Link between occupation and cancer
The association between occupation and cancer has been known for centuries and in some instances this link has lead to the identification of carcinogens.
The International Agency for Research on Cancer (IARC) has for decades maintained a rigorous program evaluating and ranking substances according to their capacity to cause cancer in humans. A number of the agents classified by IARC as carcinogens have primarily occupational exposures. The exposures ranked as Group 1 carcinogens (carcinogenic to humans) and Group 2A carcinogens (probably carcinogenic to humans) and that occur in an occupational setting are outlined in Table 1 below. Many other widely used occupational agents remain under review by the IARC as Group 2B (possible human carcinogens).
In addition, IARC have evaluated a number of work processes and occupations for their capacity to cause cancer in humans. While risk is higher (or probably higher) for people working in these settings or occupations, specific carcinogens have not been identified. Table 2 outlines the work processes and occupations ranked by IARC as carcinogenic or probably carcinogenic to humans. The level of evidence about the connection between an exposure and a particular cancer varies for different exposure-cancer pairs, even for those exposures defined as human carcinogens.
IARC acknowledges the complexities of identifying lists of potential occupational carcinogens including:
- information on industrial processes and exposures is often poor;
- exposures to well-known carcinogens occur at different intensities in different occupations; and
- levels of exposure can change over time in a given occupation as industrial processes or materials change.
Therefore any list of occupational exposures can only refer to the relatively small number of exposures that have been investigated for carcinogenic risk. The same factors complicate the estimates of the burden of cancer attributable to occupation.
|Exposure||Cancer type||Main industry or use|
|Group 1 carcinogens|
|2,3,7,8-tetrachlorodibenzo-para-dioxin, 2,3,4,7,8-pentachlorodibenzofuran, and 3,3’,4,4’,5-pentachlorobiphenyl||All cancers (soft-tissue sarcoma, non-Hodgkin lymphoma, lung)||Metal, electrical, combustion by-products|
|4,4′-Methylenebis(2-chlorobenzenamine) (MOCA)||NA **||Polyurethane industry|
|Arsenic and arsenic compounds||Lung, skin||Glass, metals, pesticides|
|Asbestos||Mesothelioma, lung, larynx, ovary (pharynx, stomach, bowel)||Insulation, construction|
|Benzene||Leukaemia (lymphoma, myeloma)||Solvent, fuel|
|Benzo[a]pyrene||NA **||Coal industry, aluminium production|
|Beryllium and beryllium compounds||Lung||Aerospace, metals|
|Bis(chloromethyl) ether (BCME) and chloromethyl methyl ether (CMME)*||Lung||Plastic|
|Cadmium and cadmium compounds||Lung||Pigment, battery|
|Chloromethyl methyl ether*||Lung||Chemical|
|Chromium[VI] compounds||Nasal cavity, lung||Metal plating, pigment|
|Coal-tar pitch||Lung (bladder)||Construction, electrodes|
|Diesel engine exhaust||Lung||Transport, mining|
|Dyes metabolized to benzidine||NA **||Pigment|
|Ethylene oxide||(breast, non-Hodgkin lymphoma, multiple myeloma, chronic lymphocytic leukaemia)||Chemical, sterilant|
|Formaldehyde||Nasopharynx, leukaemia (sinonasal)||Plastic, textile|
|Gallium arsenide||NA **||Semiconductors|
|Mineral oils, untreated and mildly treated||Skin||Lubricant|
|Mists from strong inorganic acids||Larynx (lung)||Chemical|
|Nickel compounds||Nasal cavity, lung||Metal, alloy|
|Radon-222 and its decay products||Lung||Mining|
|Shale oils||Skin||Lubricant, fuel|
|Silica, crystalline||Lung||Construction, mining|
|Soot, as found in occupational exposure of chimney sweeps||Skin, lung||Combustion by-product|
|Sulfur mustard (mustard gas)*||Lung (larynx)||Chemical weapon|
|Talc containing asbestiform fibres||Lung||Paper, paint|
|Welding arc (UV radiation)||Ocular melanoma||Welding|
|Wood dust||Nasal cavity||Wood|
|Group 2A carcinogens|
|Benzidine-based dyes||(Bladder)||Pigment, leather|
|ά-Chlorinated toluenes (benzal chloride, benzotrichloride, benzyl chloride, benzoyl chloride)||-||Pigment, chemical|
|Cobalt metal with tungsten carbide||(Lung)||Hard metal production|
|Diazinon||(non-Hodgkin lymphoma, leukaemia, lung)||Agriculture, insecticide|
|Glyphosate||(non-Hodgkin lymphoma)||Agriculture, herbicide|
|Lead compounds, inorganic||(Lung, stomach)||Metals, pigments|
|Malathion||non-Hodgkin lymphoma, prostate||Agriculture, insecticide|
|Polychlorinated biphenyls||(Liver, lymphoma)||Electrical components|
|Trichloroethylene||(Liver)||Solvent, dry cleaning|
|Vinyl bromide||-||Plastic, textile|
Note: Suspected target organs are given in parentheses
* Agent mainly of historical interest
