|The Week That Was
Feb. 11, 2006
The newly-established International Panel to Stop the Incipient Ice Age (IPSIIA) will celebrate its founding in a Baltic Cruise this summer with series of mini-symposia aboard ship and in various ports in a region that was covered with kilometer-thick sheets of ice during the first half of the Holocene - as recently as 5000 years ago. Building on a successful "dry run" in 2004 with co-founder of IPSIIA Dr. Klaus Heiss, we will start and return to Copenhagen, visiting all or some the following ports: Stockholm, Helsinki, St. Petersburg, Tallin, Gdansk, and Oslo in a 10-day cruise (most likely Aug 23 to Sept. 2).
For planning purposes, pls indicate yr interest and preferred alternate time frame. Cost per person will be about $2000, depending on date and type of cabin. We may also be able to get special transatlantic airfares to Copenhagen.
Further news: For those who are professionally inclined, the European Meteorological Society meets in Ljubljana, Slovenia, Sept 4-8, 2006.
The Strategic Petroleum Reserve is unlikely to protect against supply interruptions and should be sold off (Item #1).
The history of the "Spanish" flu pandemic of 1918 may hold some useful lessons. Did it start in Kansas as a horse flu? And why did it preferentially kill young , healthy people? (see Item #2) This information was found online at: _http://www.acsh.org/factsfears/newsID.694/news_detail.asp
California could soon ban all toxic compounds in consumer electronics sold in Cal (Item #3).
(R-NM) and Bingaman (D-NM) plan on legislation to mandate restrictions
on CO2 emissions (Item #4) - as a way to impose Kyoto on the US.
The anthropogenic Greenhouse effect has been greatly exaggerated. The observational evidence does not support the results of the climate models. But without such validation, there is little reason to trust model predictions of future Global Warming or to use them for policy decisions that can have severe impacts on national economies.
The country -
and the world --face real and pressing problems: Poverty, disease , and
terrorism. Global warming is a non-problem, most forms of mitigation are
deplorable, dangerous diversions of resources we cannot afford to waste.
Andrei Illarionov, a former economic adviser to Russian President
Vladimir Putin and staunch opponent of the Kyoto Protocol, deplores current
events in Russia (Item #5)
Says NASA Tried to Silence Him (Item #6):
But see comments
by Wallace Manheimer, Roy Spencer, and Fred Singer
How to question scientific authority - at a time when peer-review
no longer guarantees sound science (Item #7).
And now to Climate Science itself:
Eric Steig throws
cold water on climate effects from changes in ocean circulation (Item
R. G. Harrison and D. B. Stephenson, Proceedings of the Royal Society
A, January 2006, present empirical evidence for a nonlinear effect of
galactic cosmic rays on clouds - and climate. They measure cloudiness
by ratio of diffuse and direct solar radiation. It's good to have this
confirmation of the cosmic-ray - climate effect, first discussed by Svensmark
and Marsh and generally ignored by climate modelers.
Finally, a reader sends another example of scientific double-speak
hard to avoid the conclusion that
" really means
The rise in fuel prices that followed Hurricanes Katrina and Rita has prompted many members of Congress to call for new and expanded federal reserves of crude oil, diesel fuel, home heating oil, jet fuel and propane. Proponents of stockpiling claim that if the government were to hoard those commodities when prices were low, it could unleash them on the market when supplies are tight, thus dampening price increases and stabilizing the market.
But the experience in this country with the strategic petroleum reserve strongly suggests that such government-managed stockpiles are a waste of taxpayers' money. Rather than increasing the stockpile, the reserve should be emptied and closed.
Public stockpiles are far more expensive to maintain than many analysts realize. For example, after adjusting for inflation, the petroleum reserve has cost federal taxpayers as much as $51 billion since it was created in 1975. If you divide that sum by the amount of oil in the reserve, that's $80 per barrel by the end of 2003.
Of course, even at that price, some would argue that the reserve is still worthwhile under certain circumstances. That's because many economists maintain that it's not the cost of oil that harms the economy during a price spike, but the microeconomic uncertainty caused by supply disruptions, the costs of adjusting to high prices and the political reaction to soaring energy prices. If large volumes of federal oil were released at the early stage of a supply shock, it could temper those effects.
