Tag Archives: Simon Chapman

Why researchers have a duty to try and influence policy

The Conversation

Simon Chapman, University of Sydney

Very early in my career, I was invited to afternoon tea with the head of the Commonwealth Institute of Health at Sydney University, where I worked. The best bone china was produced and pleasantries exchanged. The agenda soon became clear.

He laboured into a parable about the difference between young and old bulls when locked in a small yard. He told me young bulls run hard at the gate, exhausting and sometimes harming themselves.

But old bulls are generally patient and placid. They always know the farmer will open the gate and they’ll walk out and soon get among the pasture and the cows.

Young bulls should learn from old bulls, he told me.

I knew exactly why he’d called me. For some months, I’d been in the forefront of a small group of public health people who were confronting the advertising industry’s self-regulation body with data about the appeal of Paul Hogan, who fronted the massively successful Winfield cigarette advertising campaign. Hogan’s own TV program had huge appeal to children. The advertising campaign was, therefore, in flagrant breach of the industry’s own guidelines and so needed to be stopped.

After 18 months of trying to ignore us, we won. We quickly discovered while the advertising industry could ignore our letters, going public turned 10,000 watt arc lights on the self-regulation farce. Over that time the media often interviewed us. A headline after we won said our slingshot had cut down the advertising ogre. Hogan said he’d been sent from the field for kicking too many goals. That was in fact our argument.

My “young and old bulls” mentor later told me he’d been tapped by the Vice Chancellor to tighten the reins, after receiving complaints from connections with the tobacco industry.

Then, and even today, there still remain large remnants of the attitude in universities that scientists and researchers should avoid talking to the media. News media are frequently disdained by academics as trivialising and superficial, something from which those with ambitions of gravitas should keep well away.

A long history

The roots of this go way back. In 1905 Sir William Osler a foundation professor at Baltimore’s Johns Hopkins Hospital, warned against “dallying with the Delilah of the press”. More than 100 years later, a 2006 report by the UK Royal Society noted 20% of UK scientists believed colleagues who engage with the media are “less well regarded” by their peers.

Public engagement was something “done by those who were ‘not good enough’ for an academic career”. Those who did so were seen by some as “light” or “fluffy” and, wait for this, more likely to be women. While 60% of UK researchers wanted to engage with politicians about their research, far fewer (31%) wanted to engage with journalists.

The cocooned naivety of this position is quite staggering.

Knowing someone, but never meeting

Early in Nicola Roxon’s tenure as Australian health minister I approached her after a talk she gave at a conference. “I don’t think we’ve ever met,” I said. “No, but I feel I’ve known you all my adult life,” she replied.

This could have only meant she knew me through the media.

There is an abundance of research showing people get a huge amount of their information and understanding of health issues from the news media. Equally, most politicians and their advisors rarely read scholarly papers in research journals. They form their understandings of the issues in their portfolio in a variety of ways. But like us all, they are daily exposed to information and discussion about health and medicine through the media they consume voraciously every day.

I had an instinct about the importance of all this right from the beginning of my career and so quickly took to trying to get my research covered in the media; I gave high priority to making room in my day to provide commentary about the areas in which I worked.

Here, I quickly learned the constraints on time and space meant something richly nuanced and complex always needed to be condensed into just two or three sentences in print media reports, or 7.2 seconds in television news. When I started taking opportunities to write opinion page and feature articles, the access to my work and commentary on controversies in public health rapidly accelerated.

Visibility brings access

The visibility this brought opened many doors to senior policy advisors and politicians. I also frequently had the experience of dozens of people telling me across a day they had read and enjoyed a piece I’d written in a newspaper that morning, or a breakfast radio interview as they got ready for work. Most of these colleagues work in adjacent areas of public health and would have only occasionally read my research work in journals.

My own GP and other clinicians have often told me about patients who brought in one of my newspaper articles to ask about it. This was especially true about pieces I wrote on the risks and benefits of prostate cancer screening. This feedback inspired a 2010 book – Let Sleeping Dogs Lie?: what men should know before getting tested for prostate cancer. Colleagues and I published it as a free ebook and it’s been downloaded over 35,000 times.

My 85 articles in The Conversation have been read over two and a half million times. Just two of them have together been read over 1.8 million times. By contrast, the most read of over 500 papers I’ve published in peer reviewed journals has been read only 150,000 times. Many are lucky to get even 5000 readers. Being locked behind subscription paywalls doesn’t help.

Who are the ‘influencers’?

A few years ago, colleagues and I researched the characteristics associated with peer-voted “influential” researchers. We invited all Australian researchers who had published 10 or more papers in particular fields of public health to name five Australian researchers who were “most influential” in each of these fields. We then interviewed the top five from each field.

Overwhelmingly, nearly all said they believed researchers had a responsibility and even a duty to produce work that might help shape policy and practice. Most of these were very comfortable in actively pursuing media opportunities to bring understanding of their work to the public. Those who weren’t comfortable in the media were very happy for others to do this on their behalf.

This approach started with choosing research questions they hoped would provide strategically useful information to inform policy. Their approach then passed through the necessary steps of grant application craft to best ensure it was funded through the highly competitive National Health and Medical Research Council process that now sees only 17% of applications funded.

These two steps are meat and potatoes for all funded research.

But it was in post-publication behaviour where influential researchers differ. They actively promote their work – not just to other colleagues in seminars and conferences, but to the public and those who might act on it politically.

And after all, isn’t helping evidence-based policy and practice the whole point of wanting to do the research in the first place? Why else would you bother?

Don’t just ‘stick to the facts’

Some critics of researchers with media profiles argue researchers should just “stick to the facts” in media interviews. Our study participants saw this as naïve because “people always want to know what the policy implications are”.

A total of 94% of those we interviewed disagreed with the view it was inappropriate to express opinions in the media about public health policy. Journalists might begin with a research finding or an expert clarification of a new report. But they invariably then asked what needed to be “done” about the problem, typically by government.

Journalists and audiences would meet with incredulity any researcher who tried to end an interview when there were questions about policy reform “oughts”, or claimed to have no opinion on what should be done. We expect those who know most about health problems to have views about what should be done to solve them and the courage to put these forward, even if they imply criticism of governments or powerful interest groups.

Speak up, speak up

Trump’s recent gagging of all government environmental agency staff is surely the start of a process that will spread to government funded universities in the USA. There has never been a more important time for researchers all over the world to speak up about their work, it’s implications and how societies and governments should act on it.

I’ve just published a collection of 71 of my essays and op eds across a large variety of public health issues. Like this column, the book is called Smoke Signals, and is published by the Sydney University Press imprint, Darlington Press. It’s available in paperback or as an ebook.


This article will be the subject of ABC Radio National’s Ockham’s Razor on Sunday, February 26, 2017 at 7.45am.

