AUSTRALIAN @ INSTITUTE OF OCCUPATIONAL HYGIENISTS DIESEL PARTICULATE MATTER AND OCCUPATIONAL HEALTH ISSUES Position Paper Association number: A0017462L ABN: 50 423 289 752 ISBN-13: 978-0-9577703-2-4 Prepared by: AIOH Exposure Standards Committee Updated August 2017 Authorisation: This Position Paper has been prepared by the AIOH Exposure Standards Committee and authorised by AIOH Council. Contact: AIOH Office | 03 9338 1635 | admin@aioh.org.auTable of Contents Australian Institute of Occupational Hygenists Inc (AIH). 3 Exposure Standards Committee Mission Statement 3 Statement of Position Regarding AIOH Position Papers 3 Consultation with AIH members... 4 Thirty-seventh AIOH Council 4 List of Abbreviations and Acronyms... 5 Definitions. 6 1. Background 9 2. What is diesel particulate matter (DPM)? 9 3, How do we measure it? 10 4, Hazards associated with DPM... 10 44. Lung cancer 10 42. Non-malignant respiratory disease 15 43. Other disease or effects 16 5, Major uses / potential for exposure (in Australia) 16 6. Risk of health effects 7 61. Traditional diesel exhaust versus new technology diesel exhaust. 7 62 Quantitative risk of lung cancer. 18 7. Available controls 20 8 Current applicable legislation and standards 2 9. AIOH recommendation 22 10.References and sources of additional information 23 Fsared br AGH Ecacume Suvinds GomesAustralian Institute of Occupational Hygenists Inc (AIOH) The Australian Institute of Occupational Hygienists Inc (AIH) is the association that represents professional occupational hygienists in Australia, Occupational hygiene is the science and art of anticipation, recognition, evaluation and control of hazards in the workplace and the environment. Occupational hygienists specialise in the assessment and control of: + Chemical hazards (including dusts such as silica, carcinogens such as arsenic, fibrous dusts such as asbestos, gases such as chlorine, irritants such as ammonia and organic vapours such as petroleum hydrocarbons); + Physical hazards (heat and cold, noise, vibration, ionising radiation, lasers, microwave radiation, radiofrequency radiation, ultra-violet light, visible light); and * Biological hazards (bacteria, endotoxins, fungi, viruses, zoonoses), Therefore, the AIOH has a keen interest in the potential for workplace exposures to Diesel Particulate Matter (OPM), as its members are the professionals most likely to be asked to identify associated hazards and assess any exposure risks. The Institute was formed in 1979 and incorporated in 1988. An elected governing Council, comprising the President, President Elect, Secretary, Treasurer and three Councillors, manages the affairs of the Institute, The AIOH is a member of the International Occupational Hygiene Association (IOHA). The overall objective of the Institute is to help ensure that workplace health hazards are eliminated or controlled. It seeks to achieve this by: + Promoting the profession of occupational hygiene in industry, government and the general ‘community. + Improving the practice of occupational hygiene and the knowledge, competence and standing of its practitioners. * Providing a forum for the exchange of occupational hygiene information and ideas. + Promoting the application of occupational hygiene principles to improve and maintain a safe and healthy working environment for all. + Representing the profession nationally and internationally. More information is available at our website — hitp://www.aioh.org.au. Exposure Standards Committee Mission Statement The AIOH established the Exposure Standards Committee to provide expert guidance and comment to the exposure standards setting process at a State and National level and internationally where appropriate, through development of AIOH Position Papers, AIOH guidance publications or ‘comment on relevant Standards, Regulations and Codes of Practice. The Committee's remit is to confirm that the exposure standards numbers, and Standards and Codes of Practice, are changed for valid occupational hygiene and scientific reasons. Statement of Position Regarding AIOH Position Papers The AIOH is not a standard setting body. Through its Position Papers, the AIOH seeks to provide relevant information on substances of interest where there is uncertainty about existing Australian exposure standards. This is done primarily through a review of the existing published, peer- reviewed scientific literature but may include anecdotal evidence based on the practical experience of certified AIOH members. The Position Papers attempt to recommend a health-based guidance exposure value that can be measured; that is, it is technically feasible to assess workplace exposures against the derived exposure value. It does not consider economic or engineering feasibility. As far as reasonably possible, the AIOH formulates a recommendation on the level of exposure that the typical worker can experience without significant risk of adverse health effects Any recommended guidance exposure value should not be viewed as a fine line between safe and unsafe exposures. They also do not represent quantitative estimates of risk at different exposure —— saa aieeuees Genie:levels or by different routes of exposure. Any recommended exposure value should be used as a guideline by professionals trained in the practice of occupational hygiene to assist in the control of health hazards Consultation with AIOH members AIOH activities are managed through committees drawn from hygienists nationally. This Position Paper has been prepared by the Exposure Standards Committee, with comments sought from AIOH members generally and active consultation with particular members selected for their known interest and/or expertise in this area. Various AIOH members were contributors in the development of this Position Paper. Key contributors included: Alan Rogers, Brian Davies, Tim White and lan Firth, Thirty-seventh AIOH Council President: Philip Hibbs (NSW) President Elect: Brian Eva (VIC) Secretary: Raelene Young (VIC) Treasurer: Jeremy Trotman (VIC) Councillors: Tracey Bence (WA), Andrew Orfanos (NSW), Perdita Dickson (VIC) == saa aieeuees Genie:List of Abbreviations and Acronyms ACES AIOH ALARP B75 co corp DE DEP DEEP DEMS DNA DPF DPM Ec EPA FEF oc FEV, FVC HEI HP HSE IARC gE 1om ISBN mgim? miisiKw pgim* um MAK MDG MSHA NeI NIOSH nm No Advanced Collaborative Emissions Study Australian Institute of Occupational Hygienists As low as reasonably practicable Biodiesel 75% blended with 25% diesel Carbon monoxide Chronic obstructive pulmonary disease Diesel exhaust Diesel exhaust particulate Diesel Emissions Evaluation Program Diesel Exhaust in Miners Study Deoxyribonucleic acid Diesel particulate fier Diesel particulate matter Elemental carbon Environmental Protection Agency (USA) Forced expiratory flow at 25-75% of forced vital capacity Forced expiratory volume after 1 second Forced vital capacity Health Effects Institute Horsepower Health and Safety Executive (United Kingdom) International Agency for Research on Cancer Immunoglobulin E Institute of Occupational Medicine International Standard Book Number