The panel’s recommendations
This section explains the panel’s report methodology, analytical criteria, and fourteen recommended additions.
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Methodology
The panel’s key sources of evidence included guidance notes from the ILO and Safe Work Australia, and advice published by NIOSH, IARC and OSHA. These organisations provide reputable studies as they possess the resources to undertake long-term epidemiological studies with large sample sizes.
Guidance notes from the ILO were particularly useful as they provided the panel with background information relevant to determining causal relationships between the factor (such as infrared radiation) and the resulting illness (such as heat-induced cataracts).
Where the above organisations may not have provided advice on a pairing, the independent panel made use of other peak body publications, technical reports, peer-reviewed literature, and in-depth specialist works assessing the relationship between the disease/exposure pairings. For papers to be included, they must have been published within an appropriate date range, contain sufficient statistical data on causality, and be fully available for the panel to read.
Where appropriate, the panel also drew on their clinical experience to assist in their assessments of each disease/exposure pairing. The three panel members had diverse backgrounds in epidemiology and research providing them with a wealth of professional knowledge to draw from.
Analytical criteria
In line with the overall review framework agreed to by Cabinet, the panel used the Bradford Hill Criteria when conducting their evidence review on each disease/exposure pairing. This is an internationally recognised review criteria comprising nine principles used to evaluate epidemiological evidence to establish causation between a presumed cause (exposure) and observed effect (disease). Table One below outlines the principles of the Bradford Hill Criteria.
Table One: Technical criteria for Schedule 2 review
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Criteria to establish a causal relationship |
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|---|---|
| Criteria | Description |
| Strength of association | The greater the impact of an exposure on the occurrence or development of a disease, the stronger the likelihood of a causal relationship. |
| Consistency or reproducibility | Consistent findings observed by different persons in different places with different samples strengthen the likelihood of an effect. |
| Specificity | Causation is likely if there is a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship. |
| Temporality of time sequence | The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay). |
| Biological gradient | Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence. |
| Biological plausibility | From what is known of toxicology, chemistry, physical properties, or other attributes of the studied risk or hazard, it makes biological sense to suggest that exposure leads to the disease or injury. |
| Coherence | A general synthesis of all the evidence (e.g., human epidemiology and animal studies) leads to the conclusion that there is a cause-effect relationship in a broad sense and in terms of general common sense. |
| Analogy | The use of analogies or similarities between the observed association and any other associations. |
| Experimental evidence | This can be considered if relevant. |
|
Criteria to establish if the causal connection between the disorder and employment is sufficiently strong enough to enable automatic acceptance of a claim |
|
| Criteria | Description |
| Insufficient causal evidence | Diseases will be excluded if evidence of the causal connection between the disorder and employment is not sufficiently strong to allow a connection to work to be automatically accepted. ‘Sufficiently strong’ here is not generally quantifiable. For each condition on Schedule 2 it will need to be based on an expert assessment of the evidence available and its quality. |
| Proportion of work cases | Diseases will only be included if employment is the cause of the disorder in a significant majority of the cases of that disorder in a subset of the population, identified based on the subset’s exposure to particular work tasks, or particular work environments. |
The panel’s recommended additions to Schedule 2
Following their evidence review, the panel recommended fourteen disease/exposure pairings for inclusion on Schedule 2. Each of the fourteen pairings recommended for inclusion on Schedule 2 demonstrated strong, consistent, well-defined relationships between the exposure to a factor at work and development of corresponding disease/illness. There was also biological plausibility that exposure to the substance could cause the corresponding disease/illness and presented a dose-response relationship which means increased levels of exposure were associated with an increased risk of developing the disease/illness.
Table Two below outlines the fourteen pairings recommended for inclusion on Schedule 2 by the panel.
