Workplace Exposure Standard (WES) review

Transcription

1 Workplace Exposure Standard (WES) review PORTLAND CEMENT (CAS NO: ) March 2018

2 CONTENTS 1.0 Introduction Physical and chemical properties Exposures Health effects of Portland cement Non-cancer Cancer Absorption, distribution, metabolism and excretion ACGIH evaluation and rationale DFG evaluation and rationale HSE evaluation and rationale Exposure standards and guidance values in use around the world New Zealand ACGIH DFG HSE 17

3 6.0 Analytical methods for the assessment of airborne Portland cement Discussion and recommendation 20 appendices Appendix 1: Glossary 23 Appendix 2: References 25 tables 1 Chemical and physical properties of Portland cement 5 2 Exposure standards for Portland cement from around the world 15

4 2 1.0 Introduction

5 1.0 Introduction This WorkSafe New Zealand (WorkSafe) review considers whether the WES for Portland cement should be changed. It considers the potential for exposures to Portland cement in New Zealand, the health effects and risks, exposure standards from other jurisdictions around the world, and the practicability of measuring exposures. The review includes a recommendation to change the WorkSafe WES, which is currently set at a WES-TWA of 10 mg/m 3 (Inhalable particulate fraction), as published in the Special Guide Workplace Exposure Standards and Biological Exposure Indices, 9th Ed., (WorkSafe, 2017). Terms that are bold (first occurrence only) are further defined in the Glossary. 3

6 4 2.0 Physical and chemical properties

7 2.0 Physical and chemical properties Portland cement is a fine powder, usually grey in colour. Portland cement is heterogeneous mixture of minerals manufactured by combining calcium, silicon, aluminium and iron. Gypsum (calcium sulphate) is added during a final grinding process, to regulate concrete setting time. Portland cement is made by heating the starting materials (about 85% lime and silica) to 1500 C to drive off water and carbon dioxide, creating clinker consisting of tricalcium silicate (3CaO.SiO 2), dicalcium silicate (2CaO.SiO 2), tricalcium aluminate (3CaO.Al 2O 3) and tetracalcium aluminoferrite (4CaO.Al 2O 3.Fe 2O 3). The clinker is cooled, combined with gypsum (CaSO 4) and finely ground to the required sieve size (ACGIH, 2010). An alternative description is the: TSCA Definition 2017: Portland cement is a mixture of chemical substances produced by burning or sintering at high temperatures (greater than 1200 C (2192 F)) raw materials which are predominantly calcium carbonate, aluminum oxide, silica, and iron oxide. The chemical substances which are manufactured are confined in a crystalline mass. This category includes all of the chemical substances specified below when they are intentionally manufactured in the production of Portland cement. The primary members of the category are Ca 2SiO 4 and Ca 3SiO 5. Other compounds listed below may also be included in combination with these primary substances: CaAl 2O 4; CaAl 4O 7; CaAl 12O 1; Ca 3Al 2O 6; Ca 12Al 14O 33; CaO; Ca 2Fe 2O 5; Ca 2Al 2SiO 7; Ca 4Al 6SO 16; Ca 12Al 14Cl 2O 32; Ca 12Al 14F 2O 32; Ca 4Al 2Fe 2O 10; Ca 6Al 14Fe 2O 15. (NIH, 2017). The 2006 UK Health and Safety Executive (HSE) review noted that chromium VI may be present in Portland cement, and was associated with reported skin sensitisation reactions (HSE, 2006). The 2010 ACGIH review noted that crystalline silica may be present in Portland cement, and was associated with silicosis (ACGIH, 2010). Chemical and physical properties of Portland cement include: Specific gravity 2-4 ph Solubility Slightly soluble in water (0.1-1%). Reactivity HSNO classifications 1 Incompatible with acids, ammonium salts and aluminium metal. Portland cement does not have an individual approval under HSNO but may be used as a single component chemical under an appropriate group standard. TABLE 1: Chemical and physical properties of Portland cement 1 (EPA, 2017). 5