milligrams (10 grams) per cubic metre metres cubed per second per kilowatt micrograms (10° grams) per cubic metre. micrometre (10* metres) Maximale Arbeitsplatzkonzentration Mining Design Guideline Mines Safety and Health Administration (USA) National Cancer Institute National Institute for Occupational Safety and Health nanometres Nitric oxide == <=No, Nitrogen dioxide Nsw New South Wales oHss Occupational Health & Safety PAH Polycyclic aromatic hydrocarbon PEFR Peak expiratory flow rate PEL Permissible Exposure Limit PMas Particulate matter with a diameter of 2.5 micrometres or less ppm parts per million aid Queensland Qcn Queensland Guidance Note REC Respirable elemental carbon RR Relative Risk Re Coefficient of Determination (measure of variance) SEG Similar exposure group SIMTARS Safety in Mines Testing and Research Station SMR Standard mortality ratio (observed deaths / expected deaths) Tc Total carbon TWA Time Weighted Average UK United Kingdom US/USA United States of America WA Wester Australia WEL Workplace Exposure Limit Definitions * Diesel exhaust: A complex mixture of toxic gaseous, adsorbed organics and particulate ‘components found in the raw exhaust emissions from diesel engines. + Diesel particulate matter: The particulate fraction of diesel exhaust. Hazard: Means potential to cause harm. Potency: Expression of relative toxicity of an agent, or measure of its strength, as compared to other toxic agents. + Risk: Means the probability of harm actually occurring + Toxicity: The quality of being toxic or poisonous, generally dependent on dose to cause harm == saa aieeuees Genie:AIOH Position on diesel particulate matter and its potential for Occupational Health Issues Key messages + Diesel particulate matter (DPM) at high concentrations is irritating to the eyes and respiratory system + Long-term low concentration exposure to DPM from older type diesel engines can also lead toa slight increase in the risk of cancer of the lung. + The AIOH believes that exposure may be adequately controlled by conventional means such as low emission engines and fuel, good engine maintenance, use of exhaust filtration systems, exhaust ventilation and segregation of workers from areas of high concentration + There are differences of opinion and interpretation regarding the degree of potential for cancer effects of DPM. The AIOH strongly encourages the “precautionary principle” approach in the management of diesel emissions. + AIOH recommends limiting worker exposure to DPM to as low as reasonably practicable {ALARP) below an 8-hour time weighted average (TWA) guidance exposure value of no more than 0.1 milligram (mg) submicron fraction elemental carbon in each cubic metre (m*) of air. In addition, a TWA value of 0.05 mg/m’ should be applied as an action level which triggers investigation of the sources of exposure and implementation of suitable control strategies. Summary This paper was compiled to give guidance on the assessment, evaluation and control of ‘occupational exposure to diesel particulate matter (DPM), with an emphasis on recommending a health-based guidance occupational exposure value. It is an update of the previous Position Paper on DPM issued by the AIOH in 2013, which in turn was an update of the 2007 version. This third update reflects the AIOH overview of the National Cancer Institute (NCI) / National Institute for Occupational Safety and Health (NIOSH) epidemiological ‘Diesel Exhaust in Miners Study’ (DEMS) and its recent review by the Health Effects Institute (HEI) and the Institute of Occupational Medicine (IOM), and the rationale behind the Intemational Agency for Research on Cancer (IARC) 2012 reclassification Although the adverse health effects of the gaseous fraction of diesel emissions have been known for some time, only in the last two decades has research indicated that the particulate component of the diesel exhaust has the potential to induce various health effects. In addition, diesel exhaust emissions are known to be associated with non-health aspects such as malodour, visual and nuisance pollution. Methods to monitor workplace exposures to diesel particulate (capture of the submicron aerosol fraction and analysis as elemental carbon; EC) are now readily available and control technologies have been developed for industries of known elevated exposure (e.g. underground mining). It should however be noted that EC is a surrogate for DPM, as it provides the best fingerprint of diesel particulate emissions, is relatively free of interferences and is chemically stable, unlike the adsorbed organic carbon fraction. Based on animal and epidemiological studies, it is now apparent that exposure to DPM from traditional diesel engines presents an increased risk of lung cancer. The 2012 IARC classification of diesel engine exhaust as a Group 1 carcinogen is a continued progression of toxicological and epidemiological information that has been accumulating in the literature over the past 30 years. However, due to information deficiencies in the literature, particularly regarding lack of data on past exposure conditions, including the multistage surrogate data used in the 2010 NCI/NIOSH study, the AICH has serious concerns as to the degree of potency being assigned to diesel particulates by some regulatory authorities. == saa aieeuees Genie:The NCI/NIOSH study has been subject to a number of critical reviews in the literature, the most recent by Méhner and Wendt (2017) who are from the German Federal Institute of Occupational Safety and Health and advisors to the German MAK Commission and the Commission of Hazardous Substances, The recent HEI review found that, while the NCI/NIOSH study was found to have many strengths, there were some key limitations and uncertainties in terms of the exposure estimates and the application of such exposure-response data for quantitative risk assessment. The IOM review found evidence of a weak dose response relationship with wide confidence intervals for lung cancer for the NC//NIOSH study group, hence uncertainty about which exposure- response function is the most appropriate to use to describe risks associated with DPM exposure, particularly at higher levels. They suggest it may therefore be impractical to set a meaningful health-based limit on occupational exposure to DPM, although the evidence is strong enough to recommend controlling exposures to DPM to the lowest level that is technically achievable, Méhner and Wendt (2017) concluded that the currently published studies provide little evidence for a definite causal link between DE exposure and lung cancer risk. It should also be noted that the vast majority of considered exposure in the NCI/NIOSH study came from diesel engines produced in the 1970's and earlier. The altered chemical emission profile found with contemporary engines, improved mining ventilation and improved fuels is now quite different to past DPM exposures upon which the toxicological and epidemiology studies were based. There is little doubt that this area of the health debate will continue for some time within the scientific and