Carcinogenicity Category 1 or 2 (formerly 6.7) or other carcinogen notation
For cancers induced by exposure to airborne contaminants, the time between the initial exposure and diagnosis of disease is usually several years. This latency period may vary with the particular substance, the intensity and length of exposure, and the individual.
The existence of exposure thresholds defining no-effect levels has been theorised, but such thresholds for humans cannot be precisely identified and confirmed from the evidence provided by epidemiological or animal studies.
Substances which have been identified as known, presumed, or suspected human carcinogens have this notation.
Under HSNO legislation, two categories of carcinogens are described. They are used throughout this guideline for HSNO-approved hazardous substances.
Carcinogenicity Category 1 (formerly 6.7A) – Substances that are known or presumed human carcinogens
The placing of a chemical in Category 1 is done on the basis of epidemiological and/or animal data. An individual chemical may be further distinguished as known or presumed to have to have carcinogenic potential for humans.
Based on strength of evidence together with additional considerations, such evidence may be derived from human studies that establish a causal relationship between human exposure to a chemical and the development of cancer (known human carcinogen). Alternatively, evidence may be derived from animal experiments for which there is sufficient evidence to demonstrate animal carcinogenicity (presumed human carcinogen). In addition, on a case by case basis, scientific judgement may warrant a decision of presumed human carcinogenicity derived from studies showing limited evidence of carcinogenicity in humans together with limited evidence of carcinogenicity in experimental animals.
Carcinogenicity Category 2 (formerly 6.7B) – Substances that are suspected human carcinogens
The placing of a chemical in Category 2 is done on the basis of evidence obtained from human and/or animal studies, but which is not sufficiently convincing to place the chemical in Category 1. Based on strength of evidence together with additional considerations, such evidence may be from either limited evidence of carcinogenicity in human studies or from limited evidence of carcinogenicity in animal studies.
Substances that are not covered by HSNO legislation, but are carcinogenic to humans, have been noted as such.
Wherever practicable, substances that have been identified as confirmed or possible workplace carcinogens should be replaced by less hazardous substances. If this is not feasible, the hierarchy of control specified in the GRWM(external link) must be strictly applied.
Where appropriate, exposure or biological monitoring should be employed to demonstrate that exposure is being kept to the lowest practicable level. All workers likely to be exposed to carcinogens must receive information about the hazards they face, and training in minimising exposure to those substances.
Inhalable fraction and vapour
The inhalable fraction and vapour (ifv) notation is used when a material exerts sufficient vapour pressure such that it may be present in both particle and vapour phases, with each contributing to a significant portion of exposure.
Interim WES or BEI
WorkSafe considers interim WES and BEI may not be protective for all workers. As such, caution should be applied in using the WES for health risk assessment.
WorkSafe intends to review or change the WES or BEI in the future for the following substances:
- Diethyl sulphate: Interim WES-TWA of 0.01ppm. Propose to review WES again in the future.
- Flour dust: Interim WES-TWA of 1mg/m³. Propose to change to WES-TWA of 0.2mg/m³ in the year 2024.
- Hydrogen sulphide: Interim WES-TWA of 5ppm and WES-STEL of 10ppm. Propose to change to WES-TWA of 1ppm and WES-STEL of 5ppm in the year 2024.
- Nitrogen dioxide: Interim WES-TWA of 1ppm. Propose to review WES again in the future.
- Phosphine: Interim WES-TWA of 0.3ppm and WES-STEL of 1ppm. Propose to change to WES-TWA of 0.05ppm and WES-STEL of 0.2ppm in 2024.
- Titanium dioxide: Interim WES-TWA of 10mg/m³. Propose to review in 2024 given publication of new information from cited sources.
- Vanadium, as V: Interim WES-TWA of 0.05mg/m³, as V for V and its inorganic compounds, except CI pigment yellow 184. Propose to review WES again in the future.
- Vinyl acetate: Interim WES-TWA of 5ppm and WES-STEL of 10ppm. Propose to review the WES again in the future.
- Wood dust, softwood: Interim WES-TWA of 2mg/m³. Propose to change to WES-TWA of 1mg/m³ in the year 2024.
- Isocyanates, all, (as -NCO): Interim WES-TWA of 0.02mg/m³ and WES-STEL of 0.07mg/m³. Propose to change in 2024 to: WES-TWA of 0.0001mg/m³ and WES-STEL of 0.0005mg/m³ with Skin notation.
