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Work cancer prevention kit:
Part 1 Contents Section 1 Introduction Burying workplace cancers You don’t hear much about occupational cancer. You hear about cancer the tragedy for the individual, cancer the challenge for the medical profession, cancer the result of smoking and bad diet. But at least one in every 10 cancers – and probably many more – are the result of preventable, predictable workplace exposures. The International Labour Organisation’s estimate of over 609,000 work-related cancer deaths worldwide each year is almost certainly a substantial under-estimate, but still amounts to one work-related cancer death every 52 seconds. Asbestos is the biggest industrial killer of all time, and kills thousands from cancer every single week, at least one death every five minutes. But it is not banned worldwide. Dozens of other substances known to cause cancer are used, quite literally, in industrial quantities in our workplaces, frequently with few controls. This is not yesterday’s problem. At work, we face a barrage of rapidly evolving substances, work methods, processes and environments with little thought given to the health consequences that will face society – workers, families, entire communities - a working generation down the road. Because today’s exposures cause cancers at least two decades
later, it is a problem that doesn’t cause alarm bells for corporate
executives who are answerable to shareholders from annual general
meeting to annual general meeting. Instead, the causes are covered-up,
the bodies are buried and the killing continues.
Burying the evidence The world is facing a cancer epidemic which has been almost entirely missed in official statistics. Occupational cancer is killing thousands worldwide every day, but is not receiving adequate attention from workplace enforcement or public health bodies. Cancer is a very modern killer. Lung cancer reports were relatively rare at the start of the 21st century. The massive increase in smoking in the 20th century was an indisputable and major cause of the lung cancer explosion. But coincident with the explosion in smoking, was an explosion in workplace exposures to a continually widening pool of workplace substances that had been poorly studied and which were, for much of the century, poorly controlled. There are now approaching 100,000 synthetic chemicals used in our workplaces. Many more people today are exposed to many more substances. While smoking cessation has become a major public health priority and has spurred an entire prevention industry, no similar campaign has been waged to address the carcinogens encountered and inhaled by millions at work. The International Labour Office (ILO) ranks occupational cancer as the top work-related cause of death worldwide, accounting for almost a third of all deaths linked to workplace factors, more than circulatory disease, infections or accidents. Primary prevention – removing the risks – could prevent all occupational cancers. But wherever you work, too little official regard for the risks has meant precious little regard for prevention.
Working out the relative contribution of lifestyle, diet, pollution, occupation and other factors to the overall cancer toll is at best informed guesswork. In a move that has led to occupational cancer being a forgotten prevention priority, governments routinely cite a 1981 report to the US Congress – the Doll/Peto report (1) - which estimated that 4 per cent, with a range of certainty of 2 per cent to 8 per cent, of cancer mortality was due to occupational causes.
Women scarcely featured in the large industrial US workplaces considered by the study, and breast cancer – a major killer in women – is ignored. And African-American workers, concentrated in the most hazardous manual jobs, were excluded entirely from the analysis. But this isn’t the whole story. Not everyone is at risk. The great majority of occupational cancers are concentrated in blue collar jobs, meaning those workers face a massively increased risk, while others face virtually none. For some workers in some jobs – certain asbestos and rubber industry workers, for example - work was in effect a death sentence.
Thousands have gone on to die from cancers they just shouldn’t have developed, at least according to the Doll/Peto estimate, including the family members of workers exposed to asbestos, who got a second hand “paraoccupational” dose from the contaminated clothes and hair of a family member. • Why the official cancer estimates
are wrong.
Recent reassessments of the real work cancer toll in the US, Australia, the UK and elsewhere have given some indication of how far Doll/Peto fell short of the real risk. Studies of actual work-related cancer levels have put the true contribution of work to cancer deaths at up to five times the level reported by Doll/Peto. A World Health Organisation report in 2006 (2) said: “The estimates of the proportion of cancer deaths in the general population attributable to occupational exposures in developed countries are in the range of 4-20 per cent.” It added: “Occupational cancer is entirely preventable and interventions at the workplace can save millions of lives every year.” Recent reviews suggest a workplace contribution of between 8 and 16 per cent of all cancers (3). An International Labour Organisation (ILO) estimate, cited in the American Journal of Industrial Medicine in January 2007, concluded the attributable fraction of occupational cancers in industrialised countries is 13.8 per cent for men and 2.2 per cent for women. ILO’s cautious estimate puts the global human toll at over 600,000 deaths a year – one death every 52 seconds (4). This would translate to around 10 per cent of all cancer deaths every year. The authors, which included the then director of ILO’s Safework programme, concluded that while at the moment the relative importance of cancers as a cause of work-related deaths is higher in developed nations, the export of hazardous jobs and processes as a component of rapid industrialisation meant “developing countries are encountering work-related hazards more frequently than developed countries did at the time of their industrialisation, which took place over a relatively long time period. Work-related diseases will grow in relative significance in the future as a component of the morbidity and mortality of society as a whole.” A 2006 paper in the Australian and New Zealand Journal of Public Health (5) contained an explicit criticism of the Doll/Peto figures. The authors reported: “Because of outdated data, and gaps in knowledge of which chemicals cause cancer and the magnitude of the risk of cancer from each carcinogen, these are very likely to have been considerable underestimates.” They add: “We estimate that approximately 10.8 per cent of cancer cases (excluding non-malignant skin cancers) in males and 2.2 per cent of such cancer cases in females are caused by occupational exposures.”
