Steve Sailer on the "lead pollution causes crime" theory

I commented on the subject on 6th -- JR

As part of my continuing series on the causes of the 60s, let’s consider Kevin Drum’s revival (”America’s Real Criminal Element: Lead”) in Mother Jones magazine of the recurrent theory that lead poisoning leads to the decline of civilization.

When I was young, it was popular to blame the decline and fall of the Roman Empire on the ancients’ fondness for this soft and versatile metal. (Have you ever noticed that nobody is much interested in how the Roman Empire managed to last so long?)

That exposure to this heavy metal can be dangerous to humans has been recognized since the days of Hippocrates and Pliny the Elder. But lead was so useful in so many ways that more than a few American municipalities proudly named themselves after their lucrative lead resources. Leadville, Colorado is America’s highest elevated incorporated city. There are several Galenas, one of which is a tourist town in Illinois. There’s a Smelterville, which sounds like a city made up for The Simpsons but is actually a real place in Idaho.

Ironically, Drum stands the dominant narrative about the 60s on its head. Instead of the 60s representing enlightened emancipation from the shackles of 50s conformist culture, Drum finds the 60s, with their rising rates of crime and illegitimate births, to be the result of brain damage.

“If there are connections between lead poisoning and crime, there’s gold to be made in unraveling them.”
Known side effects of lead poisoning include lower IQ and reduced impulse control, which are in turn associated with poor decision-making, such as becoming a criminal or a single mom.

The lead-crime theory is, in essence, uncomplicated: Lead was added to gasoline between the World Wars, and a generation or so later, Central Park was full of muggers. Spiro Agnew couldn’t have come up with a funnier diagnosis of the 60s than what Drum has talked an increasing number of liberals into believing.

The theory is almost as malleable as the metal. If crime is high among blacks in a car-dependent Sunbelt city, it’s because particles from leaded gasoline are still in the soil. But if crime is high in an old industrial city where poor blacks mostly took public transportation, it could be due to lead paint.

Drum and Nevin attempt to blame lead poisoning for much of the difference between black and white crime rates. Nevin, for example, notes that the notoriously violent Robert Taylor Homes were built near Chicago’s Dan Ryan Expressway. (Ironically, one reason why mid-century liberals in Chicago had favored the construction of gleaming new housing projects was because of the tragic deaths of tenement toddlers who ate chips of lead paint they had peeled off the decaying walls.)

Yet one of the more obvious differences between Chicago’s black and white areas is the heavier traffic in the expensive, safe zones. People who can afford cars tend to move away from black slums, leaving them bleak. In the Chicago area, race and class palpably determine the homicide rate. For example, compare the next-door neighbors Oak Park and Austin west of The Loop. The Eisenhower Expressway runs through Oak Park, but not through Austin. Yet the homicide rate is several dozen times worse in Austin.

Drum, who lives in Irvine, at least should be familiar with Southern California, where South-Central is fairly light in traffic compared to the jammed freeway interchanges of upscale West LA and Sherman Oaks.

And across the country, the densest neighborhoods are typically the various Chinatowns, which suffer little street crime and enjoy high math scores.

Yet as far as Theories of Everything go, lead-caused-the-60s-crime-wave is one of the less derisible. Lead is bad for you, and it might have had noticeable effects on society as a whole.

The problem is coming up with ways to test the theory. A half-dozen years ago, I blogged (”Lead Poisoning and the Great American Freakout”) about the research that Drum finds so convincing today. One reality check immediately suggested itself: Back in the late 1960s, densely populated Japan was notorious for automobile-induced air pollution. Yet crime didn’t rise in Japan. The country remained an orderly, intelligent, non-impulsive culture.

That’s one strike against the theory. Another problem is that Jessica Wolpaw Reyes’s attempt to correlate small differences from when American states began phasing out leaded gasoline in the 1970s to when crime began declining in the 1990s isn’t convincing to many besides Drum. Reyes came up with statistically significant results for total violent crimes, but not for homicides (the most accurately counted crime), nor for property offenses.

