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Hazards issue 117, January-March 2012
Why won’t HSE treat cancer with deadly seriousness?
Simon Pickvance has proof the UK is ignoring an occupational cancer epidemic. And the workplace health expert has first-hand experience of what this official inaction can mean. In 2010, he was diagnosed with the most feared work cancer around.

This man knows all about cancer
Hazards issue 117, January-March 2012



Simon Pickvance knows numbers are important. Numbers – statistics, victims – establish priorities. Which is why he’s baffled by the Health and Safety Executive’s approach to occupational cancer. He says for years HSE has been in denial about a workplace problem that dwarves the annual death count from murders and road traffic accidents combined.

“It just doesn’t seem to want to believe in ‘causes’,” says Pickvance, who is based at Sheffield University where he is researching occupational bladder cancer risks. He says when he is on the cancer ward receiving treatment for mesothelioma, the incurable asbestos cancer resulting from his time working on construction sites, “I see people on the ward and for them it is a bit of a relief to know there is a cause. You want to know ‘why me?’”

How to make bladder cancer disappear

Simon Pickvance believes bladder cancer exposes a flaw in HSE’s figures that systematically disappears real cancers from the statistics, by dismissing or ignoring risks by job, by industry or by substance. [more]

HSE has instead adopted a ‘not me’ strategy. From formaldehyde to trichloroethylene to wood preservatives to toxic metals like lead, HSE responded to alerts about cancer risks with a defence of the status quo. In some cases, like formaldehyde, its first instinct was to back the industry ‘no problem’ line.

Despite saying it prioritises evidence-backed measures to reduce the workplace cancer risk, HSE routinely refuses to do exactly that. In 2011, it stood by a dust exposure limit it acknowledges makes workers sick and inevitably contributes to the biggest single group of occupational cancers – and the biggest cancer killer overall – cancer of the lung. It continues to resist pressure to introduce a safer dust standard which it has been estimated could save many hundreds of lives a year (Hazards 116).

In other examples, like the recent concerns about shiftwork and breast cancer, HSE - an organisation Pickvance points out “has dismantled its medical wing and fired almost every employee with a medical background” - presumes to know better than the UN’s International Agency for Research on Cancer (IARC). Whereas IARC concluded in 2007 shiftwork is a ‘probable’ cause of breast cancer in humans and urged preventive action, HSE first expressed scepticism in a response to Hazards and now says it is waiting for “a more robust assessment of whether the association can be regarded as an established risk.”

And shiftworkers, who might have expected early action to reduce a ‘probable’ breast cancer risk, are still waiting.


We don’t work that way

For nearly three decades, HSE stood by a ‘best available estimate’ of 6,000 UK occupational cancer deaths a year, based on an industry-friendly 1981 US paper (Hazards 99). In 2008, this figure was revised up to around 8,000 deaths and over 13,500 new cases a year, when HSE finally got around to attempting a genuine UK based analysis (Hazards 111).

Clock ticking on cancers

Cancers caused by the jobs we do kill one person in the UK every 30 minutes around the clock, even official estimates suggest. [more]

But, Pickvance says, HSE didn’t invite too many surprises when it commissioned epidemiologist Lesley Rushton of Imperial College London to crunch the numbers. At the centre of HSE’s problems is the choice of epidemiology, a tool which had some worth when millions worked in mines, mills and manufacturing and where the workforce and the conditions remained virtually unchanged over decades. But it is singularly ill-fitted to the modern, fast evolving, smaller, more varied and more transient workplace and worker.

IARC looks for relevant toxicology and industrial hygiene when evaluating an occupation,” Pickvance explains. “It reads case reports as well as statistical analyses. But epidemiologists think in terms of large groups of workers with similar exposures – clerical or sales workers aren’t like that. These are diverse groups. Some of the workers – petrol station attendants before the era of self-service, for example - may be at high risk, whereas the rest are at no greater risk than the general population.”

Rushton’s tally, he says, was hampered by an “extremely narrow” brief and was informed by assumptions that time after time took bodies out of the body count. “You end up with something that is not fit for either purpose – to set the priority of cancer prevention among HSE priorities, or to prioritise substances and occupations for cancer prevention.”