Dr Clapp said: “I believe occupational lung cancer is the leading work-related cancer followed by bladder cancer, non-Hodgkin's lymphoma, and leukaemia. Our review paper gives the scientific studies which back this up, along with the various exposures that cause these cancers. “For example, for lung cancer, we review the evidence that metals, solvents, ionising radiation, reactive chemicals like BCME, environmental tobacco smoke, air pollution, polycyclic aromatic hydrocarbons, pesticides and fibres like asbestos and silica cause lung cancer. This adds up to a substantial burden, and some of these exposures - like asbestos and ionising radiation in underground miners - act synergistically with cigarette smoke and vastly increase lung cancer risk.” He added “there is no way to put a precise number on this because cancer is such a ‘multifactorial’ disease and even small exposures can be a critical piece of the pie when lots of people are exposed. The reason we have so much cancer is because we are exposed to so many carcinogens; we need to turn that around both by producing and using fewer carcinogenic materials and not exposing workers and others to them.” Dr Samuel Epstein, emeritus professor of environmental and occupational medicine at the University of Illinois at Chicago, puts the occupational figure in the Clapp range, saying “based on minimal estimates” occupational carcinogenic exposures are responsible for 10 per cent of overall cancer mortality adding that for certain occupational exposures, mortality rates are much higher (7). He said “lifestyle academics” including Sir Richard Doll “have consciously or unconsciously become the well-touted and enthusiastic mouthpiece for industry interests, urging regulatory inaction and public complacency”, adding the “puristic pretensions of ‘the lifestylers’ for critical objectivity are only exceeded by their apparent indifference to or rejection of a steadily accumulating body of information on the permeation of the environment and workplace with industrial carcinogens and the impact of such involuntary exposures on human health.” According to Epstein, any adherence to the Doll/Peto figures is folly because their paper “excluded from analysis people over the age of 65 and blacks, just those groups with the highest and increasing cancer mortality rates. Not content with such manipulation, they claimed that occupation was only responsible for 4 per cent of all cancers, without apparent consideration of a wide range of recent studies dealing with the carcinogenic effects of such exposures… The wild 4 per cent guess was matched by ‘guesstimates’ that diet was determinant in some 35 per cent of all cancers.”
Old cancers, new cancers It can take a generation of exposures and a generation of deaths for traditional studies to spot an occupational cancer risk, unless the cancer is very rare in the general population. With the exception of the asbestos cancer mesothelioma, however, the most common occupational cancers are also common in the wider community. New industries are emerging all the time, providing potential new processes and new exposures. Little is known about the possible long-term health effects the of vast number of nano-products in development or already in production, for example, but the lesson of history is that today’s wonder product can be tomorrow’s toxic nightmare (9). Without a precautionary approach to the substances we use and the environments we create at work, we risk condemning thousands of workers to preventable deaths. Still, occupational cancer remains a low priority, with a misconception that better understanding and better regulation have relegated occupational cancer to a lingering but fast decline dangerous legacy of past practices and exposures. In fact, regulation has not been a cancer cure. Unlike the case of infectious diseases, where a response is frequently swift and draconian, there are typically long delays between the identification of a carcinogenic agent and adoption of adequate measures of prevention. Even then, measures are usually late and incomplete, and will leave a generation to await their fate as a result of prior exposures. Instead, the assumption that it is “the dose the makes the poison” has been behind a piecemeal and slow, incremental reduction in workplace exposure limits, for workplaces where carcinogens are handled, quite literally, in industrial quantities. For many substances this presumed dose-response relationship is dangerous flawed. The asbestos related cancer mesothelioma is a case in point, occurring now in people who had only incidental exposure to asbestos. Only a handful of workplace substances have ever been banned on grounds of carcinogenicity. Most countries still allow the use of asbestos products, despite it being the most prolific ever industrial killer which may claim 10 million lives before it is banned worldwide (8). An early, precautionary move to safer alternatives would have saved millions. Commercial interests ensured that did not happen. While official agencies worldwide have stuck with Doll/Peto’s 1981 estimates of risk, a generation has gone by and new evidence has come to light, including evidence for cancers dismissed entirely by the report or only included in very limited circumstances. A 2004 paper reported the risk of ovarian cancer increases with increased exposure to diesel exhaust at work. It found individuals with the highest cumulative exposure to diesel exhaust had more than 3.5 times the risk of ovarian cancer (10). A 2005 paper concluded exposure to wood dust increased the chances of developing not only nasal cancer but also lung cancer, finding the risk of lung cancer was increased by 57 per cent with wood dust exposure in absence of smoking, by 71 per cent for smoking in the absence of wood dust