8 6 3.0 Exposures

9 3.0 Exposures Portland cement is the most common type of cement in general use as a basic ingredient of concrete, mortar, stucco, and non-speciality grout. Occupational exposure occurs during production of Portland cement, and during use. Workers can be exposed to dust in a range of particle sizes where the ratio of inhalable to respirable size fractions will vary within and between different production facilities. Studies in two production facilities indicated that particles tended to be larger in the clinker cooling and storage operations, and finishing mills (5-10 m) than during crushing, kiln operations, and storage/load out (2.5-5 m). The study authors concluded that the respirable size fraction was the most appropriate gravimetric fraction for exposure monitoring (ACGIH, 2010). The number of persons exposed or potentially exposed to Portland cement in New Zealand is unknown. Workers may be occupationally exposed to Portland cement via inhalation or dermal contact during its manufacture or use. Statistics New Zealand 2016 data indicate that 72,000 New Zealand workers were working in the areas of cement, lime, plaster and concrete product manufacturing; building construction; and, heavy and civil engineering construction, with 5,400 in the cement, lime, plaster and concrete product manufacturing area alone (Statistics New Zealand, 2017). 7

10 4.0 Health effects of Portland cement IN THIS SECTION: 4.1 Non-cancer 4.2 Cancer 4.3 Absorption, distribution, metabolism and excretion 4.4 ACGIH evaluation and rationale 4.5 DFG evaluation and rationale 4.6 HSE evaluation and rationale 8

11 4.0 Health effects of Portland cement The health effects of cement dust have been investigated. 4.1 Non-Cancer Cement dust is corrosive to the eyes and skin, particularly on contact with moisture when calcium hydroxide (ph of 10 to 12) forms from strongly alkaline calcium oxide. Cement dust on the mucosal surface also leads to strongly alkaline reactions and may cause considerable irritation to the mucosa or even ulcerations (DFG, 2012). Cement containing chromium has long been known to induce cement dermatitis, an allergic reaction of the skin to chromate. Adding iron(ii) sulphate reduces water-soluble hexavalent chromium to trivalent chromium, which remains bound in the alkaline milieu of cement as poorly soluble chromium hydroxide/chromium oxide. The introduction of low-chromate cement has been associated with a decreased incidence of sensitisation of construction workers to chromate (DFG, 2012). The respiratory tract is the main target organ in humans after repeated inhalation exposure. Impairment of pulmonary function and clinical signs similar to chronic obstructive pulmonary disease (COPD) were often diagnosed in the exposed persons. Pneumoconiosis or pleural changes are of subordinate relevance (DFG, 2012). A 2016 study included 4,966 workers in 24 cement production plants (Nordby, et al., 2016). Based on 6,111 thoracic aerosol samples and information from questionnaires the study authors estimated arithmetic mean exposure levels by plant and job type. Dynamic lung volumes were assessed by repeated spirometry testing during a mean follow-up time of 3.5 years (range years). The outcomes considered were yearly change of dynamic lung volumes divided by the standing height squared or percentage of predicted values. Individual exposure was classified into quintile levels limited at 0.09, 0.89, 1.56, 2.25, 3.36, and 14.6 mg/m 3, using the lowest quintile as the reference. Employees that worked in administration were included as a second comparison group. Exposure was associated with a reduction in forced expiratory volume in 1 second (FEV1), forced expiratory volume in 6 seconds and forced vital capacity. Statistically significant reductions were reported for FEV1, FEV6 and FEV1/FVC at and above , and mg/m 3 respectively. The FEV1 % 1 analysis predicted yearly decline in lung volumes of 12 and 22 ml, over and above the decline expected with age, at and mg/m 3 exposure quintiles compared with the lowest exposure quintile ( mg/ m 3 ). A 22 ml yearly decline in lung volume over 20 years would lead to a loss of more than 400 ml, which is considered a clinically relevant amount. The authors considered that exposure at the higher levels found in this study may lead to a decline in dynamic lung volumes, and thus concluded that exposure reduction is warranted (Nordby, et al., 2016). 1. FEV1 %: FEV1 as a percentage of the European predicted values, providing standardisation for height, age and sex, without comparing individual values to European values (Nordby et al, 2016). 9