Pickvance says Rushton’s figure produced for HSE is conservative for an embarrassment of reasons, including:

• The study only considered group 1 and 2a carcinogens, discounting possibles in the lower 2b category where there is evidence of risk, but not enough suitable studies to establish the link with certainty. Even some group 1 risks, like passive smoking, are excluded.
• HSE's analysis generally relied on large studies, but researchers have pointed out that many smaller workplaces like car repair shops and small scale building work can result in routine and considerable exposures.
• The study uses an HSE estimate of the numbers of lung cancers caused by asbestos exposure, which knocks at least 1,000 cancer deaths a year - and possibly more than 3,000 - off more usually cited figures.
• The occupational risks from certain cancers, for example leukaemia and non-Hodgkin's lymphoma, are virtually dismissed, despite evidence of a significant risk in other countries.
• Rates of certain cancers, for example, work-related cases of prostate cancer, are seriously downplayed.
• Other nations and statutory and health agencies recognise risks from more substances, more occupations and for cancers at shorter latency periods.

Real life bodies don’t play by the epidemiologists’ rules. Epidemiologists want a named job or exposure to cause a particular cancer – so wood dust causes nasal cancer, PVC causes liver cancer, asbestos causes mesothelioma.

“The target organ approach is a very damaging argument – most things have a broad spectrum, it’s just that epidemiology isn’t clever enough to see it,” says Pickvance. Even quite large increases in the numbers of the more common cancers are entirely and irretrievably invisible to traditional epidemiological number-crunching.

WRONG FOOTED  When traces of radioactive contamination were detected in January 2012 on shoes worn by workers at the Dounreay nuclear site (above), Dounreay Site Restoration Limited was quick to say there was “no harm to staff or the environment.” But there was radiation. HSE lacks the tools to determine cancer risks from the small and varied exposures of this kind many of us now tot up over a working lifetime.

Still, Pickvance believes Rushton’s figures, however limited and which she herself describes as ‘conservative’, still suggest a worker dies every 30 minutes every day around the clock and should have been enough to prompt an all-hands-to-the-pump urgent HSE action plan.

He thinks the evidence demands a more preventive approach that starts with what we know; substances and jobs cause cancer, and we have the means at our disposal - a bit of application and brain power - to substantially reduce that risk. “There needs to be a change of attitude, a lower tolerance. We need zero tolerance of chemical exposures. We’ve got to get precautionary.”

But that’s not what is happening, says Pickvance. Instead, HSE went for plan (b), dubbed ‘paralysis by analysis’. Rushton was commissioned to undertake more research, using the same flawed methods and generating results years down the line that would inform a non-strategy by a watchdog that no longer has the resources to police safety, having long given up any pretence of preventing occupational ill-health.

“The HSE approach means we will be looking in the wrong places for major cancer hazards at work. There’s less of an HSE campaign now than five years ago, just a few gestures. There’s a pervasive lack of willingness to believe things are dangerous – it’s a cultural problem about HSE,” Pickvance says.

Industry stalls action on standards

Many of our workplace exposure standards are based on those developed in the US. Which is a shame, as these are routinely stalled for years by the industries that would be required to implement improvements if a new standard was to emerge. Cancer causing diesel exhaust and silica are two current examples of this deadly delaying tactic. [more]

HSE’s website notes: “HSE’s approach to reducing the incidence of long latency diseases, with a specific focus on cancer is evidence-based, focusing in particular those activities and industries that present the greatest risks and working with stakeholders to identify sustainable solutions.”

HSE is using a low cost, low impact strategy based on a brutally butchered body of evidence that HSE’s own research has shown to be spectacular flop (Hazards 99). “The past experience of HSE’s own estimates has been that numbers exposed are often revised upwards, sometimes by a factor of 10,” comments Pickvance.

In 2007, for example, when HSE has considerably more resources and still had an explicit occupational disease reduction plan, it reviewed exposure patterns for the carcinogen crystalline silica. HSE admitted internally this revealed it had dramatically underestimated the numbers exposed and the extent of those exposures.