exposure, and by 187 per cent for individuals who were exposed to both smoking and wood dust (11). A September 2005 paper concluded exposure to polycyclic aromatic hydrocarbons (PAHs) dramatically increased the risk of laryngeal cancer, up by 5.2 times (12). A 2004 paper linked workplace exposure to the pesticide chlropyrifos to a doubling of the lung cancer risk (13). And a slew of papers have linked occupational factors to the development of gliomas, including exposure to arsenic, mercury and pulp products (14), work in pulp mills (15) and other occupations (16). Firefighters have a clearly increased risk of cancer caused by exposures at work, studies have shown. A November 2006 analysis of 32 US and European studies covering 110,000 firefighters found rates of testicular cancer were 100 per cent higher and prostate cancer 28 per cent higher than expected. There was also a 50 per cent increasing in non-Hodgkin’s lymphoma and multiple myeloma (17). On 31 October 2005, the Canadian province of British Columbia (BC) followed other provinces and recognised leukaemia, brain cancer and five other kinds of cancer as occupational hazards for long-time firefighters. The new law recognises primary site brain cancer, primary site bladder cancer, primary site kidney cancer, primary non-Hodgkin’s lymphoma, primary site ureter cancer, primary site colorectal cancer and primary leukaemia as occupational diseases associated with long-time work as a firefighter. This change to the BC Workers Compensation Act creates a “rebuttable presumption” which means the onus will be on compensation authorities or the employer to bring forward proof to establish why a worker should not be eligible for compensation rather than placing the burden of proof on a sick firefighter. Similar presumptions have been enacted for firefighters in the provinces of Alberta, Manitoba, Saskatchewan and Nova Scotia. Across much of Canada and in parts of this US this risk is legally recognised and officially compensated (18), although firefighters elsewhere are rarely compensated or warned of potential risks. But for jobs with less obvious, visible exposures, the chances of a warning or any hope of compensation are usually far more remote. Yet even with “clean” technology and improved, modern, workplace safety practices, the risks can be real. A 2006 US study found staff employed at IBM computer factories, using the firms own ‘Corporate Mortality File’, had high rates of a range of cancers, linked to exposures to chemicals and electromagnetic fields (19). Studies have found similar problems in computer factories in other countries (20).
The result of governments and statutory agencies failing to recognise the real extent of the occupational cancer problem, instead reproducing as “fact” now discredit estimates based on bad research on US workplaces over a quarter of a century ago, has been a wholly preventable public health disaster. Many occupational carcinogens are still encountered regularly in the workplace and today’s working generation is still being exposed to substances and environments that will cause tomorrow’s cancers. And the risk of exposure may, in fact, be increasing. Figures from the French national statistic office DARES published in 2005 revealed more than 1 in 8 workers was exposed to workplace substances that can cause cancer. The analysis of the 2003 SUMER survey indicated that 13.5 per cent of the total French workforce was exposed to one or more of a list of 28 workplace carcinogens (21). The figure was higher than estimates a decade earlier. Blue collar workers were eight times as likely to be at risk, with 25 per cent exposed. Eight products, all common in UK workplaces, contributed more than two-thirds of all exposures – mineral oils, three organic solvents, asbestos, wood dust, diesel exhaust fumes and crystalline silica. The World Health Organisation (WHO) ‘Global burden of disease’ study in 2002 (22) concluded 20-30 per cent of males and 5-20 per cent of females in the working-age population could have been exposed to an occupational lung cancer risk during their working lives, for example, asbestos, arsenic, beryllium, cadmium, chromium, diesel exhaust, nickel and silica. The European Union’s CAREX database of occupational exposures to carcinogens estimated that in the early 1990s 22-24 million workers in the then 15 European Union member states were exposed to possible carcinogens. The most common exposures were solar radiation, environmental tobacco smoke, crystalline silica, radon and wood dust (23). Overall, 32 million workers, 23 per cent of the working population, had workplace exposures associated by the CAREX database with an occupational cancer risk. The most common exposures were solar radiation, environmental tobacco smoke, crystalline silica, radon and wood dust. Occupational cancer is a global problem and could grow in significance. ‘Global estimates of fatal work-related diseases’, a January 2007 paper in the American Journal of Public Health co-authored by the then-head of ILO’s Safework programme, concluded: “The proportion of malignant neoplasms [cancers] and circulatory system diseases is significant in almost all regions, and it might still grow in the future because the proportion of communicable diseases is expected to diminish.” According to the paper, occupational cancer is in both the established market economies far and away the most common cause of occupational disease fatalities, causing over half of the deaths. It was the top cause of work-related death in China, too. That over 1 in 5 workers face a workplace cancer risk shouldn’t be a surprise. About 95 per cent of causes of lung cancer were identified in workplace studies, and if you discount drugs over threequarters of all causes of cancer were identified in studies of workers (24).