12 4.0 Health effects of Portland cement A systematic literature review assessing the association between exposure in the cement production industry and non-malignant respiratory effects concluded that a lack of power, adjustment for possible confounders, and other methodological issues limited many of the studies and no firm conclusions could be drawn (Fell and Nordby, 2017). The authors noted there were few longitudinal data, but that recent studies report a dose-response relationship between cement production dust exposure and declining lung function indicating a causal relationship. Crosssectional studies show reduced lung function levels at or above 4.5 mg/m 3 of total dust and 2.2 mg/m 3 of respiratory dust. Odds ratios for symptoms ranged from 1.2 to 4.8, while FEV1/FVC was 1 6% lower in exposed than in controls. Cohort studies reported a high yearly decline in FEV1/FVC ranging from 0.8% to 1.7% for exposed workers. One longitudinal study reported airflow limitation at levels of exposure comparable to 1 mg/m3 respirable and mg/m 3 total dust. A dose response relationship between exposure and decline in lung function has only been shown in one cohort (Fell and Nordby, 2017). 4.2 Cancer The results of several epidemiological studies have substantiated the suspected increased risk of cancer of the larynx from exposure to Portland cement although the studies have deficiencies such as small case numbers and at times inadequate consideration of the alcohol consumption confounder, socio-economic status and simultaneous exposure to limestone (DFG, 2012). The ACGIH 2010 review noted that although mortality studies are suggestive of increased deaths from stomach and colorectal (McDowall, 1984; Jakobsson et al, 1990 and 1993), bladder (Rafnsson and Johannesdottir, 1986) and lung cancer (Rafnsson and Johannesdottir, 1986; Rafnsson et al, 1997; Smailyte et al, 2004) among workers exposed to Portland cement, the data were not consistent, with negative studies also being reported for these sites, and there were concerns with possible confounding and other methodological issues in several of the positive studies (ACGIH, 2010). A more recent review and meta-analysis of cancer risks in Portland cement production workers examined 14 occupational cohort and 12 case-control studies found no convincing evidence of increased risks for cancer (Cohen, et al., 2014). Meta-relative risks for cancer incidence were null for lung and stomach cancer, but of borderline statistical significance for colorectal cancer (SIR = 1.38; 95% CI ). 4.3 Absorption, distribution, metabolism and excretion Portland cement particles are absorbed orally and by inhalation (DFG, 2012). The 2012 DFG review found that there were no data available for toxicokinetics or metabolism (DFG, 2012). 4.4 ACGIH evaluation and rationale The 2010 American Conference of Governmental Industrial Hygienists, ACGIH review noted that: Previous TLVs for Portland cement were based on a nuisance dust or Particulate Not Otherwise Specified (PNOS) classification that is no longer supported by ACGIH. Furthermore, Portland cement, being a highly alkaline material, has demonstrable toxicity to the respiratory tract, with increased pulmonary symptoms and significant decrements in lung function indices among cement production workers (Abrons et al., 1988; AbuDhaise et al., 1997; Ali et al., 1998; Kalacic 1973a, b; Mwaiselage et al., 2004, 2006; Saric et al., 1976; Noor et al., 2000; Yang et al., 1996). 10

13 4.0 Health effects of Portland cement Respiratory function changes and symptom rates have been found to increase with length of exposure to cement dust and with increasing exposure levels (Abrons et al., 1988; Mwaiselage et al., 2004, 2006; Saric et al., 1976; Yang et al., 1996). Abrons and colleagues (1997) also reported an increased prevalence of pleural abnormalities associated with current exposures and job tenure, with an odds ratio of 1.5 for pleural abnormalities associated with total dust levels of 5 mg/m 3. Fell and colleagues (2003) found no effect on respiratory symptoms or pulmonary function at respirable levels of 0.9 mg/m 3 and total dust levels of 7.5 mg/m 3. Mean respirable levels of 4 mg/m 3 (range mg/m 3 ) were associated with decreased lung function relative to workers exposed to an average of 0.4 mg/m 3 (range: mg/m 3 ) (Yang et al., 1996). Calculated adjusted odds ratios for wheezing of 1.2, 1.6 and 2.0 were associated with respirable exposures of 1, 3 and 5 mg/m 3, respectively (Abrons et al., 1988). Respirable levels of 5 mg/m 3 resulted in a 5-10% drop in peak expiratory flow (Abrons et al., 1988). Cross-shift reductions in pulmonary function have been noted at respirable levels of 5 mg/m 3 (Ali et al., 1998). Work by Mwaiselage and colleagues (2004, 2006) suggested that cumulative exposures should be less than 100 mg/m 3 -year total dust to prevent reductions in lung function; the same authors found significant cross-shift decrements in PEF in relation to exposure levels, with an expected decrement of -10% at 10 mg/m 3 respirable aerosol, and -2.2% to -3.2% at 1 mg/m 3 respirable aerosol. An increased asthma prevalence (14.1%) was noted in workers with a geometric mean exposure of 1.6 mg/m 3 respirable aerosol relative to the rate (8.8%) among workers with a geometric mean exposure of 0.5 mg/m 3 respirable aerosol (AbuDhaise et al., 1997). Overall, the data suggest that X-ray changes, decrements in pulmonary function and increased respiratory symptoms occur at total dust levels around 5 mg/m 3 and higher. Increased symptom rates, asthma and lung function effects are associated with respirable aerosol levels above 1 mg/m 3. Because symptoms associated with upper and lower airway structures have been reported in relation to Portland cement dust, a size-specific TLV expressed as inhalable particulate matter would usually be recommended. Unfortunately, no data exist for inhalable aerosol levels in relation to either total dust or respirable aerosol samples in this industry. Some particle size data for Portland cement dust were identified, suggesting that collecting the respirable fraction is the appropriate gravimetric measurement for exposure monitoring based on particle size (Ranpuria et al., 2009). For these reasons, the recommended TLV-TWA is expressed as a respirable particle matter. Mortality studies are suggestive of increased deaths from stomach and colorectal cancers (McDowall, 1984; Jakobsson et al., 1990, 1993), bladder (Rafnsson and Johannesdottir, 1986) and lung cancer (Rafnsson and Johannesdottir, 1986; Rafnsson et al., 1997; Smailyte et al., 2004) among workers exposed to Portland cement. However, the data are not consistent, with negative studies also being reported for these sites, and there are concerns with possible confounding and other methodological issues in several of the positive studies. While gastrointestinal cancers caused by Portland cement may be biologically plausible, the data are presently insufficient to warrant an A2 cancer designation. Furthermore, there are no animal data to support an A2 or A3 designation. Consequently, an A4, Not Classifiable as a Human Carcinogen, notation has been assigned. Insufficient data are available to assign Skin or Sensitizer (SEN) notations. (ACGIH, 2010). (References cited in ACGIH, 2010). 11