For stonemasonry, for example, both HSE and the industry thought no workers were exposed to respirable crystalline silica (RCS) levels above 0.1mg/m3. But the review suggested 3,150 workers could be exposed above this level, and 1,425 were potentially exposed to 0.3mg/m3 or more. In construction, it estimated 30 per cent of workers in “significant risk activities” could be receiving regular exposures in excess of 0.1mg/m3.

A 2009 HSE benchmarking study on respirable silica exposures did not offer much reassurance. In the brick sector, it concluded “previous recent HSE and industry estimates of silica exposures may be lower than actual exposures.” It added: “29 per cent exceeded 0.1mg/m3 8hr as a time-weighted average (TWA.) This includes 5 per cent which indicated RCS exposure above 0.3mg/m3.”

In stonemasonry, nearly 20 per cent exposures were above 0.3mg/m3, with the report warning “results suggest that earlier industry estimates of silica exposures are considerably lower than actual exposures.” In construction, the report noted: “Employers have underestimated the extent of exposures, and in many cases have not made the implementation of exposure control a priority (revealed when assessed by ‘control competence’.)”

Silica is not a tough one. We know it causes cancer, as well as lung and autoimmune diseases. Sorting it is about old-fashioned dust control, which is simple and frequently inexpensive. If HSE can’t crack problems like silica at work – or even have a clue about the extent of the problem – then it is little wonder its attitude to prevention is even more lacklustre when it comes to tougher challenges. To really get to grips with the workplace cancer issue would require HSE to find all the problem jobs and substances, and work out what do about them.

Pickvance says there is a need for “an all out search for carcinogens at work – something trade unions are still better placed to take on than HSE.” This should look at exposures, occupation by occupation, and should identify the high risk groups within those occupations. Unions should look too at case studies and industrial hygiene and toxicology studies which could flesh out the picture.

Pickvance adds that unions should beware epidemiology, a blunt tool ill-fitted to find new risks or old risks in new groups, risks in modern, often transient workplaces and jobs, and those low risks spread across very large occupational groups.

“Basically, the risks in the jobs we do today.”



How to make bladder cancer disappear

Simon Pickvance believes bladder cancers caused by work demonstrate how HSE systematically disappears real cancers from the statistics, by dismissing or ignoring risks by job, by industry or by substance.

The figures compiled by epidemiologist Lesley Rushton for HSE suggest over 500 people develop occupational bladder cancer each year, and around 250 people die of the work-related condition. That in itself is shocking enough – it’s a bigger annual toll that fatal injuries at work. But Pickvance is concerned by serious omissions from the HSE body count.

‘Ticking timebomb’ of bladder cancer

Lawyers are warning of a ‘ticking timebomb’ as workers exposed to carcinogenic chemicals from the 1950s to the 1970s develop potentially fatal cancers. Pauline Chandler from the law firm Pannone says she is noticing a “small but highly significant” rise in bladder cancer cases being referred to her. [more]

Rushton was very picky about what made it onto her list of chemicals associated with bladder cancer. On top of this, she opted to exclude substances that have been linked to bladder cancer but that are more commonly associated with other types of cancer. So, potential causes of bladder cancer including asbestos, cadmium, lead and trichloroethylene were ruled out.

Passive smoking isn’t included, but will for years to come contribute to the occupational cancer count as a result of past exposures. And despite the workplace smoking ban, which came into effect in 2007, many workers including prison officers and home carers are still exposed to high levels of secondhand smoke as their workplace is classified as someone else’s “home”.

Pickvance adds: “Environmental tobacco smoke may be the reason for raised rates of bladder cancer amongst waiters and waitresses – think back to the smokey restaurants of the 60s and 70s.