Yet two strikes isn’t bad for a causes-of-crime theory. It holds up better than the famous Freakonomics abortion-cut-crime surmise.

Exactly how deleterious this metal is at low levels, at what ages, and through which modes of transmission remains murky. This doesn’t mean that lead wouldn’t cause increased crime by lowering IQ, all else being equal. But perhaps lead poisoning also diminishes crime by making its victims more sluggish, lacking in the initiative to go out and commit felonies.

On the other hand, perhaps lead pollution can help explain a little of the differences we see in black homicide rates between cities.

After Hurricane Katrina in 2005, I was widely denounced for pointing out that the bad behavior visible on television wasn’t necessarily representative of average African Americans. You shouldn’t assume the typical black would behave as badly as New Orleans’s blacks, who had been more homicidal than most other cities’ blacks for years, even before Katrina.

This was especially true of the Crescent City’s flood-prone and poverty-stricken Lower Ninth Ward neighborhood. Back in 2005, I speculated that the traditional high crime rates of New Orleans’s blacks were due to the city’s let-the-good-times-roll culture being unsuited for African Americans, who need more socially conservative cultures.

Yet perhaps lead plays a role in New Orleans as well. Heavy metals would tend to build up in the Lower Ninth Ward’s below-sea-level soil.

Notoriously, scientific papers end with a pronouncement that More Research Is Needed. It’s been six years since I first pointed out some of the flaws in the papers upon which Drum relies. Yet for all their weaknesses, they remain the state of the art in thinking about the impact of lead pollution on crime

SOURCE






Asthma: This junk science just takes your breath away

The claim that the smoking ban has reduced asthma rates is a case study in using ‘research’ to justify coercive policy

Earlier this week, the journal Pediatrics published a study which claimed that childhood asthma rates fell after the English smoking ban was introduced in 2007. But a closer examination suggests the claims have been puffed up – not that the media seemed to mind.

The study concludes: ‘The implementation of smoke-free legislation in England was associated with an immediate 8.9 per cent reduction in hospitalisations for asthma along with a decrease of 3.4 per cent per year.’

A quick look at the personnel involved should immediately arouse suspicion. The lead author is listed as Christopher Millett, an Australian social scientist who has worked in ‘obesity prevention’ and assists Stanton Glantz’s campaign to get smoking out of the movies. Glantz himself - founder of Americans for Nonsmokers’ Rights and a veteran campaigner for smoking bans - is a co-author. The study should be seen as another entry in Glantz’s unenviable canon of junk science, and as a case study in the media’s role in creating panics and distorting policy.

The ups and downs of asthma

First, it is necessary to understand a few things about asthma. Although many people intuitively believe that there is a close relationship between smoking and asthma, this is not borne out by empirical evidence. As the British Medical Journal (BMJ) noted in 2005: ‘A broad consensus exists that in most Western countries the prevalence of asthma increased over the last four decades of the twentieth century.’ This huge rise in asthma rates is totally inconsistent with the belief that smoking causes or exacerbates asthma, since we all know smoking rates declined sharply over the same period.

Asthma rates go up and down quite inexplicably. After rising at an astonishing rate for years, there was a large drop in childhood asthma cases in the UK from the early 1990s until 2001, since when rates have stayed fairly flat.

The reasons for this are not known, as the BMJ article notes: ‘While theories abound, we must admit that neither the rise nor the recent flattening or fall in the prevalence of asthma can be explained on the basis of current knowledge. Any single explanation would need to account for both the rise and fall of the prevalence of asthma. A substantial change in prevalence would require a large change in an important risk factor to which a large proportion of the population was exposed. Various explanations have been proposed to explain trends and geographical variations in asthma, including air pollution, tobacco smoke, aeroallergens, diet, and infections in early life, but none has been shown by epidemiological studies to fit the above requirements.’

A quick survey of other countries highlights the confusion. In Canada, the number of children with asthma rose in the 1990s, but the number of childhood asthma attacks fell. Childhood admissions for asthma in Australia fell in the 1990s, but rose in the 2000s, at a time when smoking bans were introduced. Adult admissions continued to fall, however. In America, rates of asthma - including childhood asthma - have been flat or rising slightly since 2001. And in the Netherlands, there was a huge increase in childhood asthma prevalence in the 1980s and 1990s which ended around 1995. As authorities have noted, ‘there has been no satisfactory explanation for this observation’.