14 4.0 Health effects of Portland cement 4.5 DFG evaluation and rationale The German research foundation DFG (Deutsche Forschungsgemeinschaft) in a 2012 review of their MAK value summarised: Portland cement dust is corrosive to the skin and eyes. Carcinogenicity. Epidemiological studies on Portland cement provided sporadic evidence of a carcinogenic potential in the larynx as the target organ. Some studies showed an increased risk of laryngeal cancer for the occupational group of construction workers who had been exposed to Portland cement (with earlier co-exposure to lime), but there was no doseor exposure-response relationship. No animal studies are available on the carcinogenic effects of Portland cement. Due to the epidemiological findings, a suspected carcinogenic potential in humans cannot be ruled out for Portland cement. Therefore, Portland cement has been classified in Carcinogen Category 3B. MAK value. Several epidemiological studies described irritant and inflammatory reactions after exposure to Portland cement dust, mainly in the upper respiratory tract. Since the toxicological profile is determined by irritation, etc., chemical irritation in the upper respiratory tract should be avoided. The results available from studies with humans show that the general threshold limit value for dust of 4 mg/m 3 (I fraction) [inhalable fraction] does not provide protection against irritation caused by Portland cement. The available evidence describes adverse effects at high Portland cement concentrations and indicates the presence of a dose-response relationship. However, no MAK value can be derived from the available studies. Therefore, a scientifically based MAK value cannot be established. The previous MAK value has been withdrawn. Germ cell mutagenicity. On the basis of the available data, genotoxicity is not suspected. Portland cement is therefore not classified into any of the germ cell mutagen categories. Prenatal toxicity. There are no valid studies available for developmental toxicity. Since no MAK value has been established, Portland cement has not been classified in any of the pregnancy risk groups. Sensitization. Several studies demonstrated a decrease in the incidence of chromate sensitization among construction workers exposed to cement after the introduction of low-chromate cement. It is not possible to conclusively assess whether this measure helps to completely avoid sensitizations since the findings were possibly influenced by other exposures and further factors such as various percentages of old sensitizations and different cohort characteristics, etc, and there was only a relatively small number of cases. Studies on the threshold concentration for the induction of an allergic reaction to chromate showed that sensitization is very unlikely to be induced by a chromate concentration of less than 2 ppm in Portland cement dust. 2 Therefore, low-chromate cement formulations are currently not designated with Sh [ Sh designation indicates substances with the potential to cause skin sensitisation]. However, it cannot be ruled out that low-chromate Portland cements may also induce allergic reactions in the case of an existing chromate sensitization. 2 Low-chromate cements have a chromium VI content of less than 2 ppm (DFG, 2012). 12