Prison workers face smoking dangers

While other workers benefit from lower cancer and heart disease risks resulting from the workplace smoking ban, workers in prisons do not, their union has said. In February 2012 the Prison Officers’ Association (POA), which has over 35,000 members, warned that prisoners’ cells are classed as a ‘home’ and so are exempt from the legislation which came into effect in 2007 to protect workers from passive smoking.
      The union has presented evidence to the Ministry of Justice showing prison staff are “exposed to considerable quantities of secondhand smoke during their work time.” A pilot study found in one prison non-smoking prison officers had levels of cotinine – a nicotine metabolite - close to the levels measured in bar workers before the smoking ban.
      The union noted: “Further data collection is urgently required to provide accurate estimates of secondhand smoke exposure for prison officers, taking into account the smoking patterns of prisoners and work patterns of prison officers.” POA said it was calling on the government “to protect staff and prisoners against the effects of secondhand smoke. The POA also reiterate their call for a complete ban on smoking in prisons.”

Pickvance took a different approach. Restricting himself only to those substances where there is ‘strong’ or ‘good’ evidence of a bladder cancer risk, Pickvance compiled a list of 29 workplace substances - more than three times as long as the nine used in HSE’s estimate. Add in those where evidence is ‘limited’, and the list extends to 47 substances
[table 1].

The same winnowing down of the numbers occurred when Rushton considered occupations with a bladder cancer association. A sequence of jobs with serious risks including coke production, town gas production, rubber manufacture and petroleum refining are absent. Some of these jobs no longer exist, but at least some of the workers who did them will still be alive, suffering from cancer or at risk.

Other jobs are omitted where at least some of workers under that job title would potentially have significant exposures to known risks [table 2] – sales workers (diesel in petrol stations); clerical workers (printing inks); health professionals (cytotoxic drugs); electronics and electrical assembly workers (lead, cadmium in soldering, arsenic in electronics); miners (mineral oil, diesel exhaust).

Other occupations omitted have known excesses, but further work is needed to establish a cause [table 3]. This includes waiter/waitresses, paper workers, cooks and firefighters. There are a number of ‘rebuttal presumption’ compensation schemes, particularly in North America, that recognise bladder cancer as an occupational disease of firefighters. Eight US states recognise explicitly occupational bladder cancer in firefighters in their compensation schemes, as do seven Canadian provinces.

The validity of this longer list of occupations and substances preferred by Pickvance is reinforced by a 2008 analysis of 21,000 bladder cancer cases in Sweden published in the American Journal of Industrial Medicine. The joint US-Swedish research team led by Robin Taylor Wilson of Penn State Cancer Institute “shows that Rushton’s paper missed out so many jobs for which good evidence existed of bladder cancer cases. There are also so many carcinogens identified by the study that should have been included in Rushton’s analysis, but weren’t.

“All of the suspect occupations I identified bar those where Sweden lacks the industry concerned, are confirmed.” Pickvance added that because of the scale and “far greater statistical power” of Taylor Wilson’s research, jobs invisible to Rushton and HSE become “foreground occupations – often with no immediately obvious carcinogens in a large number of occupational groups.”

This, he says, demonstrates why HSE needs an on-the-ground presence to police exposures and exposure levels and to determine what at work might cause these unexplained but real excesses. Taylor Wilson suggests work factors could be responsible for the excesses of bladder cancer observed in women in clerical and waitressing jobs, and could be account for about 1 in every 6 bladder cancer cases in women.

Other unpleasant trends in modern day working life, like disappearing lunch and tea breaks and restrictions on toilet breaks, could be amplifying the risks. “Not being able to go for a pee is not just a potential cause of kidney infections, it also increases the time that carcinogens in the bladder come into contact with the bladder wall,” Pickvance says. “The ‘contact’ theory is thought to be a factor in the increased risks of bladder cancer amongst drivers. You have to be exposed to a carcinogen – think exhaust fumes – but not being able to stop for a pee makes things worse.”

A 2010 study of unionised British workplaces by the Labour Research Department (LRD) found inadequate toilet facilities and restrictive toilet break rules were commonplace. The transport sector was particularly badly affected, along with industries such as mining, construction and quarrying – all of which involve exposure to bladder carcinogens like diesel exhaust. Other studies have suggested over half of British workers are too busy to take toilet breaks.

Pickvance says HSE’s faith in its strategy should have been dented by its own reports. An HSE study of workers in the rubber and plastics industry using the bladder cancer causing chemical MbOCA, confirmed when HSE stopped looking, the industry abandoned safe working practices, with workers contaminated all the way from the canteen to the loading bay.