Industry’s influence Even if we evaluate all the available evidence, we may not be evaluating the evidence we need, or evidence that honestly reflects the real occupational risks. According to Stirling University’s Dr Jim Brophy: “The reaction of manufacturers that produce or employ products that might be deemed to be carcinogenic has at times been to suppress the damning research rather than to take steps to prevent harm to the exposed populations.” Dr James Huff, who headed IARC’s chemical evaluation programme until 1980, said in 2003 that the agency had lost its position as “the most authoritative and scientific source” on cancer risks “due to the increasing influence of those aligned with the industry point of view regarding chemicals and their inert hazards to public and occupational health.” He found representatives with industry sympathies or affiliations routinely outnumbered those aligned with public health at IARC evaluation meetings (25). In the decade from 1993, ratings for eight chemicals were upgraded, but 12 were downgraded. In the preceding decade, before industry asserted its influence on the decision making process, no IARC assessments were downgraded. In fact it can take a concerted campaign to get action to prevent cancer risks, even when the evidence of harm is overwhelming. A lowering of the maximum permissible workplace exposure levels for benzene was strongly opposed by industry, which is still resisting recognition of the risks of low concentrations (26). According to Dr Lorenzo Tomatis, who headed the IARC programme until 1993, industry is now dictating terms. “The prevailing assumption, also used as an improper justification, was that the production of certain goods is necessary and vital, even when it was only aimed at increasing consumption of inessential goods, and that the risks involved in their production are an unavoidable price that society must pay.” He said this “disregarded the evidence that the highest price is paid by a particular sector of the population, in which morbidity and mortality are considerably higher than those in the rest of the population.” An unjust public health disaster This unequal risk of occupational cancer means a minority of the population are facing an enormously elevated, serious and preventable risk. That risk is not being taken seriously and those cancer cases are not, on the whole, being prevented. Work-related cancer is far more common in blue-collar workers – there is an undeniable correlation between employment in lower status jobs and an increased risk (24). Studies have found, for example, that 40 per cent of the lung and bladder cancer cases in certain industrial groups can be caused by occupational exposures (27). French statistics office figures published in 2005 found 1 in 8 workers were exposed to carcinogens at work, but that the figure was 25 per cent for manual workers and just 3 per cent for managers (29). And the exposures causing these cancers are not the result of informed, lifestyle choices. They are the consequence of being required to spend the working day in a place that contains carcinogens and where decisions about how they are used and controlled are almost entirely outside the influence of the person facing the risk. The World Health Organisation’s occupational health and safety newsletter in 2006 said “affects certain groups of the society much more than others. Furthermore, occupational risks for cancer are taken involuntarily, as opposed to some major lifestyle risks.” (2). The asbestos cancer mesothelioma is one of the most stark examples. A 2004 British Medical Journal editorial on the UK asbestos cancer epidemic noted: “For a man first exposed as a teenager, who remained in a high risk occupation, such as insulation, throughout his working life, the lifetime risk of mesothelioma can be as high as one in five. There are now over 1,800 deaths per year in Britain (about one in 200 of all deaths in men and one in 1,500 in women), and the number is still increasing” (28). According to the 2005 UMASS Lowell report (6): “Unequal workplace exposures among different populations provide further indications of the ability of occupational exposures to cause harm.” It adds that studies in the US steel industry found the highest rates of lung cancer – 10 times expected – were in non-white workers, employed in the highest risk jobs. This racial inequality in occupational cancer risks has been reported in a number of studies (29). Long-term benzene workers are 30 times more likely to die of leukaemia, the UMASS Lowell report says, and adds: “More than half of asbestos workers have died of cancer and the relative risk of lung cancer among asbestos workers who smoke is 55,” or 55 times the general level in the population. According to the CAREX report for Great Britain (30), all the workplace exposures to carcinogens were restricted to about one-fifth of the working population. If the occupational cancer risk was equal across the population, based on HSE’s figure of 6,000 deaths a year, this would equate to 1 per cent of all deaths being caused by occupational cancers in any given year. However, the responsible exposures are limited to a much smaller group who bear most of the risk, suggesting that 5 per cent or more of deaths in this group could be caused by occupational cancers. The 2006 WHO report (2) made a similar point. “Occupational cancers concentrate among specific groups of the working population. For those people the risk of developing a particular form of cancer may be much higher than for the general population. For example, an estimate of a 3 per cent of total cancer deaths due to occupation in the general population may increase to 12 per cent in the very broad category of male blue collar workers and up to 80 per cent among populations exposed to carcinogens.” According to Stirling University’s Dr Jim Brophy: “Even the lowest estimates of occupational cancer risk for the overall population translate to a 25 per cent risk in the exposed population. I think work-related cancer is being diluted as workers at high risk are thrown in with the general population. A revised public health strategy would emphasise government regulations and accountability to curtail worker and community exposures to carcinogens rather than relying on individual behaviour modification or allocating the bulk of research cash to discovering a cure for cancer.” It is not just about prevention of cases of occupational cancer, it is also about efforts to make sure those cancers do not kill. For now, occupational cancer remains a virtually invisible killer. Those who have already faced the exposures that will result in them developing cancer are not being told of that risk and are not getting the surveillance that might allow an early and possibly lifesaving intervention.