PES: Prescribed exposure standards
Some substances can penetrate intact skin, and this may result in a higher substance uptake than would have been expected from inhalation only. Uptake through the skin is not usually the most significant route of absorption, but there are exceptions. For example, skin contact with organophosphate pesticides is thought to account for the majority of uptake experienced when working with these substances.
As the WES only takes into consideration the inhalation component, care should be taken when interpreting air sampling results where there is also a possibility of significant uptake through the skin. Respiratory protection may give a false sense of security. This is particularly important where vapour phase skin absorption occurs, as there may be no obvious contact between the skin and the substance. Biological monitoring for exposure may be a useful supplement to air sampling in these situations.
Substances that are considered to have potential for significant skin absorption have a ‘skin’ notation. Where a class or a group of substances are identified with a ‘skin’ notation, that notation may or may not apply to every substance in the group. Risk assessment for these substances should consider if skin absorption is a route of entry requiring control.
Exposure to some substances can lead to the development of an allergic sensitisation, usually affecting the skin or respiratory system. High exposures may hasten the onset of the allergy, but once developed in an individual, very low exposures can provoke a significant reaction. It is uncommon to become sensitised to a compound after just a single reaction to it.
Even though low exposure standards have been specified for known sensitisers, the levels do not necessarily provide adequate protection for an already sensitised person. Avoiding further exposure may be the only option for these individuals.
A number of substances, including acid anhydrides, isocyanates and chromium compounds, are known to be both respiratory and skin sensitisers, capable of causing allergic asthma, allergic contact dermatitis, or both. The risk of respiratory versus skin sensitisation may depend on the particular substance, as well as its physical state, exposure route, method of use, and the individual worker.
Substances that are considered to have potential for sensitisation have a ‘sen’ notation (not specified), ‘rsen’ notation (respiratory sensitiser), or ‘dsen’ notation (dermal sensitiser).
Some gases and vapours, when they are present in the air in significant concentrations, behave as asphyxiants by reducing the concentration of oxygen.
The oxygen content of air should be maintained at 19.5–23.5% under normal atmospheric conditions to manage health risks associated with oxygen.
Atmospheres that are deficient in oxygen do not provide adequate sensory warning of danger, and most simple asphyxiants are odourless. In some cases, death can occur in only a few minutes.
Some simple asphyxiants can also present an explosion hazard if present in high volumes. It is therefore essential that the presence, hazards and controls of simple asphyxiants are communicated to workers. Substances that are considered asphyxiants are identified with a ‘sa’ (simple asphyxiant) or ‘sax’ (simple asphyxiant – may present an explosion hazard) notation.
Some substances can cause hearing loss either in conjunction with noise exposure, or without concurrent noise exposure. These substances are known as ototoxins and they can affect the cochlea and/or the auditory neurological pathways. They present a risk via the inhalation route of exposure, and some present a risk via skin absorption.
Workplace Exposure Standards have not been adjusted to reflect risk of hearing impairment. As such, a cautious approach should be applied when using WES for a substance that has ototoxic potential. In addition, risk is likely to be higher if there is exposure to multiple ototoxins. As a combination of exposure to noise and ototoxins has an additive or possibly synergistic effect on risk of hearing loss, occupational noise management programmes should consider ototoxin exposure management.
Some aromatic and aliphatic hydrocarbon solvents are known ototoxins and include acrylonitrile, alcohol, carbon disulphide, ethyl benzene, heptane, n-hexane, perchloroethylene, styrene, toluene and trichloroethylene. Other ototoxins include arsenic, carbon monoxide, cobalt, hydrogen cyanide, lead, mercury, organophosphate pesticides, trimethyl tin, manganese and mercury. Substances that are considered to have potential for ototoxicity have an ‘oto’ notation.
BEI sample collection and time definitions
Prior to (next) shift
Following a period of 16 hours with no exposure. (Appropriate for substances ‘promptly’ but not rapidly eliminated.)
End of shift
The last two hours immediately following the end of the working day. (Appropriate for substances ‘rapidly’ eliminated, whose measured levels could have fallen substantially if sampling was delayed until just prior to the next shift.)
End of work week
After at least four days with exposure. (Appropriate for substances eliminated more slowly and thus incompletely over 24 hours, causing some accumulation, with the highest levels observed on the last day.)