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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On the pleasure of smoking

The Conversation

Simon Chapman, University of Sydney

Repeatedly, studies have found a large majority of smokers regret ever starting to smoke: 85% in this study, 90% in this four nation study. Each year, some 40% of smokers make an attempt to stop, with most relapsing within weeks.

Many fork out considerable money in pharmaceuticals along the way in the attempt to shake their smoking. Snake-oil, evidence-free quick-cure merchants advertising on telegraph poles for “laser therapy quitting” happily make up to A$500 from the more gullible.

With 12.8% of Australians aged 14 and over smoking daily, and 90% of these regretting they ever started, today just 1.28% are contented smokers. Recent evidence shows 55% of young smokers now approve of plain packaging with their ghoulish, unavoidable picture warnings. Can there be any product that enjoys less consumer satisfaction and customer loyalty?

One of the most common taunts pro-smokers hurl at tobacco control advocates with great relish is the claim they are enemies of pleasure: they just can’t stand the thought or sight of people taking pleasure from smoking. Perhaps they are right. Airport smoking rooms strike me as about the most fun and pleasure you could get. The queues of non-smokers you see waiting to get in just to experience it all pretty much clinch that argument.

The picture being painted here is of elegant smokers, hand gesturing and exhaling as in Richard Klein’s Cigarettes are sublime constantly pleasuring themselves in a way denied to non-smokers who have not woken up to the joys of nicotine.

But what is it that nicotine addicts like about pulling the chemical deep into their lungs some 90,000 times a year?

In 1994, the New York Times published the ratings of two of the USA’s most renowned addiction specialists, Neil Benowitz and Jack Henningfield, on the relative addictiveness of nicotine, caffeine, heroin, cocaine, alcohol and marijuana (cannabis). They rated each of these on a scale of one (most serious) to six (least serious).

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Both rated nicotine higher in dependence than all the other drugs. By “dependence” they meant how difficult it is for the user to quit, the relapse rate, and the percentage of people who eventually become dependent.

Nicotine withdrawal also rated high (third behind the often discussed agonies of alcohol and heroin withdrawal). Both experts rated nicotine fourth behind cocaine, heroin and alcohol when it came to reinforcement (essentially, the pleasure given by the drug). But both rated nicotine last on intoxication, behind even caffeine.

Taking all this together, a picture emerges of nicotine dependent people regretful they started smoking, living in full knowledge of their high dependency, experiencing often unpleasant withdrawal symptoms when they have not been able to smoke for a while, and being relieved of this unpleasantness quickly when lighting up another cigarette.

Nicotine withdrawal symptoms include headache, nausea, constipation or diarrhoea, fatigue, drowsiness and insomnia, irritability, difficulty concentrating, anxiety, depressed mood, increased hunger and caloric intake and of course, constant tobacco cravings.

Smokers know from the earliest days of their addiction these feelings can disappear within a few seconds as the nicotine is rapidly transported from their lungs to their brains where dopamine is released and experienced as pleasurable.

Smokers often insist the pleasure from this release can somehow be experienced independently of the pleasures of the nicotine withdrawal symptoms rapidly dissipating.

So what is the “pleasure” being experienced here? When you have a toothache and this is relieved by a strong analgesic, your mood can quickly elevate as the codeine begins to work.

The argument that smoking and inhaling nicotine is “pleasurable” is a bit like saying being beaten up every day is something you want to continue with, because hey, it feels so good when the beating stops for a while.

Holiday periods like the upcoming Christmas break are time-honoured opportunities for smokers to make quit attempts. I used to smoke (in late school and to my mid 20s). I thought smoking was a great way to make a statement about myself that would impress those I cared to impress and irritate those I cared to irritate. But I always thought it tasted disgusting, was a stupid thing to continue and threatened to limit my early career opportunities.

I recall just drifting out of smoking, a pathway common to many ex-smokers. And like many smokers, I recall it being anything but difficult or torturous. This is one of the best kept secrets in tobacco control. While there are many smokers who struggle to quit and fail many times, there are many more who found the experience easier than they expected, sometimes far easier.

There are many more ex-smokers in Australia than smokers. The common narratives of quitting smoking ushering in the pleasures of tasting food and drink better, feeling physically better and of course the pleasure of having more disposable income can be compared with the supposed pleasures of smoking. Good luck if you are planning to quit. It’s the single most important thing you can do to improve your health.

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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If smoking doesn’t kill, Mike Pence, neither does the plague

The Conversation

Simon Chapman, University of Sydney

US Vice President elect Mike Pence (who has been the recipient of funding from Big Tobacco) once famously wrote:

Time for a quick reality check. Despite the hysteria from the political class and the media, smoking doesn’t kill. In fact two out of every three smokers does [sic] not die from smoking-related illness and nine out of ten smokers do not contract lung cancer.

Pence is referring here to what epidemiologists call the “case fatality rate”: the proportion of deaths from a smoking-related illness to the number of new smoking-related illnesses diagnosed. According to him, the case fatality rate for long term smoking was “only” one in three, meaning only one in three long-term smokers die from a smoking-related illness (such as cardiovascular and respiratory diseases, and smoking related cancers), which somehow meant to him smoking doesn’t kill.

By Pence’s reasoning there are many other diseases that “do not kill”. This extensive list of various diseases’ case fatality rates shows many well known highly fatal diseases with case fatality rates lower than 33%.

These include oropharyngeal anthrax (anthrax that manifests in the mouth and throat), yellow fever, treated bubonic plague, diphtheria, meningococcal disease, legionnaires’ disease, dengue fever and untreated typhoid. The 1918 Spanish ‘flu which was estimated to have killed 50-100 million people globally, had a paltry case fatality rate of around 2.5%.

Pence was also wrong about the rate at which smoking kills. A landmark study of over 34,000 British male doctors (females were excluded when the study commenced in 1951 because there were insufficient numbers of women doctors at the time) has long been the benchmark for the risks of long term smoking.

When the study reported its 50 year follow-up of the cohort, it found “the eventual risks vary from about one half to about two thirds” of all doctors who had smoked had died from a tobacco-related disease.

An Australian study of 204,953 people also confirmed the two in three death rate from smoking.

Today smoking kills some six million people a year globally, and will kill one billion people this century if present trends continue.

The US is the only significant country to have not ratified the World Health Organisation’s Framework Convention on Tobacco Control (the US tends to not sign global treaties). Under a Trump administration, will we see the end of regulation and strict marketing protocols? Will the US be the only nation to ever see a rise in smoking rates after decades of continual falls?

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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Alan Jones goes after wind farms again, citing dubious evidence

The Conversation

Simon Chapman, University of Sydney

Last week, Sydney radio announcer Alan Jones lambasted those concerned about climate change and what he called “renewable energy rubbish”.

Jones has been loose with the facts in the past, having been Factchecked in 2015 after confusing kilowatts with megawatts and quoting a cost for wind power he later confessed “where the 1502 [dollars per megawatt hour that he stated] comes from, I have absolutely no idea”.