regulatory community, due in part to limitations in the epidemiological studies. Limitations are imposed by the requirements for suitable large sized study populations necessary to study common cancers such as lung cancer; the issues in dealing with a 30 to 40-year latency; the absence of actual exposure data over the long latency period; and the control of confounders, particularly due to the overwhelming effects of tobacco smoking on lung cancer outcome in the population. Given the difficulties of finding rigorous and statistically valid historical exposure data, particularly in regard to potency, the issues may never be completely or adequately resolved, Notwithstanding the lack of a well-defined universal dose response relationship, experience has shown that when workplace exposures are controlled below 0.1 mg/m? DPM (measured as submicron elemental carbon), irritant effect decreases markedly. Méhner and Wendt (2017) note that an upper bound for the cumulative exposure of 2.5 mg/m*-years respirable elemental carbon (REC) seems to be sufficient to prevent a detectable increase of lung cancer risk. This value they put as corresponding to an average annual exposure value of 0.05mgim® REC assuming an ‘exposed’ working life of 45 years. In the absence of any more definitive data, the AIOH supports the maintenance of DPM levels (measured as submicron elemental carbon) as low as reasonably practicable’ (ALARP) below an 8- hour TWA guidance exposure value of 0.1 mg/m’, with the provision of applying a TWA value of 0.05 mg/m* as an action level which triggers investigation of the sources of exposure and implementation of suitable control strategies. The AIOH is of this opinion, as such a limit is a balance between the factors of minimising irritation and minimising the potential for risk of lung cancer to a level that is not detectable in a practical sense in the work force. The most effective means of restricting DPM exposure is to apply the hierarchy of controls; for example: + elimination of diesel equipment through the use of alternative powered equipment, where feasible (e.g. electrical), provision of low emission diesel engines and fuel, provision of air conditioned (filtered) operators’ cabins, exhaust ventilation, good engine maintenance, use of exhaust filtration systems, administrative controls (e.g. limits on overtime and tag boards), "The meaning of reasonably practicable’ is as sot outin section 18 of the Work Health and Safety Act (2011), Essentially, it means that al practical precautions need to be idented for controls followed by a process to determine reasonableness. —— saa aieeuees Genie:+ worker education and training, and * use of appropriate respiratory protection. It should be understood that more than one control strategy will likely be required to reduce worker exposures to ALARP levels. Whatever strategy is adopted it should be under-pinned by an effective maintenance program so that emission reductions are sustained Health risk relative to the recommended 0.1 mg/m® guidance exposure value and the 0,05 mgim? action value dealing with the need for controls and health surveillance should be determined by a Certified Occupational Hygienist applying ‘Occupational Hygiene Monitoring and Compliance Strategies’ as published by the AIOH eae This position paper is the fourth document produced by the AIOH on DPM. Each has amalgamated the experiences of the AIOH Exposure Standards Committee members and other senior AIOH members who have for decades been involved in investigating, researching, monitoring and implementing control strategies to minimise worker exposure to DPM. In so doing they have been at the forefront of advising industry, state and federal government departments and various mining regulators on the issue. Each document follows its predecessor and builds on any updated or changing data. The sequence of papers is as follows: + Davies, B & Rogers, A (2004). A Guideline for the Evaluation and Control of Diesel Particulate in the Occupational Environment, The Australian Institute of Occupational Hygienists, Inc. ISBN 0 9577703 5 9. + AIOH (2007). Position Paper — Diesel Particulate and Occupational Health Issues. The Australian Institute of Occupational Hygienists, Inc. May 2007 + AIOH (2013). Position Paper — Diesel Particulate and Occupational Health Issues. The Australian Institute of Occupational Hygienists, Inc, May 2013. This current version of the DPM Position Paper is the outcome of review of an ever-increasing published literature on the topic, often at times with opposing views, and AIOH member comment received on a draft version of this paper. The literature on DPM is extensive and a complete review is beyond the scope of this Position Paper. A recent report by the Health Effects Institute (HEI, 2015b) reviewed over 200 references and an Institute of Occupational Medicine report (MacCalman et al, 2015) overviewed more than 60. This paper contains over 50 references including several reviews and meta-analyses selected to illustrate points considered relevant 2. What is diesel particulate matter (DPM)? Over the past 115 years the invention of a compression ignition engine by Rudolph Diesel in the 1890's has contributed significantly to the productivity of many nations, owing to the widespread use of larger diesel powered equipment in most industrial activities. The down side in terms of occupational health has been the exposure of a large number of workers to the complex mixture of toxic gaseous, adsorbed organics and particulate components found in the raw exhaust emissions; here referred to as diesel exhaust (DE). The gaseous phase of diesel exhaust is a complex mixture consisting principally of the products of complete combustion, small amounts of the oxidation products of sulphur and nitrogen, and ‘compounds derived from the fuel and lubricant. It consists largely of the same gases found in air, such as nitrogen, oxygen, carbon dioxide and water vapour, as well as carbon monoxide (Elliot et al, 2012). The particulate fraction of the diesel exhaust aerosol (here referred to as DPM) consists of a solid carbon phase and ultrafine droplets of a complex mix of semi-volatile organic compounds. The solid particulate fraction consists mainly of very small particles (typically 15-30 nm diameter) that rapidly agglomerate together to form “chains” or clumps of particles, which are themselves typically ——— sn Sy<1 ym aerodynamic size. High resolution electron microscopy has demonstrated that the basic diesel particle consists of an irregular stacked graphitic structure, nominally called elemental carbon. The graphitic nature and high surface area of these very fine carbon particles means they have the ability to absorb significant quantities of hydrocarbons (the semi-volatile organic carbon droplets and vapours) originating from the unbumt fuel, lubricating oils and the compounds formed in the complex chemical reaction during the combustion cycle. In terms of health outcome, the very small Particle size of DPM is important as this means it can reach the deep parts of the lungs. The AIOH considers that the particulate fraction of DE is most likely associated with any carcinogenic potential. Regulatory trends in emission controls and fuel quality have led to alterations in the chemical fingerprint of DE, such that modern engines, particularly those post 2007, now emit much lesser quantities of carbon particulates (EC), less sulphur (as sulphates) and as a consequence there are more detectable numbers of ultrafine droplets of semi-volatile organic compounds (as these are less readily adsorbed onto the surface of the reduced quantities of carbon particulates). 