** Not applicable (agent classified on the basis of mechanistic evidence)
|Work process or occupation||Cancer type|
|Group 1 carcinogens|
|Aluminium production||Lung, bladder|
|Boot and shoe manufacture and repair||Nasal cavity, leukaemia|
|Chimney sweeping||Skin, lung|
|Furniture and cabinet making||Nasal cavity|
|Haematite mining (underground) with exposure to radon||Lung|
|Iron and steel founding||Lung|
|Isopropanol manufacture by the strong-acid process||Nasal cavity|
|Painter||Lung, bladder (leukaemia in offspring with maternal exposure)|
|Paving and roofing with coal tar pitch||Lung|
|Rubber manufacturing||Leukaemia, lymphoma, bladder, lung, and stomach (prostate, oesophagus and larynx)|
|Group 2A carcinogens|
|Manufacture of art glass, glass containers and pressed ware||(Lung, stomach)|
|Carbon electrode manufacture||(Lung)|
|Hairdresser or barber||(Bladder, lung)|
|Petroleum refining||(Leukaemia, skin)|
Note: Suspected associated cancers are shown in parentheses
In Australia, mesothelioma caused by asbestos exposure is probably the best known occupational cancer. However, some carcinogens to which the general public can be exposed, such as ultraviolet (UV) radiation from sunlight and second-hand tobacco smoke, are also important carcinogens in an occupational context.
A 2012 study prioritised occupational carcinogens in Australia based primarily on the potential for occupational exposure and evidence of use in Australian industry, as there was limited exposure information at the time the study was conducted. Carcinogens were prioritised through an assessment framework based on evidence of carcinogenicity using IARC criteria, use in occupational circumstances and use in Australian industry. The priority list (see Table 3) comprises 38 established or probable carcinogenic agents present in Australian workplaces and is designed to guide priorities for preventive action in the Australian setting.
In terms of occupational exposure, the most common carcinogens are estimated to be solar UV radiation, diesel engine exhaust, second-hand tobacco smoke, benzene, lead and silica. See the Impact section for more information.
Table 3. Priority carcinogens for Australia
|Combustion products||Diesel engine exhaust, polycyclic aromatic hydrocarbons (PAHs), second-hand tobacco smoke|
|Inorganic dusts||Asbestos, crystalline silica dust in the form of quartz or cristobalite|
|Organic dusts||Leather dust, wood dust|
|Metals||Arsenic and inorganic arsenic compounds, beryllium and beryllium compounds,cadmium and cadmium compounds, chromium (VI) compounds, cobalt metal and tungsten carbide, inorganic lead compounds, nickel compounds|
|Radiation||Artificial ultraviolet radiation (UVA, UVB, UVC), ionising radiation, radon-222 and it’s decay products, solar radiation|
|Other industrial chemicals||Strong inorganic acid mists, acrylamide, alpha-chlorinated toluenes, benzene, 1, 3-butadiene, diethyl sulphate, dimethyl sulphate, epichlorhydrin, ethylene oxide, formaldehyde, glycidol, 4, 4´-methylenebis(2-chloroaniline) (MOCA), nitrosamines, ortho-toluidine (2-aminotoluene), polychlorinated biphenyls (PCBs), styrene-7, 8-oxide, tetrachloroethylene (perchloroethylene), trichloroethylene, vinyl chloride|
|Non-chemical agents||Shiftwork that involves circadian disruption|
UV radiation in the form of sunlight is Australia’s most prevalent occupational carcinogen and is particularly important for outdoor workers. Over 2 million Australian workers (37% of the Australian male working population and 8% of the female working population) were estimated to be significantly exposed to solar radiation in 2011-2012 in the course of their work.
Among people exposed to UV radiation in occupational settings, exposure is more likely among males and those in lower socioeconomic and regional areas. Although sun protection is used by the majority (95%) of those exposed in occupational settings, only 9% are fully protected. Solar UVR is strongly linked to the occurence of melanoma and the risk of melanoma has been found to be significantly increased for career full-time firefighters, particularly among those who were employed for more than 10 years.
For information on the impact of UV radiation on cancer and recommendations for reducing workplace UV exposure, see the UV radiation chapter of the National Cancer Prevention Policy and the Sun protection in the workplace position statement.
All forms of asbestos are ranked by IARC as Group 1 carcinogens. Asbestos exposure is responsible for high levels of mesothelioma and lung cancer incidence and mortality worldwide and also causes laryngeal and ovarian cancer. Around 90-100% of mesothelioma cases are linked with asbestos exposure.