Jones, who chaired the much hyped but poorly attended 2013 national rally against wind farms in June 2014 (see photo) told his listeners last week wind farms are “buggering up people’s health”.

He also said “harrowing evidence” had been given by sufferers to the 2014-15 Senate Select Committee on Wind Farms chaired by (now ex-) Senator John Madigan. He along with Bob Day, David Leyonhjelm, Chris Back and Nick Xenophon have been vocal opponents of wind farms.

Their report predictably savaged wind farms, while Labor Senator Anne Urquhart’s minority report was the only one I found to be evidence-based.

Jones then went on to interview Dr Mariana Alves-Periera, from the private Lusophona University in Portugal (world university ranking 1,805, and impact ranking 2,848) whom he described as a distinguished international figure.

She was “recognized internationally” and had published “over 50” scientific papers over 30 years, something of a modest output. Jones, who may or may not have read any of these publications, told listeners her findings were “indisputable”, there was “no opposing scientific evidence” and again in emphasis, “none of [her papers] have been disputed” to which Alves-Periera agreed instantly “no they haven’t”.

This is an interesting interpretation of the scientific reception that has greeted the work of the Lisbon group on the unrecognized diagnosis of “vibroacoustic disease” (or VAD), a term they have made their own.

I first encountered Alves-Periera when she spoke via videoconference to a NHMRC meeting on wind farms and health in 2011. She spoke to a powerpoint presentation which highlighted the case of a schoolboy who lived near wind turbines. Her claim was the boy’s problems at school were due to his exposure to the turbines, as were cases of “boxy foot” in several horses kept on the same property.

Intrigued by this n=1 case report, I set out with a colleague to explore the scientific reception that “vibroacoustic disease” had met. We published our findings in the Australian and New Zealand Journal of Public Health 2013.

We found only 35 research papers on VAD. None reported any association between VAD and wind turbines. Of the 35 papers, 34 had a first author from the Lusophona University-based research group. Remarkably, 74% of citations to these papers were self-citations by members of the group.

In other words, just shy of three quarters of all references to VAD were from the group who were promoting the “disease”. In science, median self-citation rates are around 7%. We found two unpublished case reports from the group presented at conferences which asserted that VAD was “irrefutably demonstrated” to be caused by wind turbines. We listed eight reasons why the scientific quality of these claims were abject.

In 2014 Alves-Periera and a colleague defended their work in a letter to the journal and I replied. They described themselves as the “lead researchers in vibroacoustic disease”. But as we had shown, they are almost the only researchers who were ever active on this topic, with self-citation rates seldom seen in research.

Other experts have taken a different view of the group’s work. One of the world’s leading acousticians Geoff Leventhall who also spoke at the NHMRC’s 2011 meeting, wrote in a 2009 submission to the Public Service Commission of Wisconsin about the Lisbon group’s VAD work.

The evidence which has been offered [by them] is so weak that a prudent researcher would not have made it public.

Another expert said:

vibroacoustic disease remains an unproven theory belonging to a small group of authors and has not found acceptance in the medical literature

And most recently, the UK’s Health Protection Agency said the:

disease itself has not gained clinical recognition.

Leventhall concluded his review by saying:

One is left with a very uncomfortable feeling that the work of the VAD group, as related to the effects of low levels of infrasound and low frequency noise exposure, is on an extremely shaky basis and not yet ready for dissemination. The work has been severely criticised when it has been presented at conferences. It is not backed by peer reviewed publications and is available only as conference papers which have not been independently evaluated prior to presentation.

Jones told his listeners the reason wind turbines are not installed on Bondi Beach, down Sydney’s Macquarie Street or Melbourne’s Collins Street was because governments “know they are harmful to health”. His beguiling logic here might perhaps also be the same reason we don’t see these iconic locations given over to mining or daily rock concerts. Most people would understand there are other factors that explain the absence of both wind turbines, mines or daily rock concerts in such locations.

Jones has given air time to a Victorian woman who is a serial complainant about her local wind farm and who has written:

Around the Macarthur wind farm, residents suffer from infrasound emitted by the turbines, even when they’re not operating.

At a time when we are seeing unparalleled increases in renewable energy and reductions in fossil fuels all over the world, one wonders why this is still public discussion in Australia.

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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Mobile phone health alarmists bereft of credible arguments

The Conversation
Simon Chapman, University of Sydney

In May this year, I led a paper published in Cancer Epidemiology, which looked at the incidence of brain cancer in Australia between 1982 and 2012.

The first mobile phone call was made in Australia in 1987 and today their use is all but universal.

Cancer is a notifiable disease: all newly diagnosed cases are gathered from doctors by state cancer registries and nationally aggregated by the Australian Institute of Health and Welfare in publicly available data.

I summarised our study in this column, which to date has had more than 44,700 readers.


New study: no increase in brain cancer across 29 years of mobile use in Australia


We found that with extremely high proportions of the population having used mobile phones across some 20-plus years (from about 9% in 1993 to about 90% today), age-adjusted brain cancer rates have flatlined over nearly 30 years.

There were significant increases in brain cancer incidence only in those aged 70 years or more. But the increase in this age group began from 1982, before the introduction of mobile phones in 1987 and so cannot be explained by it.

The most likely explanation of the rise in this older age group was improved diagnosis that happened with the introduction of imaging machines that (for example) could more accurately diagnose some strokes as brain cancers.

In the days and weeks after publication, our paper received massive global news and social media attention, achieving an Altmetric score of 835. On the basis of the most media-covered research in all fields in 2015, this would have put it just outside the 100 highest Altmetric scores if we’d published it last year (2016 figures are published early next year).

It also drew the ire of the close-knit international network of mobile phone and wifi alarmists, who are utterly convinced mobile phones are deadly and won’t hear otherwise. Their opening salvo was to accuse me of being an undeclared phone industry stooge.

In 1997 I had been given a small grant by AMTA, the Australian Mobile Telephone Association, to conduct a national survey of how many mobile phone users had ever used their phone to call emergency services such as ambulance, police and fire. Large proportions of people had done so, probably saving many lives by alerting these services far more quickly than when having to find a landline.

I didn’t report this because I got the one-off grant 19 years ago, and all reputable journals and research agencies rule that competing interests are not lifetime but extinguish typically between one and three years after such support has expired. The grant also had nothing to do with cancer.

I also got a series of mostly verbally incontinent email. One from an excitable correspondent in Swaziland, insisted that I answer his many eureka moment insights into why what we had published was wrong in every respect. We should withdraw our paper, he demanded and tell the world we were wrong.

Predictably, several wrote to Cancer Epidemiology, setting out a litany of our egregious errors and failures to understand that an epidemic of brain cancer, comparable to the deluge of smoking-caused cancers, was just around the corner. Three of these were published this week with our response (open access until October 20, 2016).

