Tags: Cancer, cancer prevention, environment, female cancers, health, medicine, public health
Cancer prevention strategies are based on what is known about attributable causes of cancer. But does focusing on existing knowledge advance or hamper efforts to reduce cancer incidence? We evaluate two opposing perspectives to conclude that demanding highly robust data may in fact limit our ability to prevent cancers beyond the proportion caused by lifestyle choices.
In December, the British Journal of Cancer published an analysis of the fraction of cancers in the UK in 2010 which were attributable to lifestyle and environmental factors (Parkin 2011). Among the main findings were that 23% of male and 15% of female cancers were caused by tobacco use, that alcohol consumption was responsible for 3-5% of cancers in both males and females, and that obesity was responsible for 6% of female cancers [chart here].
Casual readers may be puzzled by two features of the report: firstly, although the report states it is about environmental causes of cancer, it deals almost exclusively with lifestyle choices; and secondly, although the report only identifies causes for 40% of cancers, it makes a clear statement that these factors ought to be prioritised as part of a cancer prevention programme.
Why so little discussion of the environment?
Lay readers (not epidemiologists) are likely to understand the term “environmental” as referring to anything with which the body involuntarily interacts with in the world, in particular pollutants, while lifestyle factors are likely to be interpreted as encompassing people’s choices, such as what they eat and how much they exercise.
There is a simple explanation as to why the report equates environmental causes of cancer with lifestyle causes, as Professor Max Parkin, lead author of the BJC report, explains: “Epidemiologists just split things up into environmental or genetic. Genetic is something built in from the word go, that you are born with. Everything else is an external influence, which is referred to as environmental.”
Of course, what many environmental organisations are interested in is the specific contribution which inadvertent exposure to environmental pollutants makes to the burden of cancer and other disease. On this, the report has very little to say, devoting only one chapter to occupational causes of cancer, and no space at all to environmental pollutants and chemicals as a potential cause of cancer.
Instead, the BJC report satisfies itself with identifying lifestyle causes of cancer and leaving the causes of the other 60% of cancers unaccounted for. Since most lifestyle factors are accounted for in the study, this leaves a significant proportion which must be environmental in the conventional sense. So why are they not in the report?
There is a simple explanation for this as well: there are no specific environmental causes of cancer for which there are sufficient data to calculate attributable risk. For calculating attributable risk, the BJC report required sufficient evidence on the presence and magnitude of likely causal associations with cancer risk from high-quality epidemiological studies, and data on risk factor exposure from nationally representative surveys.
“We could have written a little bit about air pollution,” says Parkin. “However, it is likely to be a minor component compared to those other things [assessed in the report]. It could be doubling the risk of cancer, but we don’t really have a very good hold on that.”
“It’s possible there are things we don’t know about which are substantial contributors to cancer,” Parkin adds. “But never say never: 35 years ago we didn’t know about HPV [human papilloma virus, a major risk factor in cervical cancer] so there might be something out there. It’s a bit odd that non-Hodgkin’s lymphoma is going up, and testicular cancer likewise. However, it is unlikely we will find [another major factor] like smoking.”
If only 40% of cancers are accounted for, why are these the most important causes to address?
The BJC figures are clearly intended to inform the UK’s cancer prevention strategy and place the emphasis on people’s choices about diet, exercise, alcohol consumption and so forth. Cancer Research UK’s Chief Executive, Dr Harpal Kumar, describes these “healthy habits” as the priority for cancer prevention (CRUK 2011). Tobacco cessation therefore continues to be the number-one priority, with reducing alcohol intake and encouraging more exercise and better diet next in the queue.
Some argue this approach does more harm than good. Professors Andrew Watterson and Rory O’Neill of the University of Stirling, Scotland, argue forcefully against the “victim-blaming” they see as implicit in a healthy habits strategy, diverts attention away from the broader, societal roots of many cases of cancer, in which “income and social class connect directly to […] poor diet […] poor housing near busy, polluting roads and […] dusty, dirty, chemical-laden jobs and long hours” play into cancer incidence.