Brophy is among a growing body of occupational health professionals who think the Doll/Peto carve up of cancer by cause did a disservice to prevention efforts, not just by getting it wrong, but by failing to fully reflect the complexity of cancer causation. “The reason we don’t see any of the occupational cancers other than mesothelioma is because at any time there are multiple causes, and where the default designation is ‘lifestyle’.” His colleague at Stirling University, Professor Andrew Watterson, agrees: “Good public health practice should now automatically recognise the multi-causality of many cancers and the significant part that work circumstances and related wider environmental factors will play. “Instead we continue to have a narrow, skewed and flawed focus on lifestyle factors that ignore other exposures to carcinogens. This may reflect government policy which bends to the wishes of employers, pushes deregulation and doesn’t have an effective policy on or properly resourced structure to address occupational and occupationally-related cancers.” The 2005 UMass Lowell report (6) notes: “The least toxic alternative should always be used. Partial but reliable evidence of harm should compel us to act on the side of caution to prevent needless sickness and death. The right of people to know what they are exposed to must be protected.” If all carcinogen use in the workplace stopped today, there would still be a working generation and hundreds of thousands of retired workers that have already faced some level of risk. For this reason, public health advocates are also arguing for more effective recording of exposures and better recognition of the link between work and health. “We should be filing compensation cases to get recognition of the links between jobs and cancer and unions should be documenting cases of illness among their members and looking for trends,” says Dr Jim Brophy. “The health service should improve its act too, and should be documenting occupational histories – if they can document a person’s smoking and lifestyle habits, why not the workplace risk factors too?”
The effective identification of workplace cancer risks has slowed. There’s good reason to believe this could be the result of a well-coordinated industry campaign to influence decisions of bodies including the International Agency for Research on Cancer (25) and the World Health Organisation, rather than any actual improvements at work. And as public funding for independent occupational health research is eroded, industry-funded research is swamping the literature, with occupational and environmental risks going underestimated or undetected as a result. A report in the October-December 2005 issue of the International Journal of Occupational and Environmental Health (IJOEH) (31), examining “business bias” in workplace studies, concludes “in spite of claiming primary prevention as their aim, studies of potential occupational and environmental health hazards that are funded either directly or indirectly by industry are likely to have negative results.” The authors say “studies of workers in oil refineries conducted with total economic independence have identified possible environmental and health risks associated with exposures to more than 50 substances classified as toxic, mutagenic, and carcinogenic, such as asbestos, arsenic, benzene, chromium, nickel, polycyclic hydrocarbons, and silica. The IARC has therefore evaluated exposures in oil refineries as probably carcinogenic to humans. By contrast, other studies undertaken with the same areas of industrial production, supported by industry and of doubtful independence, do not report the existence of any risks.” The authors add: “A review of studies of effects of exposures to selected chemicals (alachlor, atrazine, formaldehyde, and perchloroethylene) shows that 60 per cent of such studies conducted by non-industry researchers found these chemicals hazardous, while only 14 per cent of industry-sponsored studies did so…. Such studies have contributed to a harmful delay in the adoption of preventive measures and have downplayed the significance of primary prevention, especially in developing countries.” The authors of studies critical of industry can find themselves facing a barrage of attacks, both from lawyers and the industry’s own PR machine. A second paper in the October-December 2005 issue of IJOEH (32) notes corporations “work with attorneys and public relations professionals, using scientists, science advisory boards, front groups, industry organisations, think tanks, and the media to influence scientific and popular opinion of the risks of their products of processes. The strategy, which depends on corrupt science, profits corporations at the expense of public health.” The paper concludes: “The strategy developed by corporations working in concert with law and PR firms has been successful in limiting both liability and regulation.” It says concerned health professionals and others have to wage their own PR campaign “to protect rather an undermine public health” and “must form more effective linkages with unions and authentic grassroots community organisations.”