The three letters were written by five individuals, three of whom are affiliated with a non-accredited Environmental Health Trust, headed by Dr Devra Davis, the alarmist doomsayer who featured in the much-criticised ABC Catalyst program which has now been withdrawn.

Assuming they got their heads together to rain blows on our heretical findings, it was amusing to see the barely audible blanks they decided to fire.

Their main arguments were:

‘It’s too soon to see an epidemic of brain cancer’

One argued several decades of widespread phone use were needed before increases in cancer might be seen. She seemed intent on diminishing the number of years that large numbers of Australians have used mobile phones, in order to preserve her argument. She argued that only the last nine years of data since 2001 when mobile subscriptions reached 50% of the population ought to be considered in any analysis. And nine years was not nearly enough.

But by 1996, some 20% of Australian adults (some 2.9 million) were using mobile phones. Apparently we ought to have joined her in seeing this as a trivial exposed population, unworthy of consideration. Quite obviously, there’s no alleged carcinogen where 20% of the population is exposed where any credible scientist would seriously maintain such widespread exposure should be ignored in assessing population attributable risk.

Further, in one of the studies cited in a review published by our critics, excess risks of brain cancer from mobile phone use are argued as occurring following exposures of as little as between five and ten years of mobile phone use. These critics even suggested in the same paper that the international INTERPHONE study may suggest a cancer “promotion effect”, with use as few as one to four years being dangerous.

We concluded that:

This therefore looks like an argument trying to walk on both sides of the street: if a short latency period show excess risks they are deemed to be credible, while if they show no excess (as with our study) they are to be dismissed.

‘Various case-control studies show evidence of increased risk’

Case-control studies in this field have been criticised because they rely on users’ recall of the extent of phone use going back many years. Just try recall your own mobile phone use in, for example, 2003 and you will immediately understand how data obtained this way are hugely problematic.

Moreover, people with brain cancer often have memory loss. And if you have brain cancer, are part of a study considering its cause, and have been exposed to frequent claims about the hypothesis that mobile phone use causing brain cancer, the likelihood of recall bias resulting in recall of high mobile phone use is probably going to increase.

The strength of our study was the ability to look at all cases of brain cancer in Australia in the 29 years since the first call was made here. The inconvenient fact for the alarmists is that there has been no significant increase in brain cancer in either men or women compatible with the mobile phone hypothesis.

‘Decreased use of X-rays is masking an increase in cancers caused by mobiles’

Perhaps the silliest argument thrown at us was an unreferenced hypothesis that “discontinued or reduced use of established carcinogens such as X-rays” may have reduced the incidence of brain cancer from such exposures while, simultaneously, the rise of mobile phone use would have replaced those cases, thereby explaining the largely flat line incidence across our data period.

This hypothesis would need to account for how reductions in a very uncommon radiation exposure (full head X-rays) could ever possibly produce the exact same decreased incidence of brain cancer that they claim arise in daily exposure to an alleged carcinogen by most of the entire population would add to that incidence.

Our Swaziland critic finished one of his missives writing that “it behooves you, as a scientist, to take note of fatal errors in your work.” It would “behoove” mobile phone alarmists to stop unnecessarily alarming people with their weak arguments.

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.
 

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No massacres and an accelerating decline in overall gun deaths: the impact of Australia’s major 1996 gun law reforms

The Conversation

Simon Chapman, University of Sydney

Twenty years ago, Australian federal, state and territory governments united to reform our firearm laws which had allowed easy access in some states to the military-style weapons of the sort used by the gunman in Orlando, Florida. The main provisions of the new laws included:

  • a ban on semi-automatic rifles and pump action shotguns, with a market price buy-back of all now-banned guns
  • uniform gun registration
  • end of “self-defense” as an acceptable reason to own a gun
  • end of mail order gun sales.

So, after 20 years of our new gun laws, what has happened to gun deaths?

Today, our study of intentional firearm deaths in Australia between 1979 and the present has been published in JAMA (Journal of the American Medical Association).

The new gun laws were introduced because of the near-universal outpouring of revulsion Australians felt over the ability of someone to go into a public place and murder lots of people quickly with rapid-fire firearms.

In the 18 years between 1979 and April 1996, Australia saw 13 massacres (five or more victims, not including the perpetrator) where 104 victims died. In the twenty years and nearly two months since the Port Arthur massacre and the passage of the law reforms that followed swiftly afterwards, we have seen precisely none.

The Gun Violence Archive reports that in the United States, the Orlando shootings were the 1000th mass shooting incident in 1,260 days. In those incidents 1,134 people were shot dead and 3,950 were injured.

Mass killings a small fraction of all gun deaths

Australia’s 104 victims of mass shootings represent a small fraction of all people intentionally shot dead in Australia across the years we examined. For every person shot in a mass killing, 139 others suicided or were murdered with guns in incidents where less than five people died (most typically one or two).

While the gun laws were introduced explicitly to reduce the likelihood of mass shootings, we were interested in whether the removal of what turned out to be some 750,000 semi-automatic and rapid fire weapons from the community may have had collateral benefits on trends in these non-mass killings.

By one argument, the outlawing of semi-automatic rifles might have made little difference to the firearm suicide rate because such firearms are irrelevant to suicide: only one shot is generally fired when people try to suicide with a gun, so a semi-automatic is not necessary. But by another argument, any firearm- semi-automatic or not – can be used, so the removal of a large number of one category of gun might nonetheless have impacts on non-mass killings.

Here’s what we found.

From 1979 to 1996 (the year of the gun law reforms), total intentional firearm deaths in Australia were declining at an average 3% per year. Since then, the decline in total firearm deaths accelerated to 5% annually.

With gun suicide deaths, over the same comparison periods, there was a statistically significant acceleration in the downward trend for firearm suicides and a non-significant acceleration in the downward trend in firearm homicides.

We also examined total all-method homicides and suicides data to assess the possibility that reduced access to firearms saw people substitute other lethal methods to commit suicide or homicide. From 1979 to 1996, the average annual rate of total non-firearm suicide and homicide deaths was rising at 2.1% per year. Since then, the average annual rate of total non-firearm suicide and homicide deaths has been declining by 1.4%. This supports a conclusion there has been no substitution of other lethal means for suicides or homicides.

Finally, we found that the post-1996 decrease in the rates of non-firearm suicide and homicide were larger than the decreases for suicide and homicide involving firearms.

There are two likely explanations for this. Another study of the decline in suicide in Australia between 1994-2007 concluded that much of the decline was explained by changes toward the use of less fatal methods. Fewer people killed themselves using motor vehicle exhaust and this explained nearly half of the overall decline in suicide deaths.

Suicide using firearms had the highest fatality rates (74%) with self-poisonings lowest at 1.4%. That study noted that “the decline in firearm deaths over the study period was due primarily to a decline in attempts; lethality remained relatively flat.”