15 4.0 Health effects of Portland cement Absorption through the skin. No data are currently available on possible absorption of Portland cement through the skin. It is not possible to estimate the toxicological relevance of this route of exposure for systemic absorption of Portland cement or its components. Portland cement has not been designated with H for the time being. (DFG, 2012). [ H designation indicates substances where dermal absorption can contribute significantly to the toxicity profile]. 4.6 HSE evaluation and rationale The 2006 HSE review noted that: This assessment concentrates on the evidence for non-malignant respiratory disease and carcinogenicity. The primary literature on skin sensitisation has not been reviewed because the potential for cement to cause such reactions, due to the presence of hexavalent chromium, has been established by other reviews. Toxicological endpoints such as reproductive toxicity and mutagenicity have not been considered because there are no data. Concerning non-malignant respiratory disease, HSE (1994) noted evidence that repeated exposure to Portland cement has produced chronic bronchitis and impaired pulmonary function, but firm conclusions could not be drawn because of limitations of the available studies. The effects of long-term exposure remain poorly studied, particularly because there are no longitudinal prospective studies in workers exposed to cement. However, many of the 15 recent studies, all conducted outside of the UK, provide evidence of the presence of respiratory problems among cement factory workers, consistent with the earlier literature. Overall, the pattern of evidence clearly indicates that occupational exposure to cement dust has produced deficits in respiratory function. However, the evidence available at the present time is insufficient to establish with any confidence the doseresponse relationship for these effects. HSE (1994) concluded that there was no convincing evidence for an increased incidence of any site-specific cancer resulting from cement exposure, but acknowledged that the data available at that time were not consistently and reassuringly negative. Since the early 1990s, a number of relevant cancer cohort and case control studies have been published, conducted in groups exposed to cement either through employment in cement factories or in the construction industry. Among these and earlier studies, increased incidences of cancers at several sites (stomach, lungs, colon, pharynx and larynx) were noted, but taking account of limitations in the strength of the observed associations, it is concluded that a causal association between Portland cement exposure and cancer has not been established. Nevertheless, the findings of the recent studies reviewed in this document maintain the uncertainty concerning a possible risk of cancer raised by the earlier data reviewed by HSE (1994). (HSE, 2006). 13

16 5.0 Exposure standards and guidance values in use around the world IN THIS SECTION: 5.1 New Zealand 5.2 ACGIH 5.3 DFG 5.4 HSE 14

17 5.0 Exposure standards and guidance values in use around the world Table 2 below shows the Portland cement exposure standards from around the world. This information is published by the Institute for Occupational Safety and Health of the German Social Accident (Institut für Arbeitsschutz der Deutschen Gesetzlichen Unfallversicherung, 2017). JURISDICTION OR ADVISORY BODY 8-HOUR LIMIT VALUE (mg/m 3 ) SHORT-TERM LIMIT VALUE (mg/m 3 ) Australia 10 3 Austria Belgium 10 Canada Ontario 1 5 Canada Quebec Finland Germany (AGS) 5 4 Hungary 10 4 Ireland 1 7 Japan JSOH New Zealand 10 4 Singapore 10 South Korea 10 Spain 4 7 Switzerland 5 4 USA NIOSH USA OSHA UK TABLE 2: Exposure standards for Portland cement from around the world It is noted that the only organisations from whom we get information as to how and why they set occupational exposures standards on Portland cement are ACGIH, DFG and HSE. 3 This value is for inhalable dust containing no asbestos and < 1% crystalline silica. 4 Inhalable fraction. 5 This value is for respirable dust containing no asbestos and < 1% crystalline silica. 6 Total dust. 7 Respirable fraction. 8 Total dust comprising particles with a flow speed of 50 to 80 cm/sec at the entry of a particle sampler. 15

18 5.0 Exposure standards and guidance values in use around the world 5.1 New Zealand New Zealand s WES for Portland cement have been unchanged since adoption in The toxicological database reviewed above indicates that Portland cement is locally toxic to humans particularly after inhalation exposure, causing obstructive pulmonary diseases, chronic bronchitis and reduced pulmonary function, with cough, increased phlegm and dyspnoea (asthma) the most common symptoms among Portland cement workers. Based on the aforementioned documentation, and in particular the findings listed below, WorkSafe does not consider the current WES-TWA of 10 mg/m 3 inhalable fraction), to be adequate to manage health risk from inhalation exposure because of the following: A number of studies reporting the association between exposure in the cement production industry and non-malignant respiratory effects have been published, but most have limitations preventing the establishment of a robust dose-response relationship. A causal relationship between cement production dust exposure and declining lung function has been established. The 2010 ACGIH review recommended a TLV-TWA of 1 mg/m 3 respirable particulate matter, stating that the limit would likely protect the substantial majority of exposed individuals from asthma, respiratory symptoms, and lung function effects. Some studies have reported reduced lung function (reductions in FEV1, FEV6, PEF) at or about 1 mg/m 3 respirable particulate fraction, while other studies report no adverse effects at this exposure level. The respirable particle fraction is the parameter mostly reported where measured exposures have been linked to health end-points. 5.2 ACGIH ACGIH TLVs are health-based guidelines or recommendations to assist in the evaluation and control of potential workplace health hazards. The 2010 ACGIH review concluded with a recommendation that: A TLV-TWA of 1 mg/m 3 respirable particulate matter is recommended to prevent respiratory symptoms, losses in lung function, and asthma. This level is less than that associated with an increase in asthma prevalence rate, and is below the levels associated with changes in lung function and increased respiratory symptoms. Confining exposures to a TLV-TWA of 1 mg/m 3 respirable particulate matter will likely protect the substantial majority of exposed individuals from asthma, respiratory symptoms, and lung function effects. (ACGIH, 2010). Note: the ACGIH TLV-TWA of 1 mg/m 3 respirable particulate matter applies to Portland cement containing no asbestos and < 1% crystalline silica (ACGIH, 2010). 16