ILO conventions The International Labour Organisation (ILO) convention on occupational cancer makes clear, commonsense recommendations which could and should be followed everywhere. There’s good reason for occupational cancer to be an ILO priority – its says it is the top cause of work-related deaths worldwide, killing one person every 52 seconds. The ILO cancer convention, C139, requires ratifying countries to:
By ILO’s estimate, one in every six workplace cancer deaths is caused by asbestos exposure. The ILO asbestos convention, C162, calls for action to minimise risks posed by asbestos. A resolution agreed at ILO’s 2006 conference clarified the purpose of the convention. It said “the elimination of the future use of asbestos and the identification and proper management of asbestos currently in place are the most effective means to protect workers from asbestos exposure and to prevent future asbestos-related deaths.” The 2006 resolution added that the convention “should not be used to provide a justification for, or endorsement of, the continued use of asbestos.” It instead called for efforts “to promote the elimination of future uses of all forms of asbestos and asbestos containing materials.” ILO’s chemicals convention, C170, calls on employers to assess the exposure of workers to hazardous chemicals; monitor and record the exposures where necessary; maintain adequate records and ensure they “are accessible to the workers and their representatives.” ILO website
What’s wrong with Doll Peto? Two major US reports published shortly before the Doll/Peto report – one from US government organisations (33) and another backed by employers’ organisations – put the occupational cancer contribution at at least 20 per cent of all cancers, with the industry-backed report conceding occupational cancer constituted “a public health catastrophe” (34). A major review of environmental and occupational causes of cancer published in September 2005 (6) concluded: “It is difficult to estimate the impact of Doll and Peto’s views, but their 1981 article had been cited in over 441 other scientific articles by the end of 2004. More importantly, it has been cited repeatedly by commentators who argue that ‘cleaning up the environment’ is not going to make much difference in cancer rates.” While industry groups and HSE embraced the Doll/Peto estimates, others were more critical. Hazards magazine warned in 1996 that the estimate “was always suspect and is now totally discredited”. A 1995 paper in the Mt Sinai Journal of Medicine said the occupational cancer figure was too low and added it failed to take account of the limitations of the data on which it was based (35). Occupational cancers by definition only occur in those of working age and above and, because of latency periods before the development of disease, many are likely to emerge in old age. We have an aging population – as other causes of death decline more are likely to survive long enough to develop their occupational cancers. Doll/Peto not only top sliced the numbers, it only considered cancer risks posed by a list of 16 substances or industries. The International Agency for Research on Cancer (IARC), however, classifies 89 substances as definite human carcinogens, 64 as probable human carcinogens and 264 as possible human carcinogens. A 2004 paper in the journal Environmental Health Perspectives reported that this included 28 definite, 27 probable and 113 possible human occupational carcinogens (36). Occupational cancer risks to women are almost entirely ignored in the Doll/Peto analysis, which concentrated on jobs which in the preceding decades had been largely the preserve of men (37). And Doll/Peto excluded African-Americans from the analysis, a group over-represented in high risk jobs and with higher and increasing cancer rates. The impact on occupational cancer incidence of the synthetic chemicals produced in unprecedented volumes in recent decades would not have been estimated in Doll/Peto’s analysis – this only considered a small number of well established cancer risks - but could have been predicted on the basis of limited human evidence and more extensive toxicological and animal studies. According to Dr Lorenzo Tomatis, who until 1993 headed the International Agency for Research on Cancer (IARC) programme evaluating chemicals, there is a marked double standard in operation when it comes to proof of risk. “A necessary requirement for declaring an environmental chemical carcinogenic to humans is that conclusive epidemiological studies support a causal relationship, and particularly robust evidence for an association between occupational exposure and human cancer is required because a causal association is accepted, while the evidence for a contribution of dietary factors to the cancer burden is usually circumstantial and, in come cases, rather weak,” he said. He told a Collegium Ramazzini conference in September 2005: “Punctilious precision is used in calculating occupational and environmental risks, while a wide latitude is