3.__ How do we measure Methods for the quantification of employee exposure to diesel particulate have been developing over approximately 30 years. The most advanced and specific method involves capturing the submicron fraction of the workplace aerosol and then determining the amount of the core component of diesel particulate (elemental carbon; EC). EC is used as a surrogate for DPM as it provides the best fingerprint of diesel particulate emissions, is relatively free of interferences and is chemically stable, unlike the adsorbed organic carbon fraction. Recent commercial developments provide ease in routine submicron sampling using a single use impactor cassette, fitted into a respirable aerosol cyclone, which is necessary when sampling in dusty atmospheres to prevent clogging of the cassette impactor holes. The impactor plate in the DPM cassette may not be required when sampling in environments when other mechanically generated aerosols are at a very low level and / or when these aerosols are known not to contain organic carbon such as that found in coal dust, Sample analysis on the captured aerosol is best conducted using United States (US) National Institute for Occupational Safety and Health (NIOSH) method 5040 (NIOSH, 2016) for determination of carbon species (especially elemental carbon), however care needs to be exercised to minimise errors due to sampling, blank filter interpretation and instrument operating parameters (Davies & Rogers, 2004) At this stage, there is no evidence that unproven methods, which rely on measuring the number of ultrafine droplets of semi-volatile organic compounds based on insufficient primary calibration methods, provide a suitable alternative or better method of defining exposures for health assessment purposes. Real-time monitoring instruments currently on the market can be used as very useful indicative instruments, in helping identify DPM sources and to manage and reduce DPM levels. However, these need to be adequately calibrated against traceable primary standards such as for total carbon (TC) or EC. Gem Sed Ce RL 44 Lung cancer in 1988 the US NIOSH published Criteria Bulletin No.50 (NIOSH, 1988) which proposed a potential link between occupational exposure to diesel exhaust and lung cancer. The NIOSH finding was based on the consistency of toxicological studies in rats and mice and limited epidemiological evidence, mainly from railroad workers. The Health Effects Institute (HEI, 1995) undertook a review of the toxicological studies including acute and chronic effects (such as risk of lung and other cancers). It also included the 30 epidemiological studies of workers exposed to diesel emissions in occupational settings for the ——— a Syperiod 1950 to 1980. About half of these epidemiological studies indicated an increased risk of lung cancer and the remainder showed no increase in lung cancer risk. After considering the positive outcome studies only, HEI concluded that the epidemiological data was "generally consistent in showing a weak association between exposure to diesel exhaust and lung cancer” with a relative risk between 1.2 to 1.5, They issued a note of caution indicating that all of the studies lacked definitive exposure data for the populations studied and most had an inability to determine the influence of confounding factors, such as tobacco smoking. The US Mines Safety and Health Administration (MSHA, 2001) reviewed 47 epidemiological studies and determined that in 41 studies there was some degree of association between occupational exposure to diesel particulate matter and an excess prevalence of lung cancer. However, some of these studies had limited statistical power either because they included relatively few workers or had an inadequate allowance for latency or follow up period. MSHA then concluded, based on the studies with positive lung cancer outcomes and implied estimates of historical exposure levels, that exposure at a mean concentration of 0.64 mg/m? DPM for a period of 45 years would result in a relative risk of 2.0 for lung cancer. The United States Environmental Protection Agency (US EPA) conducted a health assessment for diesel engine exhaust (US EPA, 2002). They concluded that lung cancer was evident in occupationally exposed groups but could not define sufficient dose response data to produce a quantitative risk assessment. The above reviews by US EPA and MSHA had flagged an epidemiological study with a potential dose response component that was being conducted by a joint National Cancer Institute (NC!) and National Institute for Occupational Safety and Health (NIOSH) research program. This NCI/NIOSH multi study, published as the ‘Diesel Exhaust in Miners Study’ (DEMS), consisted of a cohort of 12,315 mine workers from eight underground non-metal hard rock mines with DE, operating from 1946 onward. A retrospective cohort mortality and nested case-control design was used to study associations between retrospective estimates of exposure to DE and health outcome such as mortality and lung cancer (Attfield ef al, 2012; Silverman et al, 2012). Mortality analysis indicated a lung cancer SMR of 1.21 for ever-underground workers and 1.33 for surface only workers. Using a number of steps and various surrogates of exhaust emission exposure, the researchers made estimates of retrospective exposures to respirable elemental carbon (REC — similar to submicron EC) over the previous 50 years and were able to produce in the mortality and case control analysis a dose response trend between cumulative and average intensity of exposure and relative risk (RR) of lung cancer (Stewart ef al, 2010). A trend was found for the group of underground workers, with no trend for surface workers, a finding attributed to this group's lesser exposures. The DEMS retrospective exposure methodology, which stepwise linked historical carbon monoxide (CO) data, equipment power, ventilation rates and varying mining and haulage methods over time, to contemporary EC exposures, based on log-log transformations, provided very poor correlation coefficients that were not statistically significant in each step of the analysis. The major assumption in the retrospective exposure estimations was that there is a reliable quantitative relationship between CO and REC emitted from diesel engines, However, examination of the data pairs indicates considerable scatter and there appears to be little visual evidence of a relationship and a great deal of uncertainty about any presumed relationship