Ashes (residues), coal

Toxicological Summary

Workers - Hazard via inhalation route

Systemic effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

Local effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

Workers - Hazard via dermal route

Systemic effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

Local effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

Workers - Hazard for the eyes

Local effects

Hazard assessment conclusion:

no hazard identified

Additional information - workers

Ashes (residues), coal are a complex and heterogeneous mixture of metal and metalloid oxides in variable proportions generated from burning of a combination of carbonaceous materials. Based on mass percent ranges, three major constituents of ashes (residues), coal can be identified: Silicon dioxide (SiO2, including fused and crystalline silica), aluminium oxide (Al2O3), iron oxide (Fe2O3) and calcium oxide (CaO).

For hazard assessment, the available toxicological information is taken into account along with physicochemical data, particularly on granulometry and mineralogy, since the presence of silicon dioxide in form of crystalline silica in the respirable (alveolar) fraction represents a critical factor triggering potential toxic effects upon inhalation exposure.

Acute/short- and long-term dermal exposure – systemic and local effects

Based on physicochemical properties (solid particles with low water solubility) and toxicokinetic behaviour (s. Toxicokinetics), ashes (residues), coal or its main components are not expected to be dermally absorbed and hence are not bioavailable. Furthermore, no toxic effects were observed in acute dermal toxicity studies (s. Acute toxicity); several studies showed that ashes (residues), coal are not irritating to the skin or eyes and not skin sensitising (s. Irritation and Sensitisation). Therefore, no systemic or local effects are expected after acute/short- or long-term dermal exposure to ashes (residues), coal.

Acute/short-term inhalation exposure – systemic and local effects

Based on physicochemical properties and toxicokinetic behaviour, acute/short-term inhalation exposure to ashes (residues), coal is more likely to induce local effects in the lung rather than adverse systemic effects. This applies, however, mainly to respirable particles which are expected to be slowly cleared upon deposition in the respiratory bronchioles and proximal alveoli.

In rats exposed to coal fly ash particles with a MMAD of 2.5 µm at 1400 mg/m³, 4 h/day for 3 consecutive days, no mortalities occurred and the LC50 was therefore considered to be greater than 1400 mg/m³ for these particles (Smith, 2006). Analyses of bronchoalveolar lavage and blood samples as well as histopathological examinations on lung tissue indicated the induction of inflammatory responses, such as an increase in alveolar macrophages, which are not considered as adverse effects specifically related to ashes (residues), coal, but an adaptive natural response following exposure to a high concentration of insoluble particles.

The animal exposure conditions described correspond to an 8-hour human exposure to ca. 470 mg/m³ (assuming an inhalation volume of 10 m³ under light activity conditions). Such an exposure scenario is unrealistic under normal working conditions considering the current occupational exposure limits for respirable inert dust in the European Union, which range from 3 to 10 mg/m³ (8 h TWA).

Long-term inhalation exposure – systemic and local effects

The available animal data on the repeated dose toxicity of ashes (residues), coal by inhalation exposure do not provide indications for systemic toxic effects. In fact, long-term inhalation exposure to the respirable fraction of ashes (residues), coal is most likely to result in local effects considered to be adaptive responses to the inhaled particles, which may become adverse as a result of particle overload at concentrations no longer relevant to humans in current occupational settings.

In a repeated dose inhalation toxicity study, groups of rats were exposed 8 h/day to respirable fly ash particles (MMAD 2 µm) for up to 90 days at 0.6 mg/m³, and up to 180 days at 4.2 mg/m³. No health effects were seen in the lower exposure group and only minor effects were found in the high exposure group. The observed effects included increased number and size of macrophages in bronchoalveolar lavage, and minor changes in secretion of glycoprotein (mucus), or viability, adherence and phagocytic index of ex vivo cultured macrophages. The mild effects were considered natural responses to inhaled particles and not unique to coal fly ash (Raabe et al., 1988). The systemic and local NOAEC for subchronic inhalation exposure to respirable fly ash particles was therefore 4.2 mg/m³. At the same time, this value was considered a local LOEC, since the induced effects are not regarded as adverse.

In another study in rats, subacute inhalation (6 h/day, 5 days/week for 4 weeks) of respirable coal fly ash (MMAD ca. 2-3 µm) at 10, 30 and 100 mg/m³ resulted in a slight fibrotic pulmonary reaction, slight to severe lymphocytic hyperplasia in mediastinal lymph node and slightly to moderately increased septal cellularity at 100 mg/m³. The fibrotic reaction and the overall severity grade of the other effects observed were considered adverse effects due to the high particle load, and therefore 100 mg/m³ was the LOAEC (local) in this study. At 10 and 30 mg/m³, no fibrotic reactions were observed. Both incidence and severity of other lung changes was lower and considered a natural adaptive reaction as a result of the (physical) particle insult, and not adverse effects in terms of test substance specific toxicity. Therefore, 30 mg/m³ was considered a NOAEC for local effects in the lung. No toxicologically significant systemic effect was observed at any concentration. The NOAEC for systemic effects was therefore 100 mg/m³ (Dormans et al., 1999).

Assuming an 8 h inhalation volume of 10 m³ for workers under light activity conditions, the subacute local NOAEC of 30 mg/m³ mentioned above corresponds to a mid-term 8 h human exposure to approximately 15 mg/m³ of respirable particles. Accordingly, the subacute LOAEC of 100 mg/m³ corresponds to a mid-term exposure to ca. 50 mg/m³ of respirable fly ash particles. Such exposure conditions are unlikely to occur given the current occupational exposure limits for respirable inert dust in the European Union, which range from 3 to 10 mg/m³ (8 h TWA).