Guns have the highest “completion” or fatality rate in suicides compared to all other methods, so with evidence that suicide method choice is moving more toward less lethal means, it’s understandable that overall suicide rates could be falling faster than those for firearms where there has been no change in the completion rate. If you shoot yourself you are highly likely to die, but not so with many other methods.

Another factor, which combined with the high lethality of guns when used in both suicides and assaults, is the proliferation of the mobile phone over the past 20 years. A 1997 study found 12% of 764 cell phone users had used their phone to call emergency services to a road crash and 6% to a non-road medical emergency. As we wrote in our JAMA paper:

With increasing cell phone use over the past 20 years, it is plausible that ambulances will have increasingly attended traumatic incidents like assaults and suicide attempts earlier than in previous times when landlines were only or more commonly used to make such calls. There have also been improvements in emergency care, and the lower lethality of non-firearm assault and suicide may explain the greater reductions in non-firearm homicide and suicide rates.

When it comes to firearms, Australia is far a safer place today than it was in the 1990s and in previous decades. We have the leadership of John Howard to thank for this.

Today, politicians like the National Rifle Association’s local Australian hero Senator David Leyonhjelm are doing what they can to water down aspects of our gun laws as occurred with Leyonhjelm’s deal with the government to allow the importation of the massacre-ready Adler shotgun. Will the Prime Minister after the July 2 election have sufficinet Howard-like leadership to ban the Adler?

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

 

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New study: no increase in brain cancer across 29 years of mobile use in Australia

The Conversation

Simon Chapman, University of Sydney

Earlier this year, Australia saw a whirlwind tour from the electromagnetic radiation from mobile phones alarmist Devra Davis. Davis is an international champion of the belief that populations bathed in radiation emitted by mobile phones face epidemics of disease – particularly brain cancer.

Davis’ concerns were the focus of an ABC Catalyst program which attracted widespread criticism, including from me and Media Watch. The Catalyst presenter Maryanne Demasi was nominated for the Australian Skeptics bent spoon award.

At the time of the Catalyst program for which I declined to be interviewed, I had my hands tied behind my back because, with colleagues in cancer research, I had a paper in preparation examining the possible association between the incidence of brain cancer in Australia and the inexorable rise of mobile phone use here over the last three decades. Releasing our findings would have jeopardised publication, we could say nothing about what we had concluded.

Today the paper is published in early view in Cancer Epidemiology. Here’s what we set out to examine and what we found.

We examined the association between age and gender-specific incidence rates of 19,858 men and 14,222 women diagnosed with brain cancer in Australia between 1982-2012, and national mobile phone usage data from 1987-2012.

In summary, with extremely high proportions of the population having used mobile phones across some 20-plus years (from about 9% in 1993 to about 90% today), we found that age-adjusted brain cancer incidence rates (in those aged 20-84 years, per 100,000 people) had risen only slightly in males but were stable over 30 years in females.

There were significant increases in brain cancer incidence only in those aged 70 years or more. But the increase in incidence in this age group began from 1982, before the introduction of mobile phones in 1987 and so could not be explained by it. Here, the most likely explanation of the rise in this older age group was improved diagnosis.

Computed tomography (CT), magnetic resonance imaging (MRI) and related techniques, introduced in Australia in the late 1970s, are able to discern brain tumours which could have otherwise remained undiagnosed without this equipment. It has long been recognised that brain tumours mimic several seemingly unrelated symptoms in the elderly including stroke and dementia, and so it is likely that their diagnosis had been previously overlooked.

Next, we also compared the actual incidence of brain cancer over this time with the numbers of new cases of brain cancer that would be expected if the “mobile phones cause brain cancer” hypothesis was true. Here, our testing model assumed a ten-year lag period from mobile phone use commencement to evidence of a rise in brain cancer cases.

Our model assumed that mobile phones would cause a 50% increase in incidence over the background incidence of brain cancer. This was a conservative estimate that we took from a study by Lennart Hardell and colleagues (who reported even higher rates from two studies). The expected number of cases in 2012 (had the phone hypothesis been true) was 1,866 cases, while the number recorded was 1,435.

Using a recent paper that had Davis as an author we also modelled a 150% increase in brain cancer incidence among heavy users. We assumed that 19% of the Australian population fell into this category, based on data from the INTERPHONE study an international pooled analysis of studies on the association between mobile phone use and the brain. This would have predicted 2,038 expected cases in 2012, but only 1,435 were recorded.

Our study follows those published about the United States, England, the Nordic countries and New Zealand where confirmation of the “mobile phones cause brain cancer” hypothesis was also not found.

In Australia, all cancer is notifiable. At diagnosis, all cases must by law be registered with state registries tasked with collecting this information. It has been this way for decades. So we have excellent information about the incidence of all cancers on a national basis.

The telecommunications industry of course also has information on the number of people with mobile phone accounts.

While touring Australia, Davis was confronted with the “flatline” incidence data on brain cancer. Her stock response was that it was far too early to see any rise in these cancers. She was here to warn us about the future.

However, prominent Sydney neurosurgeon Dr Charlie Teo would appear to disagree about it being too early. He told Andrew Denton on ABC-TV’s Enough Rope in 2008:

If you look at the science on mobile phones and the link with brain cancer, it is quite compelling … we know that radiation causes cancer, but it takes about ten years for it to develop, so we know that EMR electromagnetic radiation is going to take at least ten years to create brain tumours and possibly longer fifteen, twenty years.

In cancer epidemiology, the concept of the latency (or lag) period is well known. This refers to the time that it takes between initial exposure to a potentially carcinogenic agent (like cigarette smoke, asbestos, or nuclear radiation) and excess cases of cancers of interest to appear.

Davis would appear to be arguing that we would see a sudden rise many years later. That is not what we see with cancer; we see gradual rises moving toward peak incidence, which can be as late as 30-40 years (as with lung cancer and smoking).

For example, as I showed in a recent Conversation piece, this paper also reports on central nervous system cancers (including brain cancers) in those exposed to atomic bomb radiation in Japan in 1945. This graph shows 110 of 187 cases (58.8%) were diagnosed in the first 40 years (before 1985) (so before 40 years).

https://datawrapper.dwcdn.net/yJ7ej/3/

The incidence and type of cancers of those exposed to atomic bomb radiation varied over the years. And this quote from the methods section shows that there were another 27 who died before 1958 from central nervous system cancers, within 13 years of the bombs.

We excluded 73 tumours in individuals who were not in Hiroshima or Nagasaki at the time of the bombings, 35 individuals who did not have available organ dose estimates, and 27 individuals who died or were diagnosed before January 1, 1958.

Note here that A-bomb survivors were affected by ionising radiation (that is, radiation of sufficient energy to produce ionisation). This is where the energy is strong enough to remove electrons off their atoms or molecules, including causing DNA damage. Mobile phones produce non-ionising radiation which is low energy, sufficient only to ‘excite’ the electrons enough to make them just heat up.