between CO and REC, particularly in light of previously published data (e.g. CO to REC r’=0.17, engine power to CO r’=0.01) and the subsequent re-analysis of the exposure estimates by other authors (Crump & van Landingham, 2012; Crump et al, 2015), Of concern in the Attfield ef a/ (2012) study was the finding that, despite their much higher DE exposure intensity (75 times higher), the lung cancer risk for ever-underground workers was somewhat lower (only 64%) than that of surface-only workers (SMR 1.21 vs. 1.33). This resulted in steeper exposure-response slopes being observed for surface-only workers than for ever- underground workers. Even the primary internal cohort analysis did not show an association between cumulative REC exposure or average REC intensity and lung cancer mortality. A positive == saa aieeuees Genie:exposure-response relationship was only seen when the (time-dependent) binary variable “work location” was included in the model (Méhner & Wendt, 2017). IARC reconvened a working group to review new data available on evidence of carcinogenic effect but not necessarily the potency of DPM since its 1989 classification of 2A (probable human carcinogen). In June 2012 IARC classified diesel particulate extract as carcinogenic to humans (Group 1), on the basis that on its analysis there was now sufficient evidence from human and animal studies. A summary of the findings indicates the basis was due to mounting concern on findings in epidemiological studies across workers exposed in a range of settings and the 2012 NCUNIOSH ‘Diesel Exhaust in Miners Study’, all of which re-emphasised evidence on which the decision was made (IARC, 2012). The detailed review of all data and the reasoning for changes in classification was included in IARC Monograph #105. The Working Group concluded that the more informative studies, many of which controlled for tobacco smoking, consistently showed a positive association between exposure to diesel engine exhaust and the risk of lung cancer. Most of the ‘comparisons of exposed and non-exposed groups indicated modest increases in risk, and analysis showed statistically significant exposure-response trends and it was improbable that these exposure-response trends were caused by chance, bias or confounding (IARC, 2013). IARC (2013) noted that diesel engine exhausts and the mechanisms by which they induce cancer in humans are complex and no single mechanism appears to predominate, They concluded that there is strong mechanistic evidence that DE, as well as many of its components, can induce lung cancer in humans through genotoxic mechanisms that include DNA damage, gene and chromosomal mutation, changes in relevant gene expression, the production of reactive oxygen species and inflammatory responses. In addition, the co-carcinogenic, cell-proliferative and/or tumour-promoting effects of other known and suspected human carcinogens present in DE probably contribute to its carcinogenicity in the human lung, Steiner ef al (2016) concluded that adverse health effects of DE are not only due to its chemical composition, but also from the interplay between its physical properties, the physiological and cellular properties, and function of the human respiratory tract. Inhalable DE particles, which can carry condensed compounds of potentially high toxicity on their surface, are not efficiently filtered from the inhaled air and penetrate the respiratory tract deeply, depositing on or translocating across the lung epithelium to evade otherwise efficient clearance mechanisms. The overall result is the induction of oxidative stress, pulmonary, systemic inflammation and, partly as a consequence of the latter two and partly via separate pathways, the damage of genetic DNA and thereby the potential formation of mutations and ultimately tumours. In a re-analysis of two population-based lung cancer case-control studies conducted in Montreal, Pintos et al (2012) examined the risk of lung cancer among men associated with exposure to DE emissions incurred in a wide range of Canadian occupations and industries. Increased risks of lung cancer were found in both studies. The pooled analysis showed an odds ratio of lung cancer associated with substantial exposure to DE of 1.80 (95% Cl 1.3 to 2.6). The risk associated with substantial exposure was higher for squamous cell carcinomas than other histological types. Joint effects between DE exposure and tobacco smoking were compatible with a multiplicative synergistic effect. Gamble ef af (2012) concluded that the NCVNIOSH study results from all occupational cohort studies with quantitative estimates of exposure have limitations, including weak and inconsistent exposure-response associations that could be explained by bias, confounding or chance, exposure misclassification, and often inadequate latency. In sum, they thought that the weight of evidence is considered inadequate to confirm the diesel-lung cancer hypothesis. Indeed, the NCI/NIOSH study has been subject to a number of critical reviews in the literature (Gamble et al, 2012; Hesterberg et al, 2012; Crump et al, 2015; Crump et al, 2016; Mohner & Wendt, 2017) and was subject to a detailed examination by an HEI Epidemiology Panel to make a determination whether or not the DEMS data and results could now form the basis for a quantitative characterisation of the lung cancer risks associated with DE (HEI, 2015). Most uncertainty was associated with the choice of the surrogate exposures of CO and the relationships between horsepower (HP), CO and REC relative to emissions over time (see also Crump et al, 2016). The —— saa aieeuees Genie:Panel agreed that these are potentially important sources of uncertainty in the exposure estimates and therefore in the exposure-response relationships that might be derived from the study. Alternate exposure assessments were tested by the Panel that did not rely on the HP-CO-REC relationships, and the exposure-response association remained, albeit producing differing risk coefficients. DEMS was found to be a well-designed and well conducted study and had made considerable progress to addressing a number of major limitations that had been identified in previous epidemiological studies targeted at diesel exhaust exposure and lung cancer. While the study was found to have many strengths, it was acknowledged by the Panel that there were some key limitations and uncertainties in terms of the exposure estimates and the application of such exposure-response data for quantitative risk assessment. Part of the HEI review involved developing alternate risk estimates for the DEMS study using adjusted exposure estimates and adjusted smoking histories, which produced a range of outcomes demonstrating the fragility of the data selection and analysis associated with the original published data set. Nevertheless, the Panel concluded that the basic association of lung cancer with DE exposure was essentially robust to alternative modelling approaches in both the DEMS cohort and case-control studies. The studies provided results and data that provide a useful basis for