Smoking and asthma

What does any of this tell us? Not much, except that it’s futile to predict whether rates of asthma will rise or fall in the future since the causes of the condition are not well understood. Asthma rates vary enormously between countries and fluctuate greatly over time, and no one really knows why. It also shows that if smoking (let alone passive smoking) has any impact, it is not big enough to show up in aggregate data. However, as we shall see, Glantz’s new study relies on the conceit that asthma rates can be forecast with precision and that the effect of passive smoking can be identified and isolated in the aggregate data.

Although there is no link between smoking and asthma rates at the population level, some epidemiological studies have found a correlation between childhood asthma prevalence and smoking households, just as there is a correlation between asthma prevalence and income. (Perhaps tellingly, there is also a link between smoking and income; income may therefore be the third variable.)

But, as the organisation Statistics Canada notes, ‘there was no difference in the rate of past-year asthma attacks between those in smoking and non-smoking households’. Between 1994/1995 and 2000/2001, in smoking households, the prevalence of asthma among children increased, but past-year attacks among those with asthma decreased. Curiously, only children in non-smoking households experienced an increase in the prevalence of wheezing or whistling in the chest. The presence of other allergenic factors in the home (pets, for instance), which was not assessed in the Canadian survey, may be related to the increase in asthma-like symptoms among children in non-smoking households.

Step one: the dubious study

So what about Britain in recent years? After dropping off in the 1990s, asthma rates have varied only slightly from year to year since 2000 and there has been neither a rise nor a decline in the medium-term. (The failure to reduce asthma cases is a source of frustration for Asthma UK.)

The graph below shows hospital admissions for asthma among 0- to 14-year-olds in England (the group studied by Glantz and his team). It shows that the smoking ban had no effect on rates of asthma among this group. The data come from HES England and covers all National Health Service (NHS) hospitals in England. Note that these are financial years, but the smoking ban began in July (2007). The graph shows 12 years’ data, whereas the Pediatrics study shows only 8.5 years.

Between 2000/01 and 2006/07, the average number of childhood hospital admissions for asthma each year was 23,747. Between 2007/08 and 2011/12, the average number of admissions each year was 23,851. In other words, the rate remained essentially the same before and after the smoking ban. Evidence from London below (red line) shows much the same picture for adults; there are similar statistics for England as a whole and north-west England in particular.

Whichever dataset you use, it is apparent that the rate of hospital admissions for asthma was higher in 2006/07 than in any other year in the series, albeit only slightly. This is crucial for Glantz and Millett’s hypothesis because it allows them to portray the rate as rising before the ban. No such claim can legitimately be made on the basis of a one-year peak. The data show several other peaks, for example in 2001/02 and 2008/09, which did not represent the start of a long-term rise.

Given such variability, predicting the number of hospital admissions for asthma even one year in advance is a mug’s game. Nevertheless, having asserted that numbers were on the rise, the authors of the Paediatrics study use a model – in other words, make a post-hoc quasi-prediction – to suggest that the rate would have continued to rise had the ban not been introduced.

Finally, having observed that the rate did not rise in reality, they conclude that the ban resulted in there being 6,802 fewer hospital admissions for asthma than there otherwise would have been. Note that their methodology means that it is not necessary for the rate to decline at all after the ban for them to claim the smoking ban reduced asthma cases. It is only necessary for the number of admissions in Glantz’s hypothetical parallel universe to be higher than the rate recorded by the NHS.

This is sheer junk science, using a trick that has been used before for similar purposes. It’s a ‘heads-I-win, tails-you-lose’ fiddle. The only way the authors’ hypothesis could be disproved was if asthma admission rates happened to soar up at an exceptional pace straight after the ban. Even that would probably not silence them since they would only say that, had it not been for the ban, the situation would have been still worse.

More HERE  (See the original for links, graphics etc.)