19 5.0 Exposure standards and guidance values in use around the world 5.3 DFG The 2012 DFG review concluded that no scientifically based MAK [WES] value can be derived from available studies (DFG, 2012). The 1993 documentation Portland Cement (documentation Portland Cement 1998, a translation of the 1993 German version) indicated that a fibrogenic connective tissue reaction was possibly caused by cement dust. Most of the studies published since then were cross-sectional studies that were carried out in Portland cement plants outside Europe. The only study from Europe was a retrospective cohort study with a relatively small number of Norwegian cement workers (Fell et al. 2003). This study demonstrated that prolonged exposure to cement dust at a concentration of about 1 mg/m 3 (respirable fraction) is not associated with decreased pulmonary function or increased prevalence of COPD. All available studies have some shortcommings [shortcomings]. Because of the cross-sectional design, workers who had left the plants due to health problems were not recorded. Current and regularly obtained historical dust measurements at the workplace are often missing. Nevertheless, all these studies have described an increased prevalence of obstructive pulmonary diseases, chronic bronchitis and reduced pulmonary function among Portland cement workers. Cough, increased phlegm and dyspnoea were the most common symptoms. The lowest dust concentrations associated with reduced pulmonary function were 3 mg/m 3 for total dust (Mwaiselage et al. 2004) and mg/m 3 for respirable dust (Noor et al. 2000; Yang et al. 1996). The lowest concentration that was significantly correlated with an increased prevalence of respiratory disorders was 1.2 mg/m 3 respirable dust (Yang et al. 1993). The currently available data do not allow the derivation of a limit value. There is no doubt that high exposure to Portland cement by inhalation may cause clinical signs similar to COPD. Pneumoconiosis or pleural changes are of subordinate relevance. All studies in the low exposure range only included current measured values. Therefore, valid conclusions about limit values can be drawn only on the assumption that earlier exposures were certainly not lower (Abrons et al. 1988). (References cited in (DFG, 2012)). 5.4 HSE The 2006 HSE review concluded that: Overall, the pattern of evidence clearly indicates that occupational exposure to cement dust has produced deficits in respiratory function. However, the evidence available at the present time is insufficient to establish with any confidence the dose-response relationship for these effects. and Since the early 1990s, a number of relevant cancer cohort and case control studies have been published, conducted in groups exposed to cement either through employment in cement factories or in the construction industry. Among these and earlier studies, increased incidences of cancers at several sites (stomach, lungs, colon, pharynx and larynx) were noted, but taking account of limitations in the strength of the observed associations, it is concluded that a causal association between Portland cement exposure and cancer has not been established. Nevertheless, the findings of the recent studies reviewed in this document maintain the uncertainty concerning a possible risk of cancer raised by the earlier data reviewed by HSE (1994). (HSE, 2006). 17

20 Analytical methods for the assessment of airborne Portland cement

21 6.0 Analytical methods for the assessment of airborne Portland cement Portland cement is a heterogenous substance, made up of a number of chemicals and minerals. As such there is no analytical procedure that can be used to analyse specifically for this substance. The current analytical method is to measure respirable dust gravimetrically, according to AS 2985: 2009 Workplace atmospheres Method for sampling and gravimetric determination of respirable dust (Standards Australia, 2009). Using this method an air sample is collected onto a pre-weighed membrane filter using a respirable sampling train set at a flow rate of 2.2 or 2.5 litres of air per minute (depending on the specific cyclone being used). Following exposure of the filter for an appropriate period of time, the filter is re-weighed and the dust concentration calculated based on the mass of dust present and the volume of air that has been filtered. The detection limit of this method will depend on the equipment used, but should be of the order of 10 g per sample. This would allow a minimum concentration of 0.01 mg of inhalable dust per m 3 of air to be quantified over a collection period of 8 hours. 19