Table Two: The panel’s recommended additions to Schedule 2
| New entry | Erionite and malignant mesothelioma |
|---|---|
| Infrared radiation and heat-induced cataracts | |
| Nickel and nasal cancer | |
| Ammonia and chronic corneal ulcer | |
| 1,2-Dichloropropane and cholangiocarcinoma | |
| Butadiene and leukaemia | |
| Trichloroethylene and kidney cancer | |
| New entry with specific occupation or process | Welding and ocular melanoma |
| Firefighting and mesothelioma | |
| Add to existing entry in Schedule 2 | Potroom emissions and asthma (amend entry 37 which is currently: Occupational asthma diagnosed as caused by recognised sensitising agents inherent in the work process such as, but not limited to, isocyanates, certain wood dusts, flour dusts, animal proteins, enzymes, and latex). |
| Asbestos and laryngeal cancer (amend entry 2 which is currently: Lung cancer or mesothelioma diagnosed as caused by asbestos). | |
| Asbestos and ovarian cancer (amend entry 2 which is currently: Lung cancer or mesothelioma diagnosed as caused by asbestos). | |
| Vinyl chloride and hepatocellular carcinoma (amend entry 21 which is currently: Angiosarcoma of the liver diagnosed as caused by vinyl chloride monomer). | |
| Add to existing entry with specific occupation | Firefighting and bladder cancer (amend entry 33 which is currently: Bladder carcinoma diagnosed as caused by 2-naphthylamine, benzidine, 4-aminobiphenyl, N, N-Bis (2-chloroethyl)-2-naphthylamine, other aromatic amines, or poly-cyclic aromatic hydrocarbons). |
Occupations and processes
While the majority of the recommended additions are diseases or illnesses associated with specific causative agents (for example nasal cancer caused by occupational exposure to nickel), the panel has also recommended the inclusion of a specific process (welding) and occupation (firefighting) as causative factors.
Welding
The panel followed advice from the IARC’s 2012 specialised report on radiation which found strong evidence of ocular melanoma occurring in welders. However, without a full review into the carcinogenic effects of welding, the IARC’s Working Group did not feel comfortable attributing the occurrence of ocular melanoma to ultraviolet radiation alone. Therefore, the IARC Working Group’s final evaluation was that there was sufficient evidence linking the broader process of welding to the development of ocular melanoma.
Firefighting
The panel followed advice from the IARC’s 2023 specialised report on firefighters’ occupational exposures which found a causal relationship between firefighting and bladder cancer, and firefighting and mesothelioma. In their concluding notes, the IARC acknowledged that the occupational exposures firefighters face are complex and contain a variety of hazards given their diverse roles and responsibilities. As the events firefighters respond to vary so widely, their potential exposures also vary and while carcinogenicity can be proven for many of these potential exposures, the panel determined that listing all of these could be too prescriptive. Therefore, it would be more accurate to include firefighting as a causative factor for developing bladder cancer and mesothelioma.
Not recommended for inclusion
Pairings to monitor
The independent panel highlighted eleven disease/exposure pairings which, at present, did not have enough evidence to demonstrate a sufficient causal relationship. However, through the evidence review process, the independent panel found there to be a developing body of evidence to establish causality between the pairings and flagged that these should be prioritised for assessment in the next review.
Table Three below outlines the pairings flagged by the panel to be prioritised for assessment as part of the next review of Schedule 2, along with the panel’s reasoning for this.