quantitative risk assessments of exposures, in particular to older diese! engine exhaust, although the “uncertainties within each study should be considered in any attempts to derive an exposure-response relationship”. In response to a commissioned investigation by BHP-Billiton, the Institute of Occupational Medicine (IOM) analysed the available lung cancer dose response studies, relying almost exclusively on the NCUNIOSH study (MacCaiman ef al, 2015). The authors commented on the multiple complexity of the positive and negative bias inherent in the studies and came to the opinion that the exposure level estimates applied in the dose response epidemiological studies were likely to be too high, especially in the DEMS miners study, and adjusted the exposure data accordingly to lesser values Applying the adjusted data in a risk model produced predictive working lifetime lung cancer risk estimates associated with a range of 45 year working lifetime cumulative exposure levels. The result found some consistency in predictive risk outcomes at the lower level exposures, however the variability at the extrapolated high exposure levels (such as 0.1 mg/m? as the average exposure every working day for a duration of 45 years) was found to be considerable with a 20-fold difference between the lower confidence limit and the upper confidence limit. The IOM cumulative exposure value (4.5 mg/m*.years) is 4.5 times greater than the highest cumulative exposure group in log linear models applied to the combined DEMS and the two truckers (Steenland ef al, 1998; Garshick et al, 2012) and miners’ studies (Vermeulen ef al, 2014). 1OM concluded ‘There does seem to be evidence of an increasing trend in risk associated with DEP exposure, although the nature of the relationship, particularly for higher exposures, is still unclear resulting in uncertainty about which exposure-response function is the most appropriate to use to describe risks associated with DEP exposure, particularly at higher levels. Given the level of uncertainty at levels of 0.1 mg/m® (cumulative working life exposure 4.5 mg/m® years) it does not make sense to make any predictions of risk at this level.’ They also conclude that: + The derived exposure-response relationships suggest that exposure to DPM is associated with a marked elevation in lung cancer risk even at relatively low levels of exposure. + There are practical difficulties in lowering exposures to a level associated with a predicted lifetime cancer risk of less than 0.1% or even 1%. + It may therefore be impractical to set a meaningful health-based limit on occupational exposure to DPM. However, the evidence is strong enough to recommend controlling exposures to DPM to the lowest level that is technically achievable. Méhner et al (2013) reassessed lung cancer risk associated with occupational exposure to DE in German potash miners, while controlling for potential confounders such as smoking and previous occupational history, in particular uranium mining. The re-analysis revealed that while about 4% of all study subjects had worked earlier in uranium mines, 10.3% of later lung cancer cases did so. Although their absolute number was small, the corresponding relative risk estimator was significantly elevated. Their analysis did not show any notable association between cumulative REC exposure and lung cancer risk == saa aieeuees Genie:Sun et al (2014) critically evaluated 42 cohort studies and 32 case-control studies from between 1970 to 2013 to examine the association between DE exposures and lung cancer. In general, they found that previous studies suffer from a series of methodological limitations, including design, exposure assessment methods and statistical analysis used. They noted that a lack of objective exposure information appears to be the main problem in interpreting epidemiological evidence. To facilitate the interpretation and comparison of previous studies, a job-exposure matrix of DE exposures was created based on around 4,000 historical industrial measurements. The values from the job-exposure matrix were considered during interpretation and comparison of previous studies. Overall, neither cohort nor case-control studies indicate a clear exposure-response relationship between DE exposure and lung cancer. They conclude that epidemiological studies published to date do not allow a valid quantification of the association between DE and lung cancer, although such an association cannot be ruled out. They further note that causality of weak association is often difficult to establish, since it is susceptible to all forms of possible design bias. Crump et al (2015) re-analysed the DEMS case-control study by Silverman ef al (2012) and, while largely managing to reproduce its results, they found that radon exposure underground proved to be a main confounder, which Silverman et al did not include in their final models, Crump ef al (2015) also developed six new DE exposure metrics, as an alternative to the estimates used by Silverman et al. If these alternative DE exposure metrics were used, and also adjusted for the radon exposure, there was no significant association between the cumulative DE exposure and lung cancer mortality. In a further re-analysis of the DEMS work, Crump et al (2016) used new estimates of REC exposures using historical data on use of diesel equipment, diesel engine HP, mine ventilation rates, and the documented reduction in particulate matter emissions per HP in diesel engines from 1975 through 1995 to find that none of the trend slopes calculated were statistically significant. These results underscore the uncertainty in estimates of the potency of DE in causing lung cancer based on analysis of the DEMS data due to uncertainty in estimates of exposures to diesel exhaust. Méhner and Wendt (2017) noted the influence of the NCINIOSH study on the IARC (2012) classification and conducted a critical review of the studies used by the IARC working group to evaluate the relationship between DE and lung cancer, They included 18 cohort studies and 13 case-control studies. This review highlighted several methodological flaws in the studies, amongst them over adjustment bias, selection bias and confounding bias. The conclusion was that the currently published studies provide little evidence for a definite causal link between DE exposure and lung cancer risk. They did note that, based on two studies in miners, the DEMS and the German potash miners study, quantitative risk assessment may be conducted; “Considering the high DE-intensity levels in underground mines, underground workplaces seem to be the most appropriate site for deriving robust estimates for a possible dose-response relationship between DE- exposure and lung cancer risk’. They noted the unusual adjustment of REC exposure for smoking cross-classified with work location led to strong over adjustment bias and suggested an alternative hypothesis for the observed relationship would be the presence of a healthy worker effect. They suggest that the DEMS data should be reanalysed in advance to avoid bias that affects the