allowed for risks related to diet, ranging between 10 per cent and 70 per cent” (31). He added that Doll/Peto acknowledged that occupational cancinogens “tend to be those which increase the risk of some particular type(s) of cancer very substantially,” and others might not have been detected simply because they have not been investigated or because the exposure concerned a small number of individuals, and no suspicion was raised. The end result is that cancers are attributed a “lifestyle” cause with relative ease, while production and use of occupational carcinogens continues unremarked and unabated. “The emphasis given to lifestyle factors, to the detriment of information on the role of chemical pollutants, favoured the uninterrupted production of agents with negative effects on health that remain hidden or secret or are deliberately underestimated,” said Tomatis. “Furthermore, attributing most cancer cases to lifestyle, which is related to free personal choice, unduly amplifies the individual’s responsibility, diverts attention from the lack of commitment of health authorities and obscures the aetiological role of other risk factors.” Sir Richard Doll, lead author of the Doll/Peto report, played down the occupational and environmental contribution to cancer throughout the latter decades of his career, including actively opposing further control measures. In a 1996 paper in the journal Carcinogenesis (38) he wrote: “Two categories of cause remain for which I see little possibility of material benefit from their further control, namely the hazards of occupation and pollution.” For several decades, however, Doll had “secret ties to industry”, according to a report published online in the American Journal of Industrial Medicine in November 2006 (39). The professor, who died in 2005, was receiving substantial undeclared payments from a number of chemical multinationals when he co-authored the Doll/Peto report. The AJIM study, ‘Secret ties to industry and conflicting interests in cancer research’, concludes: “The most striking case is that of Sir Richard Doll, co-author (with Richard Peto) of one of the most influential papers in cancer epidemiology, one that concluded that only a small percentage of cancer was caused by environmental exposures.” The AJIM analysis said Doll had a long term financial relationship with Monsanto between 1970 and 1990, with evidence including a letter from a Monsanto epidemiologist renewing Doll's contract for US$1,500 per day. This formed part of a dossier revealing Doll's relationships with industry. In a paper dismissing vinyl chloride brain cancer risks, for example, Doll did not disclose the £15,000 plus expenses he had received from the Chemical Manufacturers’ Association and the vinyl chloride manufacturers ICI and Dow. The payments were confirmed in US court papers and in documents from Doll’s own Wellcome Institute archive in London (40).
See Work hazards cancer pevention kit: Part 4. Union resources, Organisations, Cancer causes and Further information
1. Doll R and Peto R. The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. Journal of the National Cancer Institute, volume 66, number 6, pages 1191-1308, 1981. 2. Prevention of occupational cancer, World Health Organisation (WHO) GOHNET newsletter, number 11, 2006. [pdf] 3. Burying the evidence, Hazards magazine, number 92, October-December 2005. 4. Päivi Hämäläinen, Jukka Takala, Kaija Leena Saarela. Global estimates of fatal work-related diseases, American Journal of Industrial Medicine (AJIM), volume 50, pages 28-41, 2007. [abstract]. 5. Lin Fritschi and Tim Driscoll. Cancer due to occupation in Australia, Australian and New Zealand Journal of Public Health, volume 30, number 3, pages 213-219, 2006. 6. Richard Clapp, Genevieve Howe, Molly Jacobs Lefevre. Environmental and cccupational causes of cancer: A review of recent Scientific literature. Lowell Center for Sustainable Production, University of Massachusetts Lowell, September 2005. Executive summary • Full report [pdf] 7. Cancer-gate. How to win the losing cancer war. Epstein S. ISBN 0-89503-354-2, Baywood Publishing Company Inc, USA, 2005. 8. Joseph LaDou. The asbestos cancer epidemic. Environmental Health Perspectives, volume 112, number 3, pages 285-290, 2004. 9. Hazards magazine nanotechnology webpages 10. Johannes Guo, Timo Kauppinen and others. Risk of esophageal, ovarian, testicular, kidney and bladder cancers and leukemia among Finnish workers exposed to diesel or gasoline engine exhaust, International Journal of Cancer, volume 111, issue 2, pages 286-292, 2004 [abstract]. 11. Carlos H. Barcenas, George L. Delclos, Randa El-Zein, Guillermo Tortolero-Luna, Lawrence W. Whitehead, Margaret R. Spitz. Wood dust exposure and the association with lung cancer risk. Am J Ind Med. 2005: 47: 349-57 [abstract] 12. Becher H and others. Occupation, exposure to polycyclic aromatic hydrocarbons and laryngeal cancer risk, International Journal of Cancer, volume 116, issue 3, pages 451-457, September 2005 [abstract] 13. Lee WJ, Blair A and others. Cancer incidence among pesticide applicators exposed to chlorpyrifos in the Agricultural Health Study, Journal of the National Cancer Institute, volume 96, pages 1781-1789, 2004 [abstract]. 