Table Three: Pairings to monitor for the next review of Schedule 2
| Disease/exposure pairing | Panel assessment |
|---|---|
| Asbestos and cholangiocarcinoma | The panel identified some limited evidence which suggested a potential link between asbestos and the development of cholangiocarcinoma. However, there was not sufficient evidence to warrant the panel’s recommendation at this time. |
| Carcinogenic effects of cadmium | Evidence identified by the panel was insufficient to support a causal link between cadmium exposure and the development of kidney and/or prostate cancer. |
| Coal tar pitch and bladder cancer | The panel identified a limited but emerging body of research on the link between coal tar pitches and the development of bladder cancer. However, this was not sufficiently strong to warrant the panel’s recommendation at this time. |
| Coal tar pitch and kidney cancer | The panel identified a limited but emerging body of research on the link between coal tar pitches and the development of kidney cancer. However, this was not sufficiently strong to warrant the panel’s recommendation at this time. |
| Formaldehyde and endometriosis | As part of the panel’s commitment to applying an intersectional and gender-equitable lens to this review, they looked at evidence for female-specific occupational diseases. They identified an emerging body of evidence linking formaldehyde exposure to the development of endometriosis. However, this was not sufficiently strong to warrant the panel’s recommendation at this time. |
| Formaldehyde and leukaemia | While the IARC has determined there to be a causal link between formaldehyde exposure and the development of leukaemia, this decision has been contested and the panel did not find the evidence to be sufficiently strong to prove causality. |
| Nickel and asthma | The panel identified limited epidemiological evidence to support a causal link between exposure to nickel and the development of asthma. |
| Platinum and asthma | The panel identified limited epidemiological evidence to support a causal link between exposure to platinum and the development of asthma. |
| Polycyclic aromatic hydrocarbons (PAHs) and skin cancer | The panel identified a limited but emerging body of research on the link between specific PAHs (which are by products of coal tar pitches) and the development of skin cancer. However, this link was not sufficiently strong, and the panel recognised that some coverage can be obtained under Schedule 2 already (per entry 15: Primary epitheliomatous cancer of the skin diagnosed as caused by tar, pitch, bitumen, mineral oil, anthracene, or the compounds, products, or residues of these substances). |
| Shift work and breast cancer | As part of the panel’s commitment to applying an intersectional and gender-equitable lens to this review, they looked at evidence for female-specific occupational diseases. They identified an emerging body of evidence linking shift work to the development of breast cancer. However, this was not sufficiently strong to warrant the panel’s recommendation at this time. |
| Vanadium and asthma | The panel identified limited epidemiological evidence to support a causal link between exposure to vanadium and the development of asthma. |
Not recommended for inclusion
A lack of sufficient evidence to support a causal relationship between an exposure and disease (or other illness) was the most frequently cited reason provided by the panel when not recommending a pairing for inclusion in Schedule 2.
This conclusion was often supported by the panel’s clinical experience and accompanied by the panel noting that, for the time being, many of the proposed disease/exposure pairings were best left to being assessed on a case-by-case basis (i.e., through the section 30 test) until the body of evidence develops.
For example, sensitiser asthma caused by occupational exposure to platinum was not recommended for inclusion on Schedule 2 given there was limited epidemiological evidence to support causation. Additionally, the panel noted that in their joint clinical experience, a variety of metal fumes can be a cause of occupational asthma, but this is best assessed on a case-by-case basis until more evidence is available.
Table Four below outlines the pairings assessed by the panel which were not recommended for inclusion on Schedule 2 and the reasoning.
Table Four: Pairings assessed and not recommended for inclusion on Schedule 2
| Disease/exposure pairing | Panel assessment |
|---|---|
| Irritant and allergic dermatitis for any exposure | While contact dermatitis is a common occupational disease, it is too complex to determine causality and is best left to being assessed on a case-by-case basis. |
| Acrylonitrile and associated cancers | The carcinogenic effects of acrylonitrile should be excluded from Schedule 2 for now as determining causality is complex. The panel found that this is not suitable for inclusion on Schedule 2 as there was insufficient causal evidence. |