Not everybody sees things this way, however. In a Personal View in March’s Lancet Oncology, Professor Bernard Stewart of the University of New South Wales, Australia, acknowledges that although a focus on lifestyle does not recognise the burden caused by the chemical industry and associated pollution, no intervention based around reducing involuntary exposure to pollutants (except for air pollution) should be prioritised over lifestyle choices in a cancer prevention strategy (Stewart 2012).
Stewart argues that public health strategies aimed at cancer prevention have to be based in solid data. To be solid enough, the data has to show (1) the circumstances of exposure; (2) a calculation the consequential risk of cancer; and (3) the effectiveness of measures in reducing that risk of cancer. Only if all three boxes are ticked can an intervention be properly described as preventive.
For Stewart, only air pollution has adequate data for describing exposure and establishing the burden of cancer. He describes industrial pollution and pesticide findings as “not unequivocal”. For EDCs, their role in human breast cancer is “mainly inferential” and as yet unsupported by epidemiological evidence. Nor, he says, is there any evidence that there is a case of cancer which would have been avoided had a consumer decided not to buy a particular product, or had regulators been more diligent.
This is the interpretation of the data on which the established view that personal choices provide the greatest opportunities for reducing cancer incidence, while controls on specific pollutants are understood to be individually so causally insignificant they cannot be interpreted as part of a cancer prevention strategy.
Does this lead to an effective prevention strategy?
Professor Richard Clapp of Boston (US) University’s School of Public Health is unimpressed with the findings of the BJC report and is opposed to the view that lifestyle choices should be a priority in a cancer prevention strategy. Although Professor Richard Peto says the BJC report will focus attention on the high priority areas, such as refocusing on tobacco and the continuing importance of tobacco control and efforts to change the UK diet (Peto 2011), to Clapp, this is “just more of the same”.
“The 60% unknown is the elephant in the room,” says Clapp, reiterating Parkin’s and Stewart’s view that, beyond obvious causes such as smoking, it is very difficult to attribute percentages to causes of cancer. However, he draws a very different conclusion, saying it is “counterproductive and pointless” to assign certain exposures as causing a specific fraction of cancer when it is clear that preventable occupational and environmental exposure fuel excess cancer cases and deaths. (See e.g. Clapp et al. 2007)
Clapp argues this is because the fundamental mechanism of cancer is both environmental and genetic. Exposures from outside the body combine with inherited genes and genetic mutations, all of which converge to produce cancer. Overall, there are six essential alterations which need to happen in order for the body’s defences against cancer to be overwhelmed (Hanahan & Weinberg 2011).
Clapp describes this as an integrated circuit, in which a combination of exposures is required to produce a tumour, then prevention of any one of these will prevent the tumour. While preventing any of the single major factors, such as a carcinogenic exposure, is therefore a preventive measure, it becomes impossible to calculate what proportion of cancers any particular such measure prevents.
That the effectiveness of an intervention cannot be measured is unimportant for Clapp, who says we do not need a hierarchy of interventions or to play one cause off against another; exposures from all sources should be systematically reduced: “It doesn’t matter if tobacco is responsible for 20% or 30% of cancers; if it’s a carcinogen, we should minimise the exposure.”
Is Stewart’s position of holding out on action until the data is certain help set the right priorities for a cancer strategy, or does it limit our ability to prevent cancer?
For one thing, human exposure to chemicals is uncontrolled. In the instance we find a control group, exposure is usually so thoroughly confounded with other chemicals, lifestyle choices, occupation, economic status etc. that it becomes extremely difficult to prove an association which could pass as causal.
It is therefore hard to see how we can attain Stewart’s required level of proof for preventive action, beyond the 40% we already know about (and have known about for over 30 years). Waiting for proof for a set of factors which Stewart and Parkin both acknowledge may remain unproven for many years to come, seems a missed opportunity for preventing many cancers – even if we do not know how many cancers such action will prevent.
