: particulate materials: railway(s): tunnels: ventilation: warehouses.
(paras 6 and 43)
1 Although often discussed as a single group, airborne particulates vary considerably in size and composition, depending on their source. Most originate from vehicle exhaust, in particular diesel exhausts, and they mainly consist of carbon and other organic compounds from unburnt fuel and lubricants, sulphates and nitrates and various other substances.
2 Attention from environmentalists has focused on particulate matter less than 10 m in diameter, collectively called PM10. These particulates may have a damaging physical effect on the lung surface; or in some cases initiate a chemical response constricting the airway; or in the long term may lead to the induction of cancer. The largest single source of environmental PM10in urban areas is road traffic, and within this category the largest component is that derived from diesel exhaust.
3 Short-term increases in environmental PM10are linked to slight decreases in lung function in healthy people and can increase frequency and severity of asthma attacks and other symptoms of respiratory illness. Deaths from all causes (but mainly from respiratory disease and heart disease brought on by breathing problems) increase after periods of high PM10. Furthermore, long term exposure to raised PM10levels in the environment also appears to affect the lung function, the symptoms of respiratory disease and the death rate.
4 In 1996, The Department of the Environment, (now part of the Department of Environment, Transport and the Regions (DETR)) proposed an air quality standard (AQS) of 50g/m3for airborne fine particles (called PM10s). This is based on evidence of increased morbidity and mortality, mainly amongst elderly people and those with pre-existing cardio-vascular or respiratory disease (ie it is not concerned with carcinogenicity). This is part of the Government national air quality strategy which, as well as other AQSs, will also include targets to reduce environmental air pollution and effectively control emissions especially from vehicles. Other pollutants chosen as the focus for the strategy include benzenes, CO, NO2, and polycyclic aromatic hydrocarbons (PAHs).
5 The DETR uses static sampling for measuring PM10levels in the environment and this is averaged over a 24-hour period; there is no simple method for measuring personal exposure. There is currently no established relationship between the AQS for PM10and possible health effects from occupational exposure to diesel exhaust emissions. Therefore, until further evidence is available, there is no reason to measure exposure to PM10in the workplace.
1 In 1989 a review of diesel engine exhaust by the World Health Organisation's International Agency for Research on Cancer (IARC) concluded that there was:
(1) "limited" evidence for carcinogenicity from epidemiological studies of occupational groups exposed to high cumulative levels of diesel engine exhaust;
(2) "sufficient" evidence for carcinogenicity from studies in experimental animals exposed to whole diesel engine exhaust.
Taken together IARC concluded that diesel engine exhaust fitted its carcinogenicity category 2A, ie "probably carcinogenic to humans". However this conclusion does not reflect convincing evidence of carcinogenicity relevant to humans.
2 In 1990 the Department of Health's expert Committee on Carcinogenicity (CoC) considered essentially the same evidence as IARC. They concluded that diesel engine exhaust was carcinogenic to rats and that it could be carcinogenic to humans at occupational exposure levels sustained over long periods.
3 In 1996 the CoC evaluated recent studies which looked at the carcinogenicity from DEEEs in rats and other animals, comparing it to other substances. They concluded that:
(1) the carcinogenicity of DEEEs appeared to be specific to the rat, caused by the overloading of lung clearance mechanisms with particulate and that this effect was not relevant to the assessment of risk to humans;
(2) available epidemiological evidence still indicated a carcinogenic effect from sustained occupational exposure over long periods ( >20 years), but there is no evidence of increased risk at lower cumulative exposures.
HSE accepted these conclusions.
4 Recent work in Germany indicates that small quantities of polycyclic aromatic hydrocarbons (PAHs) and other organic substances may be insufficient in themselves to explain the carcinogenicity of DEEEs. This appears to be associated with the particulate component, in particular the inert core of elemental carbon, although organic substances adsorbed onto the carbon particles are thought to play an important role.
5 As part of the same IARC studies it was shown that there exists "inadequate" evidence of carcinogenicity from whole petrol engine exhausts in both humans and in animals.
6 Occupational health studies have concentrated on the carcinogenic effect and there has not yet been a systematic review on irritancy, but accounts indicate that this is frequently encountered in the workplace.