presently published risk estimates. Based on their interpretation of the toxicological and epidemiological data, regulatory authorities in USA, Europe and Canada have concluded that sufficient evidence exists to indicate that diesel Particulate presents an increased risk of lung cancer, although the absolute quantification of potency remains unclear. The UK HSE simply cites the IARC 2012 classification of DE as carcinogenic to humans. A NSW Coal Industry cancer surveillance study has shown no significant cancer risk for underground workers exposed to high levels of diesel particulate (SMR of 0.85 all cancers, 0.74 for lung cancer) (Brown et al, 1997). This is supported by a systematic review by Jenkins ef al (2013), who identified 34 studies published since 1980 specifically examining the increased risk of cancer associated with coal mining and associated activities. Twenty-seven of these explicitly examined coal minersicoal mining as an occupational cohort or risk factor, and the liver was the only cancer site for which an increased risk was reported. == saa aieeuees Genie:It would appear that in practice if such high predicted risks were real then they would have been consistently found in many of the published epidemiological studies, where in fact no measurable increase in lung cancer risk has been detected in the vast majority of studies. For example, including the NSW coal mine workers (Brown et al, 1997) and by indirect exposure inference Western Australian (WA) underground gold miners (de Klerk & Musk, 1998). While the original NCVNIOSH DEMS study may provide some evidence of a dose response relationship with wide confidence intervals for lung cancer for this specific study group, in practice how this relationship applies to other occupational situations and differences in the altered chemical emission profile found with contemporary engines remains unclear at this stage. Given the Conflicting outcomes of the various reviews presented and the previously stated opinion regarding an association between cumulative DE exposure and lung cancer mortality, the potency of DPM as a carcinogen appears to be weak. 42 Non-malignant respiratory disease The US EPA (2002) noted that for short-term DE exposures, reversible changes in pulmonary function in humans can occur, although it was not possible to relate these changes to specific exposure levels. In studies of underground miners, bus garage workers, dockworkers and locomotive repairmen, increases in respiratory symptoms (cough, phlegm and dyspnoea) and decreases in lung function (FVC, FEV;, PEFR, and FEF»s.75) over the course of a work shift were generally found to be minimal and not statistically significant. Smokers appeared to demonstrate larger work shift respiratory function decrements and increased incidence of respiratory symptoms. The use of a biodiesel fuel (B75) lowered respirable DPM exposure and consequently some associated acute health effects (lung function), although lung and systemic inflammation were not reduced compared with diesel use (Mehus et al, 2015). In the long-term longitudinal and cross-sectional studies reviewed by the EPA (2002), a relationship was generally observed between work in a job with diesel exposure and respiratory symptoms (such as cough and phlegm), but there was no consistent effect on pulmonary function. There were various biochemical and pathophysiological alterations, such as IgE changes, altered levels of cytokines/chemokines, and goblet-cell hyperplasia, with nearly all these responses being key changes and markers of allergic inflammatory disorders of the airways such as asthma and nasal allergies. The HEI has produced a detailed review of the epidemiological studies of non-malignant respiratory disease in groups of workers exposed to diesel particulate emissions. HEI (1995) found that diesel exhaust exposures produced chronic changes in lungs of laboratory animals and this may be a problem if the effects were transferable to humans. In reviewing short-term exposure studies little evidence was found for changes in pulmonary function related to diesel exhaust exposure, and it was unclear as to what extent such acute response would indicate the potential for chronic respiratory disease. In long-term exposure studies (six of which addressed effects in miners) some studies suggested a slight decrease in lung function, but overall the studies do not provide strong or consistent evidence for chronic, non-malignant respiratory effects associated with occupational exposure to DPM. In addition, HE! found that the published mortality studies to 1995 do not provide consistent evidence of an effect of occupational exposure on mortality from non-malignant respiratory disease. Studies funded and published by HEI examined the pulmonary effects of exposure to DPM on non-smoking asthmatics (HEI, 2009). The studies indicated only minor reductions in lung function and airways inflammation indicating little biological response in these lung sensitised individuals. The studies are in line with those reporting similar effects on workers exposed to break down products from natural polymers, such as proteins and vegetable oils, occurring in the process of cooking some foods. Emerging review studies on exposures to ultrafine Particles in air pollution studies are tending to indicate that mortality and morbidity effects are better explained by PM, fraction of aerosols rather than the ultrafine fraction which is less than 100 nanometre size (HEI, 2013). == saa aieeuees Genie:Nevertheless, Hart et al (2012) found that while the available literature directly examining the effects of occupational DE on risk of chronic obstructive pulmonary disease (COPD) is quite small, it does suggest that increasing exposures are associated with increasing risk. They do however note that additional research with more advanced exposure metrics is needed to fully elucidate such an association. 43 Other disease or effects The most readily identified acute non-cancer health effect of DE on humans is its ability to elicit subjective complaints of eye, throat and bronchial irritation and neurophysiological symptoms such as headache, light headedness, nausea, vomiting and numbness and tingling of the extremities. There is considerable variability in the reported DE detection threshold. In fact, there is substantial inter-individual variability in the ability to detect odour and the level at which it becomes objectionable (US EPA, 2002). AIOH publications have noted that the level of eye and upper respiratory tract irritation is significantly reduced at DPM exposure concentrations of 0.2 mgim®, or approximately 0.1 mg/m? submicron EC (Pratt et al, 1997; Rogers & Davies, 2005). The irritation issue and data was also presented at the ACGIH Conference in Seattle in 1998. Epidemiological studies suggest that an increase of PM;s DPM in ambient air corresponds to increased myocardial infarctions and atherosclerosis. When exposed to DPM, endothelial cells exhibit increases in oxidative stress and cell death (Wang et al, 2017). Using the DEMS study data, Costello ef a! (2016) also determined that exposure to diesel exhaust underground may also increase the risk of mortality from ischaemic heart disease, Peters ef al (2013) determined that parental occupational exposure to DE may increase the risk of childhood brain tumours. IARC (2013) noted that a positive association has also been observed between exposure to DE and cancer of the urinary bladder. 