14. Navas-Acien A, Pollan M, Gustavsson P, Plato N. Occupation, exposure to chemicals and risk of gliomas and meningiomas in Sweden. American Journal of Industrial Medicine, volume 42, number 3, pages 214-227, 2002. 15. Andersson E, Nilsson R, Toren K. Gliomas among men employed in the Swedish pulp and paper industry. Scandinavian Journal of Work Environment and Health, volume 28, number 5, pages 333-40, 2002. 16. Krishnan G, Felini M, Carozza SE, Miike R, Chew T, Wrensch M. Occupation and adult gliomas in the San Francisco Bay Area. 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Also: Lorenzo Tomatis, Primary prevention of cancer: Science, socio-cultural trends and economic pressures, Scandinavian Journal of Work Environment and Health, volume 31, number 3, pages 227-232, 2005 [pdf]. 27. Vineis P and Simonato L. Proportion of lung and bladder cancers in males resulting from occupation: a systematic approach. Archives of Environmental Health, volume 46, pages 6-15, 1991. 28. Treasure T, Waller D, Swift S and Peto J. Editorial. Radical surgery for mesothelioma. The epidemic is still to peak and we need more research to manage it. British Medical Journal, volume 328, pages 237-238, 2004. 29. Murray LR. Sick and tired of being sick and tired: Scientific evidence, methods, and research implications for racial and ethnic disparities in occupational health. American Journal of Public Health, volume 93, pages 221-226, 2003. 30. Carcinogenic exposure information for Great Britain, Carex, 1998. 31. Gennaro V and Tomatis L. 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Bethesda, MD: National Cancer Institute, National Institute of Environmental Health Sciences, and National Institute for Occupational Safety and Health, 1978. 34. Proctor R. Cancer Wars. New York: Basic Books, 1995. 35. Landrigan PJ, Baker DB. Clinical recognition of occupational and environmental disease. Mt Sinai Journal of Medicine, volume 62, number 5, pages 406-411, 1995. Also: Landrigan PJ, Marsowitz SB, Nicholson WJ, Baker DB. Cancer prevention in the workplace. In: Greenwald P, Kramer BS, Weed DL, eds. Cancer prevention and control. Marcel Dekker Inc, pages 393-410, 1995. 36. Siemiatycki J, Richardson L, Straif K and others. Listing occupational carcinogens. Environmental Health Perspectives, volume 112, number 15, pages 1447-1459, 2004. 37. Zahm SH and Blair A. Occupational cancer among women: Where have we been and where are we going? American Journal of Industrial Medicine, volume 44, pages 565-575, 2003. 38. Richard Doll. Commentary: Nature and nurture: possibilities for cancer control, Carcinogenesis, volume 17, number 2, pages 177-184, 1996 [abstract]. 39. Lennart Hardell and others. Secret ties to industry and conflicting interests in cancer research, American Journal of Industrial Medicine, volume 50, issue 3, pages 227 – 233, 2007 [abstract]. 40. HSE’s low work cancer estimate discredited. Hazards magazine, number 97, January-March 2007. www.hazards.org/cancer
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HAZARDS MAGAZINE • WORKERS' HEALTH INTERNATIONAL NEWS |
The
lead author, Professor Sir Richard Doll, was at the time receiving
substantial undeclared payments from industry, including major chemical
producers and a top US chemicals trade body. And the findings just
didn’t add up. Large swathes of the at-risk workforce were excluded
from the analysis. Retired workers were excluded too – despite
being the workers most likely to develop work-related cancers. Far
more people are exposed to far more substances than they were willing
to admit.
The
widespread, unquestioning, acceptance by governments of the Doll/Peto
low figure for the occupational contribution to total cancer causation
was good news for some, but a death sentence for others. “The
companies were ecstatic when Doll/Peto came out, because it posed
the whole thing politically as a lifestyle issue,” Stirling
University occupational cancer authority Dr Jim Brophy(right) said.
“That had consequences for prevention, in that it effectively
ended any chance of a structured and well resourced strategy to combat
occupational cancer.”
According
to Dr Richard Clapp (right) of the University of Boston Medical School,
USA, co-author of the September 2005 review 
Professor
Andy Watterson (right) of Stirling University’s occupational
and environmental health research group, believes Clapp’s estimate
of real occupational cancer incidence “is about right”.
He added: “Lung cancers caused by asbestos exposure are not
picked up and other occupational cancers simply do not show up on
the official radar; the contribution of work to breast cancers is
widely neglected and there are a number of carcinogens that attack
humans – brain, nervous system, soft tissue sarcomas, cancer
of the larynx, kidneys, stomach, bone – which are not adequately
regulated.”