Australia has one of the highest rates of mesothelioma incidence in the world. Mesothelioma incidence rates have steadily increased in Australia over the last 30 years. Total cases are expected to reach around 18,000 by 2020.
Mesothelioma, resulting from occupational asbestos exposure, is one of the most comprehensively studied occupational cancers in Australia. The most extensively documented exposure to asbestos by area relates to the mining town of Wittenoom in Western Australia, where mining operations caused disease not only in the workforce, but also among residents.
A retrospective analysis of mesothelioma in Australia between 1945 and 2000 found Australia's high incidence was linked to a history of prevalent asbestos use, of all fibre types, across varied occupational and environmental settings. The Australian Mesothelioma Registry (AMR) provides estimates of asbestos exposure data based on the exposure profiles of those diagnosed with mesothelioma. Based on cases diagnosed since July 1st, 2010 over 60% of people diagnosed were identified by the AMR as having ‘possible’ or ‘probable’ asbestos exposure in an occupational setting.
While commercial production and use of asbestos have been banned in Australia for many years, inadvertent exposure remains a problem because of its widespread presence in building materials such as fibro, which is in place in thousands of established structures. Mesothelioma cases related to renovation are projected to continue to increase due to the number of homes still containing asbestos building products. Exposure to asbestos during home renovation is common. From 2005-2008 home renovators accounted for 8.4% of all men and 35.7% of all women diagnosed with mesothelioma.
Unless occupational health and safety standards are improved Australia-wide, opportunities to minimise future disease burden associated with the high prevalence of asbestos-containing materials already in the community will not be realised. "Lessons must be learned to help revive the currently waning societal commitment to occupational health and safety in Australia and elsewhere", to prevent unnecessary asbestos-caused disease. See Effective interventions for more information.
Second-hand tobacco smoke
Despite workplace bans on smoking, second-hand tobacco smoke remains one of the most common occupational carcinogens in Australia, with over 1.1 million working men and 240,000 working women estimated to be exposed.
Given the time lag between exposure and diagnosis, the full impact of tobacco smoking in the workplace has not yet been evident in cancer incidence and mortality data.
For more information, see the Tobacco control chapter of the National Cancer Prevention Policy.
Diesel engine exhaust
Diesel engine exhaust is classified by IARC as a Group 1 carcinogen. Diesel engine exhaust in one of the most common occupational carcinogens in Australia, with over 1.3 million working men and 250, 000 working women estimated to be exposed. Occupational exposure to diesel exhaust increases lung risk and probably also increases bladder cancer risk.
Professional drivers potentially exposed to diesel exhaust are at increased risk of lung cancer and probably of bladder cancer. There is good evidence that lung cancer mortality is associated with occupational exposure to diesel exhaust in miners.
Combined data from three occupational cohort studies suggest that diesel engine exhaust at levels common in the workplace and in outdoor air appear to pose substantial excess lifetime risks of lung cancer. Two independent studies of trucking industry workers  and a study of non-metal miners were included in this meta-regression. Past occupational and environmental exposure to diesel engine exhaust was estimated to be responsible for 1.3% and 4.8% of annual lung cancer deaths in the United States and the United Kingdom respectively.
Pesticides and herbicides
Worldwide, occupational exposure to pesticides and herbicides have been clearly implicated as a carcinogenic hazard, although studies have been unable to consistently identify specific agents or classes of agents.
In March 2015, the International Agency for Research on Cancer (IARC) assessed the carcinogenicity of five organophosphate pesticides. Glyphosate (a herbicide), malathion and diazinon (insecticides) were classified as probably carcinogenic to humans (Group 2A). There was limited evidence of carcinogenicity of glyphosate to humans based on non-Hodgkin lymphoma associated with occupational exposure studies in the US, Canada and Sweden as well as evidence of cancer in laboratory animals. For the insecticides malathion and diazinon, there was limited evidence of carcinogenicity for non-Hodgkin lymphoma, prostate cancer (malathion only) and lung cancer (diazinon only). The epidemiological evidence for malathion comes from studies of agricultural exposures in the US, Canada and Sweden. Malathion also caused tumours in rodents. The evidence for carcinogenicity of diazinon comes from studies of agricultural exposures in the US and Canada. While there was limited evidence of carcinogenicity in humans found, there was strong mechanistic evidence of the carcinogenicity of glyphosate, malathion and diazinon with all three agents inducing DNA and chromosomal damage in human and animal cells in vitro. The insecticides tetrachlorvinphos and parathion were classified as possibly carcinogenic to humans (Group 2B) based on sufficient evidence that these pesticides cause cancer in laboratory animals. Given the recent IARC findings, the Cancer Council recommends the Australian Pesticides and Veterinary Medicines Authority considers altering current usage and/or handling requirements for these particular herbicides.