22 Discussion and recommendation

23 7.0 Discussion and recommendation WorkSafe considers the current New Zealand WES- TWA of 10 mg/m 3 (inhalable fraction) to be inadequate to protect workers exposed to Portland cement, based on today s scientific understanding. It is proposed that WorkSafe: 1. adopt a WES-TWA for Portland cement of 1 mg/m 3 respirable particulate fraction 2. notes that the WES-TWA applies to Portland cement containing no asbestos and < 1% crystalline silica, 9 and 3. remove the WES-TWA for inhalable Portland cement. The proposed respirable WES-TWA value is based on that given by the ACGIH, and in particular on: published studies reporting the association between exposure in the cement production industry and non-malignant respiratory effects that have established a causal relationship between cement production dust exposure and declining lung function, and 1 mg/m 3 respirable particulate fraction being likely to protect the substantial majority of exposed individuals from asthma, respiratory symptoms, and lung function effects. The reviewed toxicological database indicates that it is not necessary to apply additional notations (eg skin or sen) for low-chromate Portland cement For Portland cement containing chromium (VI) or silica, consideration needs to be given to whether sampling and analysis specifically for those components should be carried out. If so, the appropriate WES for those components should be applied. 10 Low-chromate cement contains less than 2 ppm chromium VI. 21

24 Appendices IN THIS SECTION: Appendix 1: Glossary Appendix 2: References 22

25 Appendices Appendix 1: Glossary TERM ACGIH COPD DFG EPA FEV1 FEV6 FVC HSE HSNO Inhalable fraction MAK mg/m 3 ml NIH NIOSH PEF ppm Respirable fraction sen MEANING The American Conference of Governmental Industrial Hygienists (ACGIH ) is a member-based organisation, established in 1938, that advances occupational and environmental health. Examples of this include their annual edition of the TLVs and BEIs book and work practice guides. Store at Chronic obstructive pulmonary disease. Deutsche Forschungsgemeinschaft (German Research Foundation), the Permanent Senate Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Federal Republic of Germany. The science-based MAK values are recommended to the German Minister of Labour and Social Affairs for possible adoption under the German Hazardous Substances Ordinance. New Zealand Environmental Protection Authority. Volume that has been exhaled at the end of the first second of forced expiration. Volume that has been exhaled after 6 seconds of forced expiration. Forced vital capacity: the determination of the vital capacity from a maximally forced expiratory effort (i.e. the amount of air which can be forcibly exhaled from the lungs after taking the deepest breath possible.) The UK Health and Safety Executive (HSE) is the body responsible for the encouragement, regulation and enforcement of workplace health, safety and welfare, and for research into occupational risks. Hazardous Substances and New Organisms Act, New Zealand. Inhalable particulate fraction is that fraction of dust that can be breathed into the nose or mouth. Particulate size: mostly < 100 m, 50% cut point. For sampling purposes the inhalable dust is to be collected according to the method set out in AS : Workplace Atmospheres Method for Sampling and Gravimetric Determination of Inhalable Dust (Standards Australia, 2009). (cf. Respirable fraction) (Also referred to as: inhalable particulate matter). Maximale Arbeitsplatz-Konzentration, (maximum workplace concentration) is defined as the maximum concentration of a chemical substance (as gas, vapour or particulate matter) in the workplace air which generally does not have known adverse effects on the health of the employee nor cause unreasonable annoyance (eg by a nauseous odour) even when the person is repeatedly exposed during long periods, usually for 8 hours daily but assuming on average a 40-hour working week. Milligrams of substance per cubic metre of air. Millilitre, or thousandth of a litre. National Institutes of Health an agency of the U.S, Department of Health and Human Services. The National Institute for Occupational Safety and Health (NIOSH) is the United States federal agency responsible for conducting research and making recommendations for the prevention of work-related injury and illness. NIOSH is part of the Centers for Disease Control and Prevention (CDC) within the U.S. Department of Health and Human Services. Peak expiratory flow. Parts of vapour or gas per million parts of air. Respirable particulate fraction is that fraction of inhaled airborne particles that can penetrate beyond the terminal bronchioles into the gas-exchange region of the lungs (alveoli). Particulate size: mostly < 4 m, 50% cut point. For sampling purposes the respirable dust samples are to be collected according to the method set out in the Standards Australia publication AS : Workplace Atmospheres Method for Sampling and Gravimetric Determination of Respirable Dust (Standards Australia, 2009). (cf. Inhalable fraction) (Also referred to as: respirable particulate matter) A substance that can sensitise the skin or respiratory system, inducing a state of hypersensitivity to it, so that on subsequent exposures, an allergic reaction can occur (which would not develop in nonsensitised individuals). It is uncommon to become sensitised to a compound after just a single reaction to it. A New Zealand term. 23