Human data on the pneumoconiotic effects of coal fly ash (pulverised fuel ash, PFA) derived from a number of studies in UK workers of the electricity supply industry throughout 1950 to 1977 has been reviewed by Bonnell et al. (1980). The results of the studies indicate that PFA is unlikely to give rise to pneumoconiosis caused by working in coal-combusted power plants, other than in subjects with previous exposure in underground coal mining.

In a published review by Borm (1997), in vitro, in vivo and human toxicity data on coal fly ash was assessed and compared to information from coal (mine) dust (which contains up to 10% of quartz) and/or crystalline silica. In summary, in vitro studies showed that coal fly ash is generally clearly less cytotoxic than crystalline silica. In vivo exposure (inhalation and intratracheal instillation) of different animal species to coal fly ashes showed only very mild to moderate fibrosis, the observed pathology being similar to other nuisance dusts, and it appears that silica is less fibrogenic in inhaled coal fly ash than in coal mine dust. Epidemiological studies on fly ash exposed workers failed to show any convincing evidence of pneumoconiosis other than in former coal miners or emphysema as described by Bonnell et al. (1980). Other studies showed lung function impairment and respiratory symptoms in workers with long-term, high exposure (> 5 mg/m³) to coal fly ash. However, it should be considered that this effect is also results from exposure to other inorganic dusts at prolonged and high exposure (review: Oxman et al. 1993).

Borm (1997) concluded that "although most studies have not been designed to test fly ash toxicity in relation to its content of crystalline silica, there are no available data that suggest that coal fly ash is merely an addition of (crystalline) silica and other components. There is minimal knowledge on the effect of the mineralogical properties of fly ash on the activity of (crystalline) silica", and suggested a closer investigation of "matrix" effects masking the toxicity of silica in particles by complex composition.

In more recent studies on ash samples from Germany, Israel and The Netherlands addressing the mineralogy and distribution of quartz along among particle fractions, it could be demonstrated that quartz content is higher in the coarse than in the fine and respirable fractions of ashes (Meij et al., 2000; Nathan et al., 2009; Urbonas, 2010), and that crystalline silica in the respirable fraction is either present as inclusion in vitrified material or coated by layers of aluminosilicates (Meij et al., 2000; Nathan et al., 2009). Thus, the reactive quartz particle surface is not free exposed, explaining the lower toxicity of fly ash particles containing silica compared to coal (mine) dust and respirable crystalline silica.

The quartz concentration in the respirable fraction of the fly ash produced was determined to be considerably lower than in the whole ash. X-ray diffraction and scanning electron microscopy analysis showed that most of the quartz particles in the respirable fraction were coated by amorphous aluminosilicate layers. For coated particles it has been demonstrated that no pneumoconiotic effects have been observed (Nathan et al., 2009).

By means of scanning electron microscopic/X-ray microanalysis (SEM/XMA) and X-ray diffraction (XRD) analysis, it was shown that coal gasification ash (CG slag and CG fly ash), as produced in the, consisted entirely of glass and did not contain any crystalline silica forms. No cristobalite or tridymite could be demonstrated in any of the ashes studied. In Dutch power plants after combustion of the coal, about 50% of the original quartz remained in the ash, which was mostly present in the coarse fraction as free angular particles. The quartz content of the health-relevant respirable fraction was lower: less than 1% of the original quartz in coal. However, the major part of the quartz in the respirable fraction was embedded in the glass matrix of the fly ash particle. The authors stated that since the effects of quartz are surface related, these findings explain the negative results of quartz related effects of PFA (pulverized fuel ash) in epidemiological, in vitro and in vivo studies. Besides, the amount of the total α-quartz in the respirable fraction of the ashes studied was less than 0.2%, so in practice the occupational exposure limits for respirable quartz (0.075 mg/m³ in The Netherlands) will not be exceeded. It was concluded that there is no reason to assume that coal ash, as produced in the Netherlands, would induce PMF (progressive massive fibrosis) (Meij et al. 2000).

In conclusion, the whole package of information available on the physicochemical, mineralogical and toxicological properties of ashes (residues), coal do not indicate a hazard for systemic effects specifically related to their intrinsic chemical properties. Short- and long-term exposure to high airborne concentrations of ashes (residues), coal is expected to result in local responses in the lung as in the case of exposure to high airborne concentrations of nuisance dust. Therefore, the available data show no more preoccupation of toxicity of Ashes (residues), coal than for inert dust. The current occupational exposure limits for respirable dust in the European Union (3-10 mg/m³) should apply.

 

References not as IUCLID entry:

 

Borm, P.J.A. (1997). Toxicity and occupational health hazards of coal fly ash (CFA). A review of data and comparison to coal mine dust. Ann Occup Hyg 41(6):659 -676.

 

Oxman, A.D., H.S., Stock, S.R.T., Hnizdo, E. and Lanfe, H.J. (1993). Occupational dust exposure and chronic obstructive pulmonary disease. American Review of Respiratory Diseases 148, 38-48.

General Population - Hazard via inhalation route

Systemic effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

Local effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

General Population - Hazard via dermal route

Systemic effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

Local effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

General Population - Hazard via oral route

Systemic effects

Long term exposure

Hazard assessment conclusion:

no hazard identified

Acute/short term exposure

Hazard assessment conclusion:

no hazard identified

DNEL related information

General Population - Hazard for the eyes

Local effects

Hazard assessment conclusion:

no hazard identified

Additional information - General Population

Since exposure for the general public is precluded, DNELs for the general population are not relevant and thus not derived.