Pesticides are a heterogeneous group of chemicals, with different substances and mixtures in use having changed over time. Retrospective exposure assessment identifying the type and extent of individuals' exposure to pesticides is likely to result in misclassification. Inconsistency in the evidence on pesticides and cancer underscores the need for a cautious approach to working with these potentially carcinogenic substances and for more research on the potential harms associated with specific agents.
Investigation of a cohort of Australian workers exposed to pesticides did not find evidence of a relationship between occupational pesticide exposure and cancer, nor other non-injury-related mortality. However, a separate case-control study found substantial exposure to any pesticide was associated with a trebling of the risk of non-Hodgkin lymphoma. Subjects with substantial exposure to organochlorines, organophosphates, and "other pesticides" (all other pesticides excluding organochlorines, organophosphates and herbicides) and herbicides other than phenoxy herbicides had similarly increased risks, although the increase was statistically significant only for "other pesticides".
See the Cancer Council position statement on Pesticides and cancer for more information.
Ionising radiation is classified as a Group 1 carcinogen to humans by the IARC. A retrospective cohort study examined cancer incidence among Australian nuclear industry workers and found no evidence of a significant increase in cancer risk. Exposure to ionising radiation is carefully controlled under strict Occupational Health and Safety regulations and workers who have potential for exposure carry personal monitors.
Welding activities produce many hazards through the production of contaminants in welding fume and ultraviolet (UV) radiation in the welding arc, both of which have been classified as Group 1 carcinogens (carcinogenic to humans) by IARC. Exposure to welding fumes or welding arc can increase your risk of developing lung cancer and ocular melanoma respectively. There is limited evidence for increased risk of kidney and other cancers.
Welding fume is made when a metal is heated above its boiling point. The metal cools and then condenses into fume which produces fine particles that can be inhaled. Welding fumes contain potential carcinogens including metallic oxides, silicates and fluorides. A positive exposure-response association was found between welding fume exposure and lung cancer. The increase in lung cancer was unable to be explained by asbestos exposure and/or tobacco smoking.
Electric arc and laser welding give off UV radiation. UV exposure was found to increase the risk of developing an ocular melanoma generally between two and ten times. These results remained consistent even in studies that adjusted for sun exposure and/or sunbed use. Furthermore, a relationship was found between ocular melanoma and both duration of employment as welder  and eye burns.
Other occupational risk factors
There is mixed evidence for a positive association between occupational sitting and cancer. However, physical inactivity is an important cancer risk factor and should therefore be addressed in the workplace.
For more information see the Overweight and obesity, physical activity and nutrition chapter of the National Cancer Prevention Policy, and the Policy context section of this chapter.
Shift work involving circadian disruption has been classified by IARC as a probable human carcinogen (Group 2A). Shift work is common in a number of industries, including manufacturing, mining, healthcare, hospitality, communication and transport. Night work causes most disruption to the circadian clock, the 24-hour biological cycle that governs sleeping and waking in humans.
The strongest evidence for carcinogenicity of shift work is for breast cancer. Women working shift work involving nights appear to have an increased risk of developing breast cancer. There are however, some inconsistencies with a dose-response relationship between shift work and breast cancer.
Parental exposures and cancer risk in children
The impact of occupational exposures may go beyond the individual worker and contribute to increased cancer in family members. Research has suggested that parental exposure to certain carcinogens or work environments may increase cancer risk in their children – implicated exposures include vehicle exhaust, painting, wood trades, pesticides and other agricultural exposures, electronics, textiles and second-hand smoke during pregnancy. There are, however, no definitive findings that enable quantification of the risk.
See the Pesticides and cancer position statement for more information on the link between parental exposure to pesticides and cancer in offspring.
Cancer incidence and mortality in Australia is higher among less socio-economically advantaged people as measured by factors such as income, educational attainment, employment and skill levels in specific occupations. While much of this disparity in cancer incidence can be attributed to risk factors such as smoking, obesity/overweight, poor diet and sedentary behaviour – which are more prevalent among people with socioeconomic disadvantage – the risk of occupational cancer appears to be higher among socially disadvantaged people, who are more likely to be employed in relatively unskilled jobs where exposure to carcinogens is higher.
Industrial and workplace exposures to carcinogens are more common among manual workers, or employees with lower levels of job skills, education and training. In industrialised countries, occupational exposures may be responsible for about one third of the excess of all cancers occurring in people in lower socioeconomic groups.
Eliminating or reducing exposure to occupational carcinogens is therefore an important part of redressing health disparities linked to socioeconomic disadvantage in Australia.
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