We have had mobiles in Australia since 1987. Some 90% of the population use them today and many of these have used them for a lot longer than 20 years. But we are seeing no rise in the incidence of brain cancer against the background rate.

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

 

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Ten myths about smoking that will not die

The Conversation

Simon Chapman, University of Sydney

Across forty years I’ve come to recognise many factoid-driven myths about smoking that just won’t die. If I asked for a dollar each time I had to refute these statements, I’d have accumulated a small fortune.

Their persistence owes much to their being a vehicle for those who utter them to express unvoiced but clear sub-texts that reflect deeply held beliefs about women, the disadvantaged, mental illness, government health campaigns and the “natural”.

Let’s drive a stake through the heart of ten of the most common myths.

1. Women and girls smoke more than men and boys

Women have never smoked more than men. Occasionally, a survey will show one age band where it’s the other way around, but from the earliest mass uptake of smoking in the first decades of last century, men streaked out way ahead of women.

In 1945 in Australia, 72% of men and 26% of women smoked. By 1976, men had fallen to 43% and women had risen to 33%.

As a result, men’s tobacco-caused death rates have always been much higher than those of women. Women’s lung cancer rates, for example, seem unlikely to reach even half the peak rates that we saw among men in the 1970s.

Currently in Australia, 15% of men and 12% of women smoke daily.

But what about all the “young girls” you can see smoking, I’m always being told. In 2014, 13% of 17-year-old male high school students and 11% of females smoked. In two younger age bands, girls smoked more (by a single percentage point).

Those who keep on insisting girls smoke more are probably just letting their sexist outrage show about noticing girls’ smoking than their ignorance about the data.

2. Quit campaigns don’t work on low socioeconomic smokers

In Australia, 11% of those in the highest quintile of economic advantage smoke, compared with 27.6% in the lowest quintile. More than double.

So does this mean that our quit campaigns “don’t work” on the least well-off?

Smoking prevalence data reflect two things: the proportion of people who ever smoked, and the proportion who quit.

If we look at the most disadvantaged groups, we find that a far higher proportion take up smoking than in their more well-to-do counterparts have never smoked (39.5% vs 50.4%) – see table 9.2.6).

When it comes to quitting, 46% of the most disadvantaged have quit compared to 66% of the least disadvantaged (see table 9.2.9).

There is a higher percentage of the disadvantaged who smoke mainly because more take it up, not because disadvantaged smokers can’t or won’t quit. With 27.6% of the most disadvantage smoking today, the good news is that nearly three-quarters don’t. Smoking and disadvantage are hardly inseparable.

3. Scare campaigns ‘don’t work’

Countless studies have asked ex-smokers why they stopped and current smokers about why they are trying to stop. I have never seen such a study when there was not daylight between the first reason cited (worry about health consequences) and the second most nominated reason (usually cost).

For example, this national US study covering 13 years showed “concern for your own current or future health” was nominated by 91.6% of ex-smokers as the main reason they quit, compared with 58.7% naming expense and 55.7% being concerned about the impact of their smoking on others.

If information and warnings about the dire consequences of smoking “don’t work”, then from where do all these ex-smokers ever get these top-of-mind concerns? They don’t pop into their heads by magic. They encounter them via anti-smoking campaigns, pack warnings, news stories about research and personal experiences with dying family and friends. The scare campaigns work.

4. Roll-your-own tobacco is more ‘natural’ than factory made

People who smoke rollies often look you in the eye and tell you that factory made cigarettes are full of chemical additives, while roll-your-own tobacco is “natural” – it’s just tobacco. The reasoning here that we are supposed to understand is that it’s these chemicals that are the problem, while the tobacco, being “natural”, is somehow OK.

This myth was first turned very unceremoniously on its head when New Zealand authorities ordered the tobacco companies to provide them with data on the total weight of additives in factory made cigarettes, roll-your-own and pipe tobacco.

For example, data from 1991 supplied by WD & HO Wills showed that in 879,219kg of cigarettes, there was 1,803kg of additives (0.2%). While in 366,036kg of roll-your-own tobacco, there was 82,456kg of additives (22.5%)!

Roll-your-own tobacco is pickled in flavouring and humectant chemicals, the latter being used to keep the tobacco from drying out when smokers expose the tobacco to the air 20 or more times a day when they remove tobacco to roll up a cigarette.

5. Nearly all people with schizophrenia smoke

It’s true that people with mental health problems are much more likely to smoke than those without diagnosed mental health conditions. A meta-analysis of 42 studies on tobacco smoking by those with schizophrenia found an average 62% smoking prevalence (range 14%-88%). But guess which study in these 42 gets cited and quoted far more than any of the others?

If you said the one reporting 88% smoking prevalence you’d be correct. This small 1986 US study of just 277 outpatients with schizophrenia has today been cited a remarkable 1,135 times. With colleagues, I investigated this flagrant example of citation bias (where startling but atypical results stand out in literature searches and get high citations – “wow! This one’s got a high number, let’s quote that one!”).

By googling “How many schizophrenics smoke”, we showed how this percolates into the community via media reports where figures are rounded up in statements such as, “As many as 90% of schizophrenic patients smoke.”

Endlessly repeating that “90%” of those with schizophrenia smoke does these people a real disservice. We would not tolerate such inaccuracy about any other group.

6. Everyone knows the risks of smoking

Knowledge about the risks of smoking can exist at four levels:

  • Level 1: having heard that smoking increases health risks.
  • Level 2: being aware that specific diseases are caused by smoking.
  • Level 3: accurately appreciating the meaning, severity, and probabilities of developing tobacco related diseases.

Level 4: personally accepting that the risks inherent in levels 1–3 apply to one’s own risk of contracting such diseases.

Level 1 knowledge is very high, but as you move up the levels, knowledge and understanding greatly diminish. Very few people, for example, are likely to know that two in three long term smokers will die of a smoking caused disease, nor the average number of years that smokers lose off normal life expectancy.

7. You can reduce the health risks of smoking by just cutting down

It’s true that if you smoke five cigarettes a day rather than 20, your lifetime risk of early death is less (although check the risks for one to four cigarettes a day here).

But trying to “reverse engineer” the risk by just cutting down rather than quitting has been shown in at least four large cohort studies such as this one to confer no harm reduction.

If you want to reduce risk, quitting altogether should be your goal.

8. Air pollution is the real cause of lung cancer

Air pollution is unequivocally a major health risk. By “pollution”, those who make this argument don’t mean natural particulate matter such as pollen and soil dusts, they mean nasty industrial and vehicle pollution.

The most polluted areas of Australia are cities where pollution from industry and motor vehicle emissions are most concentrated. Remote regions of the country are the least polluted, so if we wanted to consider the relative contributions of air pollution and smoking to smoking-caused diseases, an obvious question to ask would be “does the incidence of lung cancer differ between heavily polluted cities and very unpolluted remote areas?”