| Alcohol, glycols or ketones and associated diseases | Methyl isobutyl ketone and methyl ethyl ketone are already covered on Schedule 2 as organic solvents corresponding to laryngeal carcinoma, chronic solvent-induced encephalopathy, and peripheral neuropathy. There was insufficient causal evidence linking alcohols and glycols to other associated diseases. |
| Aluminium and aluminosis, bauxite fibrosis, and chronic obstructive pulmonary disease | The panel’s proposed addition of asthma diagnosed as caused by potroom emissions would sufficiently address this pairing. |
| Ammonia and chronic obstructive pulmonary disease and pulmonary fibrosis | Chronic obstructive pulmonary disease and pulmonary fibrosis resulting from exposure to ammonia should continue to be considered on a case-by-case basis as it can be caused by exposures other than ammonia. |
| Antimony and nose septal ulceration, deposits on teeth or antimoniosis | Nasal septal ulceration is caused by other activities and antimoniosis is extremely rare meaning there was insufficient causal evidence throughout the panel’s review. The panel also noted that, if these were to be added, then all other causes of lung opacity would need to be ruled out. |
| Benzoquinone and vitiligo | Vitiligo is best assessed on a case-by-case basis. It is currently covered on Schedule 2 when diagnosed as being caused by para-tertiary-butylphenol, para-tertiary-butylcatechol, para-amylphenol, hydroquinone, or the monobenzyl or monobutyl ether of hydroquinone. |
| Cadmium and pulmonary emphysema, ansomia, osteoporosis, osteomalacia, itai-itai disease, nephropathy, and Fanconi disease | Pulmonary emphysema, ansomia, osteoporosis, osteomalacia, and itai-itai disease are best left to being assessed on a case-by-case basis as there are a range of causes other than cadmium exposure. |
| Carbon disulphide and chronic toxic encephalopathy, toxic optical neuropathy, ototoxic hearing loss, atherosclerosis, chronic ischaemic heart disease, secondary hypertension, and chronic kidney disease | Chronic toxic encephalopathy, toxic optical neuropathy, ototoxic hearing loss, atherosclerosis, chronic ischaemic heart disease, secondary hypertension, and chronic kidney disease are best left to being assessed on a case-by-case basis as there are a range of causes other than carbon disulphide exposure. |
| Chlorine and chronic obstructive pulmonary disease, emphysema, chronic bronchiolitis, pulmonary fibrosis, chronic rhinitis, and erosion of the teeth | Chronic obstructive pulmonary disease, emphysema, chronic bronchiolitis, pulmonary fibrosis, chronic rhinitis, and erosion of the teeth are best left to being assessed on a case-by-case basis as there are a range of causes other than chlorine exposure. |
| Copper and hepatic granuloma, chronic pulmonary fibrosis and chalcosis | Chronic pulmonary fibrosis is best left to being assessed on a case-by-case basis as it can be caused by exposures other than copper exposure; linking hepatic granuloma to copper exposure would be difficult; and chalcosis is extremely rare. |
| Cyclophosphamide and leukaemia | While the panel determined that a causal relationship between cyclophosphamide and leukaemia is possible if the affected person was manufacturing cyclophosphamide, it is significantly less likely to occur in a hospital setting. Therefore, is best left to being assessed on a case-by-case basis to check exposure status. |
| Fluorine and dental fluorosis and chronic obstructive pulmonary disease | There are no recent reports of dental fluorosis and skeletal fluorosis resulting from a workplace exposure and are both difficult to link to a work task or environment. Chronic obstructive pulmonary disease was also not recommended for inclusion on Schedule 2 as it is incidental to asthma when attributed to fluorine exposure. |
| Food flavourings and obliterative bronchiolitis | Food flavouring is too broad of a category, making it inappropriate for inclusion on Schedule 2. |
| Hard metal dust and sensitiser-induced occupational asthma and hard metal lung disease | The panel determined that it would be sufficiently covered by entry 24: diseases of a type generally accepted by the medical profession as caused by tungsten. |
| Isocyanates allergic rhinitis, allergic conjunctivitis, and chronic obstructive pulmonary disease | Allergic rhinitis, allergic conjunctivitis, and chronic obstructive pulmonary disease are best left to being assessed on a case-by-case basis as there are a range of causes other than exposure to isocyanates. |
| Lindane and non-Hodgkin’s lymphoma | Lindane as a pesticide was banned from use in New Zealand in 2009, meaning all claims would be historical. Shifting the exposure to ‘pesticides’ would be too broad. |
| Methyl ethel ketone and chronic toxic encephalopathy | Chronic toxic encephalopathy is already adequately covered by entry 35: Chronic solvent-induced encephalopathy diagnosed as caused by organic solvents, particularly styrene, toluene, xylene, trichloroethylene, methylene chloride, or white spirit. |