When the industry objected to the study’s methodology and findings, HSE removed the report from its website and scurried away to start the research again. The re-run study’s findings, published but not press released by HSE in December 2010, confirmed there had been no improvement in over a decade in the chemical industry’s control of MbOCA.


Table 1. 
What causes bladder cancer at work?

The list of occupational bladder cancer causes used by HSE was just nine items long. Simon Pickvance’s list of substances where there is ‘strong’ or ‘good’ evidence is more than three times as long [carcinogens and exposure circumstances used in HSE’s analysis in bold]

1,1-dichloroethane [Strong]
2-naphthylamine [Strong]
4,4'-Methylenebis(2-chloroaniline) MOCA (aromatic amine) [Strong]
4-aminobiphenyl [Strong]
Aromatic amines [Strong]
arsenic [Strong]
auramine [Strong]
benzidine [Strong]
Benzidine-derived dyes [Strong]
benzo(a)pyrene [Strong]
chlordimeform/4-COT [Strong]
Coal tars [Strong]
direct black 38 [Strong]
direct blue 6 [Strong]
direct brown 95 [Strong]
nitrobiphenyl [Strong]
o-toluidine [Strong]
PAHs [Strong]
Tobacco Smoke (Active smoking) [Strong]
carbaryl [Good]
Chlorination byproducts [Good]
chlornaphazine [Good]
Chlorophenols [Good]
Creosotes [Good]
Ionizing radiation [Good]
methylenedianiline [Good]
propoxur [Good]
Solvents [Good]
Trihalomethanes [Good]
antimony [Limited]
asbestos [Limited]
bifenthrin [Limited]
cacodylic acid [Limited]
Carbamates [Limited]
Chromium [Limited]
dichloropropene [Limited]
Diesel exhaust [Limited]
Dioxins/TCDD [Limited]
lead [Limited]
Nitrosamines [Limited]
o-phenyl-phenol [Limited]
Organochlorine pesticides [Limited]
p-cresidine [Limited]
Pesticides [Limited]
Pyrethins/Pyrethroids [Limited]
saccharin [Limited]
tetrachloroethylene (PCE) [Limited]

Collaborative For Health and the Environment Toxics Database. Causes of Bladder Cancer
[with strength of evidence], consulted on 13 January 2012.

Table 2. 
Other substances missed by HSE

Case reports of occupational bladder cancer risk, supported by toxicological or health surveillance evidence, exist for a number of other agents.

Substance Evidence
Cyclophosphamide Case report
Anti-neoplastic drugs Case reports. Health surveillance
Phenyl beta-naphthylamine Workplace studies, epidemiology
2-Mercaptobenzothiazole Workplace cohort
Solvent Red 164 as dye penetrant Case report
Solvent Red 19 as dye penetrant or anti-rust agent Case report
Dinitrotoluenes Workplace cohort, toxicology
Diazo printing ink Case report

Table 3.
Jobs missed by HSE

Occupations for which Simon Pickvance believes there is strong though not consistent evidence for a link with bladder cancer in the scientific literature.

Name of occupational group Comment
Sales workers There is evidence for linkage to a small list of more highly exposed sales jobs, eg. in hardware and fuel sales.
Health workers Exposures vary between different health professionals and other occupations, but evidence linking bladder cancer to exposure to anti-neoplastic drugs is strong.
Firefighters Highly diverse chemical exposures mean that occupational cancers are also diverse. Fifteen states and provinces across the US and Canada recognise bladder cancer as an occupational disease of firefighters.
Farmworkers Huge diversity of exposure to pesticides and herbicides in different kinds of agriculture probably explains the inconsistency of results.
Food preparation Possible causes include heterocyclic amines produced during cooking, and by-products of the use of chlorinated sterilising agents.
Ferrous metal production Polycyclic aromatic hydrocarbons (PAHs), mineral oil, etc.
Miners Possible causes include mineral oil from cutting and hydraulic systems, diesel fumes, coal tar, explosives.
Clerical workers A small subsector of clerical workers have had printing ink exposure to mineral oil, pigments and dyes.
Assemblers Mineral oil and solder containing lead and cadmium may account for excess cases in this occupational group.
Electronics workers Solder containing lead and cadmium may be involved.
Gas supply workers PAHs and aromatic amines, as well as brazing solder could account for the excesses reported.
Construction workers Bladder carcinogens in construction include diesel, asphalt fumes, PAHs, and coal tar pitch products.
Paper manufacture Chlorination by-products have been suggested to account for reports.
Tobacco manufacture Not known.
Cooks Heterocyclic amines are generated by cooking operations.
Other occupations with occasional reports of excess bladder cancer incidence or mortality include photographic processing, artists, waiters, welders and cleaners.