So although Stewart argues against use of the precautionary principle, it seems if we are to progress beyond the 40% of cancers attributed to lifestyle choices, we will ultimately have no choice but to work with limited data: being measurable is important, but only if your measurements help you make the optimal decision, rather than simply the optimal measurable decision.
“It is probable that limiting exposure to tobacco smoke has reduced incidence of lung cancer; there are lots of opportunities to expand that approach,” says Clapp. Watterson and O’Neill say that “social, political and physical environmental factors all play into cancer incidence and prevalence, and should form part of a coherent cancer prevention strategy.”
Although individual exposures are unlikely to make much difference to cancer risk, if there are hundreds of exposures which can be eliminated through general pollution control programmes, then significant further progress could be made. As Parkin acknowledges, “healthy habits” will not help the majority of people who don’t smoke, aren’t overweight and will get cancer anyway.
Transgenerational actions of environmental compounds on reproductive disease. Deliberate study of transgenerational effects of exposure to chemical mixtures, plastics, jet fuel, dioxin and pesticides, finding sperm death and premature female puberty.
Science highlight of the month: Scientists publish review describing regulatory testing as unfit for EDCs. In the largest review to date of studies examining low-dose effects of chemicals, scientists have concluded regulatory testing for chemical safety does not effectively examine the potential health risks of endocrine disruptors. Summaries of the findings in Yale360 and Scientific American.
In an editorial in Environmental Health Perspectives, Linda Birnbaum, Head of the US National Institute of Environmental Health Sciences, says the question is no longer whether nonmonotonic dose responses are real. “Instead, it is which dose–response shapes should be expected for specific environmental chemicals and under what specific circumstances.”
Exposure to Phthalates and Phenols during Pregnancy and Offspring Size at Birth. Consistent with findings of a previous study, observed evidence of an inverse association of 2,5-DCP and a positive association of BP3 with male birth weight.
Effects of Chronic Exposure to an Environmentally Relevant Mixture of BFRs on the thyroid and reproductive systems of adult male rats. Exposure to three commercial brominated diphenyl ethers, formulated to mimic the relative congener levels in house dust, affected liver and thyroid physiology but not male reproductive parameters.
Early breast development in girls after prenatal exposure to non-persistent pesticides. Evidence that prenatal exposure to currently approved pesticides may cause earlier breast development in girls, possibly from aromatisation of androgens.
Going to Extreme Lengths to Purge Household Toxins. A subtle and easily misunderstood NYT piece, not about middle-class paranoia, but about how inadequate regulatory control over chemical exposures in consumer goods leads to people to going to almost bizarre lengths to “shop our way to some place which protects us”.
‘Green’ cleaners without cancer-causing ingredients. The Environmental Protection Agency has found that chemicals in household cleaners are three times more likely to cause cancer than air pollution. So what’s the alternative? (And so did the Silent Spring Institute. What, as reported in Forbes, did industry think of the institute’s research? “This study presents a clear example of biased, advocacy-based research,” says William Troy, Ph.D., Scientific Advisor to the International Fragrance Association North America.)
News highlight of the month. What is really making us fat? Man-made chemicals present in homes, schools, offices, cars and food are probably contributing to the sharp rise in obesity and diabetes in western societies, according to a review of scientific literature. The Atlantic recounts various perspectives on the problem and the UK Independent provides a basic overview of the review findings. Download the report here.
Children’s car seat makers to eliminate PVC and halogenated flame-retardants. Britax and Orbit, two major manufacturers of children’s car seats and pushchairs have pledged to eliminate polyvinyl chloride (PVC) and brominated and chlorinated flame retardants from their products.
Campbell’s to end use of BPA in can linings. Campbell’s Soup Co. spokesman Anthony Sanzio said the company has been working on alternatives for five years and will make the transition as soon as “feasible alternatives are available.”
How those pesticides persist even when you wash your fruit and veg. Washing fruit and vegetables does not remove chemical pesticide residues, tests commissioned by Government food watchdogs show.