| Methyl isobutyl ketone and polyneuropathy | Polyneuropathy is already adequately covered by entry 36: Peripheral neuropathy diagnosed as caused by organic solvents such as n-hexane, carbon disulphide, or trichloroethylene; pesticides such as organophosphates; acrylamide. |
| Mineral acids and nasal septal ulceration and laryngeal cancer | Nasal septal ulceration is caused by other activities and, as smoking is the primary causal factor, attributing a work-related task or activity to the development of laryngeal cancer may be difficult. |
| Nail technician and respiratory diseases | Respiratory diseases is too broad of a category and the evidence review only identified low-quality evidence from the 1990’s and early 2000’s, but this was insufficient to support a causal relationship. |
| Nitroglycerin (and nitric acid esters) and chronic toxic encephalopathy, angina pectoris, and Raynaud’s phenomenon | It is not practical to assess Raynaud’s phenomenon in relation to a work-related task or environment. |
| Non-fibrogenic mineral dust and stannosis, baritosis, pneumoconiosis due to titanium oxide and antimoniosis | There was insufficient evidence to determine a causal relationship between this disease(s)/exposure pairing. Baritosis is best left to being assessed on a case-by-case basis as it can be caused by exposures other than non-fibrogenic mineral dust. Antimoniosis is extremely rare; if this was to be added, then all other causes of lung opacity would need to be ruled out. Additionally, entries 26, 28, 37 and 38 on Schedule 2 cover other dusts (wood, organic, flour, cotton, and grain). |
| Optical radiations and chronic blepharoconjunctivitis, chronic actinic dermatitis, and B12 deficiency | Chronic blepharoconjunctivitis, chronic actinic dermatitis, actinic cataract are best left to being assessed on a case-by-case basis to ensure work-related exposure is the attributable cause. |
| Oxides of nitrogen and bronchiolitis obliterans, chronic obstructive pulmonary disease, and B12 deficiency | Nitrogen oxides, while occupational irritants, have transient and acute effects making them unsuitable for inclusion on Schedule 2. As respiratory health effects from exposure to nitrogen oxides require high levels of exposure, the panel concluded that these are best left to being assessed on a case-by-case basis. |
| Pentachlorophenol and non-Hodgkin’s lymphoma | Given the rarity of pentachlorophenol use nowadays, it is likely that exposure or development of non-Hodgkin’s lymphoma would be historical. The carcinogenic effects of the broader category of pesticides is best left to be assessed on a case-by-case basis. |
| Pesticides and anti-coagulation syndrome due to exposure to coumarin derivatives, toxic effects caused by pentachlorophenol and carcinogenic effects of pesticides | The carcinogenic effects of the broader category of pesticides is best left to be assessed on a case-by-case basis. Additionally, cover may be provided under entry 36: Peripheral neuropathy diagnosed as caused by organic solvents such as n-hexane, carbon disulphide, or trichloroethylene; pesticides such as organophosphates; acrylamide. |
| Pharmaceutical agents and carcinogenic effects of antineoplastic drugs | While there is causal evidence of antineoplastic drugs having carcinogenic effects, this was either not specific to occupational exposure (per IARC advice), or, where theoretically possible, is unlikely to occur in a hospital setting as a high level of exposure is required. The panel determined that this was best left to being assessed on a case-by-case basis. |
| Platinum and allergic rhinitis and allergic urticaria | Given its various uses and variety of occupations which can face platinum exposure, allergic rhinitis and allergic urticaria as a result of platinum exposure are best left to being assessed on a case-by-case basis. |
| Polychlorinated biphenyl and malignant melanoma | Polychlorinated biphenyls have been banned in New Zealand since the 1980’s meaning exposure would be historic. As a result, the panel determined that this is not appropriate for inclusion on Schedule 2 and is best left to being assessed on a case-by-case basis. |
| Polycyclic aromatic hydrocarbons and lung cancer | The panel determined that lung cancer diagnosed by exposure to polycyclic aromatic hydrocarbons are adequately covered by entry 31: Lung cancer diagnosed as caused by bis (chloromethyl) ether (and chloromethyl methyl ether), cadmium, coke oven emissions, nickel, radon, silica, or soot. |
| Selenium and selenosis | Selenosis is best left to being assessed on a case-by-case basis. |
| Sulphur oxides and chronic skin and mucous membranes irritation, nose septal ulceration, chronic obstructive pulmonary disease, chronic bronchiolitis obliterans, emphysema, and pulmonary fibrosis | Chronic skin and mucous membrane irritation, COPD, chronic bronchiolitis obliterans, emphysema and pulmonary fibrosis are best left to being assessed on a case-by-case basis as there are many causal factors for these diseases. |