Back to main story


Clock ticking on work cancers

Cancers caused by the jobs we do kill one person in the UK every 30 minutes around the clock, even official estimates suggest. Occupational cancer – a workplace guide, TUC’s February 2012 analysis of the official figures prepared for HSE by Imperial College epidemiologist Lesley Rushton, says the prevention of workplace cancer has a much lower profile in the workplace than preventing injuries, “despite the fact that only 220 to 250 workers die each year as a result of an immediate injury as opposed to the 15,000 to 18,000 that die from cancer.”

TUC is calling for greater efforts to prevent cancers, through removing the cause from the workplace, better standards and enforcement and greater union involvement in finding solutions. The guide notes: “Trade unions have been at the forefront of the campaign against the use of carcinogens in the workplace. Many substances that employers once claimed were safe have only been recognised as dangerous because unions highlighted the fact that workers were dying as a result of exposure, or because unions have campaigned for their ban or control.”  

According to TUC: “Following pressure from unions, a large number of employers have managed to substitute cancer-causing chemicals with safer ones. Examples include trichloroethylene as a cleaner for metal, cancer-causing inks in printing, and formaldehyde and insulating foams in furniture.”

In an accompanying guide to the number of occupational cancers, TUC warns that a failure by the authorities to show the same sort of resolve will have tragic consequences. “What we do today will have a major impact, but it will not be seen for perhaps 20 or even 40 years,” the statistics guide notes. “By cutting regulation and enforcement it is not only fatalities from injuries that will go up, it is also future deaths from cancer.”

[back to main story]


Industry stalls action on cancer standards

Many of our workplace exposure standards are based on those developed in the US. Which is a shame, as these are routinely stalled for years by the industries that would be required to implement improvements if a new standard were to emerge. Cancer causing diesel exhaust and silica are two current examples of this deadly delaying tactic.

A February 2012 report from the US Center for Public Integrity revealed publication of a landmark US government study probing whether diesel engine exhaust causes lung cancer in miners — already 20 years in the making — was delayed further this year by industry and congressional insistence on seeing study data and documents before the public does.

Diesel exhaust fume has been recognised by the UN’s International Agency for Research on Cancer (IARC) as a probable cause of cancer in humans, confirmed in a 1998 IARC monograph. The US government’s workplace safety research body National Institute for Occupational Safety and Health (NIOSH), which has also “determined that diesel exhaust is a potential human carcinogen”, has been calling for its control in mines since the 1970s.

The results of the $11.5 million investigation by the National Cancer Institute and NIOSH remained under lock and key throughout February, after a federal judge affirmed the right of an industry group, Mining Awareness Resource Group (MARG), and a House committee to see the background documents in advance.

After considerable public disquiet and media criticism, the study of more than 12,000 miners was finally published in the Journal of the National Cancer Institute on 2 March 2012. It concluded that exposure to diesel engine exhaust significantly increases the risk of lung cancer. For the most heavily exposed miners, the risk of dying from lung cancer was three times higher than it was for those exposed to low doses. For non-smokers, the risk was seven times higher.

Joseph Fraumeni Jr, director of the National Cancer Institute’s Division of Cancer Epidemiology and Genetics, said in an NCI press release “the findings suggest that the risks may extend to other workers exposed to diesel exhaust in the United States and abroad, and to people living in urban areas where diesel exhaust levels are elevated.”

Life and death evidence of a preventable cancer risk extending way beyond miners had been kept secret, stalling preventive efforts and inevitably increasing the workplace and public cancer burden.