26 Appendices TERM SEN skin Skin Thoracic TLV TLV-TWA TSCA WES WES-TWA MEANING A notation indicating the subject substance is a sensitiser. DSEN and RSEN are used in place of SEN when specific evidence of sensitisation by the dermal or respiratory route, respectively, is confirmed by human or animal data. An ACGIH term. Skin absorption applicable to a substance that is capable of being significantly absorbed into the body through contact with the skin. A New Zealand term. A notation indicating the potential for significant contribution to the overall exposure, by the cutaneous route, including mucous membranes and the eyes, by contact with vapours, liquids and solids. An ACGIH term. Thoracic particulate fraction is that fraction of inhaled airborne particles that can penetrate into the trachea-alveolar region. Particulate size: mostly < 30 m, 50% cut point. Threshold Limit Value (see TLV-TWA below). An ACGIH term. TLV Time-Weighted Average; the TWA concentration for a conventional 8-hour workday and a 40-hour workweek, to which it is believed that nearly all workers may be repeatedly exposed to, day after day, for a working lifetime without adverse effect. An ACGIH term. The Toxic Substances Control Act (TSCA) is a United States law passed in 1976 and administered by the US EPA. It regulates the introduction of new or existing chemicals. Workplace Exposure Standard WESs are values that refer to the airborne concentration of substances, at which it is believed that nearly all workers can be repeatedly exposed to, day after day, without coming to harm. The values are normally calculated on work schedules of five shifts of eight hours duration over a 40 hour week. A New Zealand term. The average airborne concentration of a substance calculated over an eight-hour working day. A New Zealand term. 24

27 Appendices Appendix 2: References ACGIH (2017). From ACGIH, 2017 TLVs and BEIs book, 7th Edition. Copyright Reprinted with permission. Cohen, S. S., Sadoff, M. M., Jiang, X., Fryzek, J. P., & Garabrant, D. H. (2014). A review and meta-analysis of cancer risks in relation to Portland cement exposure. Occupational Environmental Medicine, 71(11), Deutsche Forschungsgemeinschaft. (2012). MAK Value Documentation: Portland cement dust. EPA Environmental Protection Authority. (2017). HSNO Classifications. Retrieved from Fell, A. K., & Nordby, K. C. (2017). Association between exposure in the cement production industry and non-malignant respiratory effects: a systematic review. BMJ Open, 7, 1-3. HSE Health and Safety Executive. (2006). Portland Cement Dust - Hazard assessment document EH75/7. Health and Safety Executive. Institut für Arbeitsschutz der Deutschen Gesetzlichen Unfallversicherung. (2017). Retrieved from NIH National Institute of Health. (2017, May 24). ChemIDplus. Retrieved from TOXNET: Nordby, K. C., Notø, H., Eduard, W., Skogstad, M., Fell, A. K., Thomassen, Y., & Skare, ø. (2016). Thoracic dust exposure is associated with lung function decline in cement production workers. Eur Respir J, 48, Standards Australia. (2009). AS 2985:2009. Workplace Atmospheres: Methods for Sampling and Gravimetric Determination of Respirable Dust. Sydney: Standards Australia. Statistics New Zealand. (2017). Geographic units by region and industry Retrieved from Stats NZ: WorkSafe New Zealand. (2017). Special Guide Workplace Exposure Standards and Biological Exposure Indices, 9th Edition. 25

28 Notes

29 Disclaimer WorkSafe New Zealand has made every effort to ensure the information contained in this publication is reliable, but makes no guarantee of its completeness. WorkSafe may change the contents of this guide at any time without notice. This document is a guideline only. It should not be used as a substitute for legislation or legal advice. WorkSafe is not responsible for the results of any action taken on the basis of information in this document, or for any errors or omissions. Published: March 2018 Current until: 2020 PO Box 165, Wellington 6140, New Zealand Except for the logos of WorkSafe, this copyright work is licensed under a Creative Commons Attribution-Non-commercial 3.0 NZ licence. To view a copy of this licence, visit In essence, you are free to copy, communicate and adapt the work for non-commercial purposes, as long as you attribute the work to WorkSafe and abide by the other licence terms. WSNZ_2969_Mar 2018

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