Yes it does. Lung cancer incidence is highest in Australia in (wait for this …) in the least polluted very remote regions of the country, where smoking prevalence happens also to be highest.

9. Smokers should not try to quit without professional help or drugs

If you ask 100 ex-smokers how they quit, between two-thirds and three-quarters will tell you they quit unaided: on their final successful quit attempt, they did not use nicotine replacement therapy, prescribed drugs, or go to some dedicated smoking cessation clinic or experience the laying on of hands from some alternative medicine therapist. They quit unaided.

So if you ask the question: “What method is used by most successful quitters when they quit?” The answer is cold turkey.

Fine print on this English National Health Service poster states a bald-faced lie by saying that “There are some people who can go cold turkey and stop. But there aren’t many of them.” In the years before nicotine-replacement threapy and other drugs were available, many millions – including heavy smokers – quit smoking without any assistance. That’s a message that the pharmaceutical industry was rather not megaphoned.

Not true. NHS poster.

10. Many smokers live into very old age: so it can’t be that harmful

In just the way that five out of six participants in a round of deadly Russian roulette might proclaim that putting a loaded gun to their head and pulling the trigger caused no harm, those who use this argument are just ignorant of risks and probability.

Many probably buy lottery tickets with the same deep knowing that they have a good chance of winning.

The ConversationSimon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

 

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The slow-burn, devastating impact of tobacco plain packs

The Conversation

Simon Chapman, University of Sydney

It is three years since Australia fully implemented its historic tobacco plain packaging law. From December 1, 2012, all tobacco products have been required to be sold in the mandated standardised packs, which, with their large disturbing graphic health warnings, are anything but “plain”.

Ever since, there have been frenzied efforts by the tobacco industry and its ideological baggage carriers to discredit the policy as a failure.

The obvious subtext of this effort has been to megaphone a message to other governments that they should not contemplate introducing plain packaging because it has “failed”: smoking, it is claimed, has not fallen any faster in Australia after plain packaging that it was already falling before. All that has occurred, they argue, is that illicit trade has increased.

The supreme irony here is of course that if such criticism was correct, then to paraphrase Hamlet’s mother Gertrude, “The tobacco industry doth protest too much, methinks.” Why would the industry and its astro-turfed bloggers waste so much money and effort denigrating a policy which was having little or no impact?

Why take the Australian government to the High Court (and fail six to one) to try and block the law? Why invest in supporting minnow tobacco-growing states such as the Dominican Republic, Honduras and Cuba in their efforts to have the World Trade Organization rule against plain packaging?

Why not just ignore an ineffective policy instead of making it only too obvious to all by such actions that it is in fact a grave threat to your industry?

Two key assumptions have underscored efforts to discredit the impact of plain packaging. First, critics assume the impacts of the law should have been evident immediately as it was implemented: as one colleague put it recently “within ten seconds of the law passing”.

Second, they assume (but never actually state) that the impact of plain packaging on smoking by children (the principal target) and adults was supposedly going to be greater than anything we have previously observed in the entire history of tobacco control.

In 1999, the late Tony McMichael, professor of epidemiology at the Australian National University, published a classic paper called Prisoners of the Proximate where he wrote about the need to understand the determinants of population health in terms that extend beyond proximate single risk factors and influences.

In tobacco control, both proximal (discrete, recent and quick-acting) and distal (on-going, slow-burn) effects of policies and campaigns can occur.
Price rises (and falls through discounting) can have both immediate and lasting effects, jolting smokers into sometimes unplanned quitting and also slowly percolating an unease about the costs of smoking that translate into quitting down the track.

Tobacco advertising bans are a good example of a policy that has such slow-burn effects across many years. Few if any quit smoking in direct response to tobacco advertising bans. They work instead by causing the next generations of kids to grow up in an environment devoid of massive promotional campaigns depicting smoking in positive ways.

I have often heard smokers say “plain packaging won’t make me quit smoking”. This is akin to the myopic self-awareness of those who swear “advertising (for any product) never influences me” while noting that it only influences the more impressionable.

Plain packs were unlikely to act suddenly in the way tax rises do, although the unavoidably huge graphic health warnings may well have acted like straws that broke the Camel’s back of worry about smoking. Their impact was far more likely to be of the slow-burn sort, where the constant reminder that tobacco, unique among all products, is the only consumer good treated this way by the law. It is exceptionally dangerous, with a recent estimate that two in every three long-term smokers will die from tobacco use.

In 1994 I wrote a now highly cited paper in the British Medical Journal which talked about the impossibility of “unravelling gossamer with boxing gloves” when it came to being certain about precisely why smokers quit. I took a day in the life of a smoker who quit, and pointed to the myriad of influences both distal and proximal that coalesce to finally stimulate a smoker to quit.

While a smoker might nominate a particular policy, conversation with a doctor or anti-smoking campaign as being “the reason” they quit, much of what went on before provides the broad shoulders of concern that carry the final attribution. There are synergies between all these factors and the demand to separate them all is like the demand to unscramble an omelette.

So what has happened to smoking in Australia since plain packs?

Data released this month from a national schools survey involving more than 23,000 high school children found smoking rates were the lowest ever recorded since the studies first commenced in 1984 (see graph). This momentum is starving the tobacco industry of new smokers, which is one important reason why all tobacco companies are now busily acquiring e-cigarette brands.

Proportion of 12- to 15-year-olds who smoke, 1984 to 2014

Trends in proportion of current (smoked in past seven days) and committed smokers (smoked on three or more of the past seven days) among 12 to 15-year old students, Australia, 1984-2014. National Drug Strategy report 2014.

With adults, National Accounts data just released show that for the 11 quarter-year periods since March 2013, consumption of tobacco products in aggregate fell an unprecedented 20.8%, while the previous 11 quarters it fell 15.7% and in the 11 before that, only 2.2%.

The latest available data on adult smoking prevalence we have is from 2013 and shows just 12.8% of Australians over 14 smoked on a daily basis. This is the lowest on record and again, the biggest percentage falls experienced since the surveys commenced (see graph).

Reductions in daily smoking among Australians aged over 14, 1991 to 2013

AIHW National Drug Strategy Household Survey 2013: preliminary findings. 2014 Author-sourced.

Meanwhile, the tobacco industry plods along funding heavily lambasted studies which purport to show none of this is happening.

The argument that plain packaging would cause illicit trade to boom was made with monotonous regularity by Big Tobacco between April 2010 when plain packaging was announced and its December 2012 implementation. When the industry lost its case in the High Court, the argument was quietly dropped.

Today, the industry explains illicit trade entirely by the heinous government tobacco tax rises cloaked in a sanctimonious rhetoric of speaking up for poor smokers and corporate citizen concern about tax avoidance bleeding Treasury. In all this it fails to mention that it has long used tax rises as air cover to quietly raise its own profit margins.