A new safer official US workplace exposure limit for deadly silica dust, a recognised cause of lung and other cancers, has also been frustrated by the business lobby for over a decade. But a bid by the Department of Labor's Occupational Safety and Health Administration (OSHA) to finally introduce stricter controls on silica has hit a second brick wall – a review process run by the White House Office of Management and Budget (OMB) that has stalled the ready-to-go standard since 14 February 2011.

Frustrated at the delays, more than 300 scientists, doctors and workplace safety experts countersigned a 25 January 2012 letter to the president, urging him to direct OMB to complete its review. OMB should have completed the review of the proposed rules within 90 days, but has delayed for nearly a year. The letter notes that OMB staff have hosted at least nine private meetings on the rules, most of which involved representatives of companies with a direct financial stake in their outcome.

Any reduction in the standard has been vigorously opposed by this industry lobby. An estimated 1.7 million US workers are exposed to crystalline silica, which kills some 200 workers each year and causes new cases of silicosis in as many as 7,300 workers, mostly in construction.

Silicosis, which also affects miners, foundry and ceramics workers and other trades where silica is used or becomes airborne as a result of work processes, is incurable but preventable. It is also linked to other lung diseases, cancer and autoimmune conditions.

The National Advisory Committee on Occupational Safety and Health, which advises the Labor Department, issued a statement in December 2011 saying it was “deeply distressed” that the proposed new regulations had been under review for so long. “The current standard is many decades old and is insufficient to protect workers from this serious occupational health hazard,” the advisory committee noted. “The silica rule delay is extraordinary and without explanation, and there is no indication as to when the review will be concluded.”

Back to main story


‘Ticking timebomb’ of bladder cancer cases

Lawyers are warning of a ‘ticking timebomb’ as workers exposed to carcinogenic chemicals from the 1950s to the 1970s develop potentially fatal cancers.

Pauline Chandler from the law firm Pannone says she is noticing a “small but highly significant” rise in bladder cancer cases being referred to her. According to the industrial disease legal expert, “my fear is that workers in a number of industries, including; the chemicals sector, paint production, rubber manufacture and pigments and dyestuffs production, will develop cancers and be unaware that they are related to their past employment.”

One recent bladder cancer case concluded by Chandler involved David Pechey. The 62-year-old worked as a chemist in the laboratories at Ciba-Geigy in Paisley, Scotland, from 1975 to 1982, before moving down to the company’s Clayton Aniline site in Manchester. Mr Pechey, who eventually went on to hold senior marketing roles with the firm, received a “substantial” five figure settlement.

The Paisley plant manufactured pigments for colouring paints, inks and plastics, exposing Mr Pechey to cancer-linked chemicals including dichlorobenzidine, dimethoxybenzidine and nitro-biphenyl. He commented: “Workers in the plant had routine urine cytology tests to check for cancer but lab personnel were not given such tests whilst I was there.”

After having a diagnosis of bladder cancer confirmed in 2007, he underwent three years of treatment before being given the all clear by medics. He said his decision to take legal action was “borne out of the desire to highlight the problem of those who, like me, found themselves exposed to carcinogenic chemicals through no fault of their own.”

His lawyer, Pauline Chandler, commented: “Sadly we are seeing an increasing number of bladder cancer cases arising from people’s negligent exposure to cancer causing chemicals.” A clause in the compensation agreement allows Mr Pechey to claim again if the cancer returns.

[Back to: How to make bladder cancer disappear]








Search Hazards

This man knows all about cancer

Simon Pickvance knows numbers are important. Numbers – statistics, victims – establish priorities. Which is why he’s baffled by the Health and Safety Executive’s approach to occupational cancer. There’s a pervasive lack of willingness to believe things are dangerous – it’s a cultural problem about HSE,” Pickvance says.


How to make bladder cancer disappear more

Clock ticking on work cancers more

Industry stalls action on cancer standards more

‘Ticking timebomb’ of bladder cancer cases more


Table 1  What causes bladder cancer at work?

Table 2  Other substances missed by HSE

Table 3  Jobs missed by HSE

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