5. _ Major uses / potential for exposure (in Australia Potential for exposure to DPM exists whenever workers are in close proximity to operating diesel equipment and is ubiquitous in low level exposure for workers in the transportation industry. In many cases the fact that the equipment is operating in the open environment significantly reduces the potential for excessive exposures. Exposure assessments conducted aboard diesel locomotives have ranged from <0.001 to 0.045 mg/m*, with a geometric mean of 0.0037 mg/m’ (as EC) (Liukonen ot al, 2002). Levels for forklift operators have ranged from 0.007 to 0.40 mg/m’, with a median of 0,075 mgim* (as EC) (Groves & Cain, 2000). Conversely, where diesel equipment is operating in confined areas (e.g. underground mines, ships’ holds, cool rooms, and large truck loading and unloading depots) there is a significant risk of exposure. Past levels in Australian underground coal mines have been measured at 0.01 to 0.37 mgim* (as EC) (Joint Coal Board, 1999; Rogers, 2005), although levels up to 2.2 mg/m* DPM have been measured, depending on job type and mining operation (Pratt et al, 1997). Levels in Australian underground metallferous mines have been measured at 0.01 to 0.42 mg/m* (as EC) (Rogers & Davies, 2001 & 2013). Considering the underground mine cohort studies used to determine quantitative exposure-response assessment, the mean REC exposure of production workers in the German potash mine study was 0,15 mg/m’, while that for underground potash mines in the DEMS were 0.12 to 0.22 mg/m’. The DE-exposure among underground workers in the DEMS was nearly two orders of magnitude higher than at typical surface workplaces with potential exposure to DE, including mining jobs at surface level (Mahner & Wendt, 2017). Investigations in 2005 and 2006 by SIMTARS also found elevated exposures in Queensland underground metalliferous mines (Hedges, 2007). However, for one mine that implemented comprehensive DPM controls, there was a decrease in the arithmetic mean EC personal exposures for all similar exposure groups (SEGs) combined from 2005 to 2006; 0.09 to 0.04 mgim’, For surface mining operations, forklift operators have been found to be the highest exposed group (Dabill, 2004) ——= saa aiaeiaes Gomeeiee:Levels in Queensland underground coal mines have been measured as annual mean values for various SEGs at between 0.04 to 0.2 mg/m* (as EC) (Manthey et al, 2013) between 2004 to 2012 for 3,253 personal samples. There were significant differences between SEGs and mines. The Development Production SEG, arguably the most at-risk group, was the most frequently sampled (32%) and had a mean DPM (as EC) concentration of 0.071 mg/m® (with 95% confidence limits of 0.066 to 0.078) in 2012. Other SEG mean exposures in 2012 were as follows: Longwall Production — 0,063 mg/m®, Underground Maintenance — 0.044 mgim*, Outbye Supplies — 0,045 mg/m°, Longwall Moves — 0.099 mgim?; Outbye Construction / infrastructure — 0.06 mgim®; VCD installers — 0.053 mg/m*; ERZ controllers — 0.039 mg/m*; and Surface Maintenance — 0.006 mg/m’. Levels in Western Australian mines as reported via the regulatory CONTAM system (Peters et al, 2016), determined from 8,614 personal EC measurements from 146 different jobs at 124 mine sites between 2003 and 2015, expressed as arithmetic mean exposures, were: 0.018-0.026 mg/m® for surface occupations (equivalent to geometric means of 0.008-0.011 mg/m’); and 0.03 — 0.10 mg/m* for underground occupation groups (equivalent to geometric means of 0.017-0.059 mgim’). For 2011, job specific EC geometric mean exposures were: 0.01-0.019 mg/m’ for surface operators over a 12-hour shift and 0.014-0.059 mg/m? for underground operators. Jobs with the highest geometric mean exposure levels underground were diesel loader operators, ground or roof support occupations (including shotcreters) and non-contract miners (including miners operating a jumbo or handheld drilling rig), with EC exposure levels of 0.059, 0.055 and 0.053 mg/m? for a 12-hour work shift at a gold mine in 2011, respectively. The prevalence of occupational exposure to DE was estimated as part of the Australian Workplace Exposure Study which involved telephone interviews with 5023 households. Qualitative ‘exposure’ assessments were made regarding assumed exposures in broad groups of industries and occupational groups, and where members of each group could possibly have experienced exposures spread across several orders of magnitude. The finding of a 13.8% exposure prevalence estimate of Australian workers is much higher than reported from other countries and is probably due to the artificiality of the definition of ‘exposure’ used in this study compared with the actual level of exposure experienced by the overall workforce (Peters et al, 2015). The claim by the authors that the lack of emissions standards for non-toad heavy and light duty equipment and that it may contribute to higher prevalence and exposure levels among Australian workers compared to other countries is not substantiated by current practices. The official government guidelines on diesel emission testing and monitoring workforce exposures and the reporting of the results to the authorities over the last 10 years are taken as being applicable in mining and tunnelling operations throughout most of Australia (refer to detail in Part 8 of this Position Paper). BHP-Billiton (McDonald, 2016) noted that the vast majority of diesel engines currently in the underground operating environment in Australia (the work environment for our industry with the greatest exposure risk) remain transitional engines (Tier 1 to Tier 3 — 1996 to 2008) and as such have levels of particulate and hazardous chemicals that are as much as 100-fold higher than Tier 4 engines (Khalek et al, 2011; 2015). This is reflected in the current personal DPM exposures presented above, where a level of 0.1 mg/m® is stil often exceeded by some underground mining SEGs, even though levels appear to be decreasing over time, particularly where a comprehensive DPM management program is implemented. With a comprehensive DPM management program, average personal EC exposures can be reduced to below 0.05 mg/m’, but the 95% upper confidence limit may stil exceed this value. 6.__ Risk of health effects 61 Traditional diesel exhaust versus new technology diesel exhaust The DEMS study (Altfield et af, 2012; Silverman et al, 2012) concluded in 1998 and lagged all exposures 15 years. Thus, the most recent engine that study included was made in 1983. The vast majority of considered exposure came from diesel engines produced in the 1970's and earlier, which produced so called traditional diesel exhaust. ———— sn Sy