As I wrote recently in The Conversation:

From August 2011 to February 2013, while excise duty rose 24¢ for a pack of 25, the tobacco companies’ portion of the cigarette price (which excludes excise and GST), jumped A$1.75 to A$7.10. While excise had risen 2.8% over the period, the average net price had risen 27%. Philip Morris’ budget brand Choice 25s rose A$1.80 in this period, with only 41¢ of this being from excise and GST.

Ireland, the United Kingdom and France have already passed laws to introduce plain packs. Norway and Canada will soon, and New Zealand, Chile, Turkey, South Africa and Brazil have also made high-level noises about joining in too. The world has a lot to thank Rudd and Gillard governments (and particularly Health Minister Nicola Roxon) for taking this initiative, and the subsequent Coalition government for continuing to support it strongly as it continues to come under attack from those it has and will continue to hurt.

The ConversationSimon Chapman, Professor of Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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What’s next, a Senate inquiry into infrasound from trees, waves or air conditioners?

The Conversation

Simon Chapman, University of Sydney

At the centre of claims about wind farms allegedly causing health problems is the infrasound that wind turbines generate as they turn in the wind.

Infrasound is sound below 20Hz, which is generally inaudible. Wind turbines are just one source of artificial man-made infrasound. Others include power stations, industry generally, motor vehicle engines, compressors, aircraft, ventilation and air conditioning units, and loudspeaker systems. Everyone living in an urban environment is bathed in infrasound for most of their lives.

As I sit at my inner Sydney desk writing this I’m copping infrasound from the planes that pass some 200-300 metres over my house sometimes many times an hour, the sound of passing road traffic on a quite busy road 100 metres from our house, and the stereo system I listen to as I write. Don’t tell anyone, but I feel fine and I’ve lived here 25 years.

But infrasound is generated by natural phenomena too. These include rare occurrences such as volcanoes and earthquakes, but also sources like ocean waves and air turbulence (wind) that countless millions, if not billions, are exposed to on most days. Anyone living close to the sea is surrounded by constant infrasound from waves.

The inclusion of wind as a source of infrasound is of particular significance to claims made that wind turbine-generated infrasound is noxious. In a Polish research paper published in 2014, the authors set out to measure infrasound from wind turbines and to compare that with naturally occurring infrasound from wind in trees near houses and from the sound of the sea in and around a house near the seaside.

The researchers used the average G-weighted level (LGeq) over the measurement period. This is the standardised measurement of infrasound which approximately follows the hearing threshold below 20Hz and cuts off sharply above 20Hz.

The infrasound levels recorded near 25 100-metre high wind turbines ranged from 66.9 to 88.8 LGeq across different recordings. Those recording infrasound in noise from wind in a forest near houses ranged from 59.1- 87.8 LGeq. The recordings of sea noise near seaside houses ranged from 64.3 to 89.1 LGeq. These infrasound levels were thus very similar cross the three locations.

The peak 88.8 LGeq was recorded very close to the turbines – virtually directly under the blades. The lower 66.9LGeq was 500m away, which is more like a common scenario for the nearest residences to turbines. Similarly, for the other sources, highest levels were nearest the source.

Wind is, of course, a prerequisite for wind turbines to turn and generate their mechanical infrasound. Here, the Polish authors noted that:

natural noise sources … always accompany the work of wind turbines and in such cases they constitute an acoustic background, impossible to eliminate during noise measurement of wind turbines.

This is a fundamentally important insight: wherever there are wind turbines generating infrasound, there is also wind itself generating infrasound. And it is impossible to disentangle the two. Indeed, every time I’ve been near wind turbines, easily the most dominant sound has been that of the wind buffeting my ears.

In 2013, the South Australian Environmental Protection Authority measured infrasound in a variety of urban and rural settings. With the latter, this included locations near and well away from wind farms.

They reported that in urban settings, measured infrasound ranged between 60-70 decibels. In fact, at two locations – the EPA’s own offices and an office with a low frequency noise complaint – building air conditioning systems were identified as significant sources of infrasound. These locations exhibited some of the highest levels of infrasound measured during the study.

They concluded:

This study concludes that the level of infrasound at houses near the wind turbines assessed is no greater than that experienced in other urban and rural environments, and that the contribution of wind turbines to the measured infrasound levels is insignificant in comparison with the background level of infrasound in the environment.

Wind farm opponents claim infrasound is the cause of this Old Testament-like plague of plagues (now numbering 244 different problems). If that were true, how is it that hundreds of thousands of Australians who are daily exposed to infrasound in cities, in their houses surrounded by dastardly infrasound-generating fans, air conditioners and stereo systems, and those who live near trees or the sound of the ocean aren’t breaking down the door of those sworn enemies of infrasound Senators John Madigan, Nick Xenophon, Chris Back, David Leyonhjelm and Bob Day who brought us their scathing report on wind farms in June?

The explanation lies in factors we recognise frequently in risk-perception studies, popularised by Peter Sandman. Sandman has produced matrices of factors which have been often found to be associated with increased levels of community “outrage” about putative environmental threats to health.

Sandman distinguishes primary from additional factors, with primary factors being those which have been shown to be more strongly associated with increased levels of community concern.

I applied these to a case study of mobile phone tower complaints in the 1990s. I’ve now constructed the table below indicating the likely applicability of these factors to the case of predicting community worry about wind farms.

People don’t worry about infrasound in wind, trees and ocean waves because these sources are natural, while the same levels of infrasound from wind turbines are considered quite differently as they are sourced from what anti-wind farm activists like to call evil “industrial” wind farms.

The rare examples of people complaining who host wind turbines on their land for rental payment, compared with the far more common situation of non-hosting neighbours complaining, illustrates the voluntary vs coerced exposure factor, as well as the fair vs unfair factor. Those not benefiting from lucrative rental payments because of unsuitable local topography, while near neighbours can, understandably feel this as unfair.

Wind turbines are very memorable and exotic (a new experience to many), while wind in trees or the pounding of the ocean is very familiar and unremarkable, both factors likely to greatly diminish concerns.

Table: Primary and additional components predicting community outrage about putative environmental risks to health: the case of wind turbines. (two ticks = applies strongly to wind turbines; one tick = likely to apply less strongly)

The 2015 Senate (majority) report into wind farms roundly rejected the idea that psychosocial factors such as nocebo effects were largely responsible for the challenging historical and geographical variance in wind farm complaints. A nocebo effect is the opposite to a placebo effect: instead of exposure to an inactive agent making people feel better because of belief that it will, nocebo effects are when a benign agent makes people feel worse because they have been told it will.

The Committee, chaired by avowed wind farm opponent John Madigan, was emphatic that infrasound was the culprit but did not produce convincing evidence for this.

If the committee is sincere in its concerns about the health effects of infrasound, will we soon learn of a new inquiry about the pernicious and unappreciated dangers of living near the sea or trees, having air conditioners, stereos, ceiling fans, or travelling in motor vehicles?

The ConversationSimon Chapman, Professor of Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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