But the government has never employed the reserve in this manner and probably never will. Politicians are simply too loath to risk a premature release of public crude because one can never know how long a supply disruption might last, how high prices might climb or whether additional disruptions are on the horizon.
In its 30-year history, the 700-million-barrel reserve, which was recently authorized by Congress to expand to 1 billion barrels, has been tapped only three major times: 21 million barrels were released at the onset of the Persian Gulf war in the early 1990's, 30 million barrels in September 2000 and 24 million barrels last year after Hurricane Katrina struck. Those releases were so small considering the size of the reserve that one wonders why politicians are so dead set on having a billion barrels.
Another reason for the reluctance to tap the reserve is the widespread belief that it should be maintained as a hedge against an embargo like the one America experienced in 1973. But embargoes are not the powerful "oil weapon" that people think they are. Once a producer sells its oil on the world market, that oil can be bought, sold and rerouted repeatedly. The producer cannot control the oil's ultimate destination. The globalization of oil markets ensures that the United States will always have access to Persian Gulf oil whether OPEC members like it or not.
But what if, instead of an embargo, there was a catastrophic disruption in supply, say the kind that might occur were Al Qaeda to seize power in Saudi Arabia? That scenario is worrisome, but the reserve would not be able to do much. No public stockpile would ever be large enough to deal with such a huge disruption. For instance, even if all of the oil in the reserve were released in 2004, it would have amounted to only 2.6 percent of the world supply -- nowhere near enough to replace the oil from a major producer on a sustained basis. Building a reserve large enough to replace Saudi production would prove outrageously expensive.
Fortunately, it is highly unlikely that political motivations would lead an oil producing state to cut its production so drastically. Those nations need oil money as much or more than oil-consuming nations need the oil. Even anti-American regimes like Iran and Venezuela's have no interest in economic suicide by suspending oil production.
Regardless, getting rid of the public petroleum reserve would not mean destroying all oil reserves. Private oil inventories are three times larger than public inventories and would be even larger if investors didn't have to worry about the government flooding the market with public oil during a price spike. Inventories, after all, are costly to maintain and will only be profitable if market actors can "sell high" during a price increase.
In fact, economists agree that every barrel of oil we put in the public reserve displaces oil that might otherwise have gone into private inventories. How much displacement occurs is unclear, but there is little doubt that it's significant.
If the reserve is thought of as an insurance policy against high prices, the cost of the policy has been more expensive than the dangers the stockpile is meant to prevent. Americans should resist the drive to expand public stockpiles. Instead, we should sell while the selling is good.
Jerry Taylor and Peter Van Doren are senior fellows at the Cato Institute.
How much do we really know about the origin and spread of the 1918 flu pandemic? Comparisons with other pandemics reveal patterns and lingering mysteries.
Watching the Animals
"The horses growing better, a cough and sore throat seized mankind." This was the news from Dublin toward the end of 1727, reported in Charles Creighton's monumental History of Epidemics in Britain -- Volume II -- From the Extinction of the Plague to the Present Time, Creighton's "present time" being 1894.
Matters had been much the same in 1688 as in 1727. A "short time before the general fever, a slight disease, but very universal, seized the horses too: in them it showed itself by a great defluxion of rheum from their noses." Creighton's source "was assured by a judicious man, an officer in the army of Ireland there were not ten horses in the regiment that had not the disease." In Dublin "not one [man] in fifteen escaped."
Then in Huxham in 1732, some months prior to an influenza outbreak, the horses were affected by "the strangles." This seriously unpleasant term seems to be the most common synonym for horse flu, though in World War I, la gourme, a term used by the French military's veterinarian staff also crept into English. (You can look it up, though Google will first ask if you didn't mean "la gourmet.") Whether called gourme, horse flu, or the strangles, this was a nasty disease. By April 1918, civilian horses in France had also been affected. The April timing is intriguing because the first reported cases of the disastrous "Spanish Flu" among humans had been in March. But that had been among soldiers at a cavalry training site in Kansas.
At a professional meeting in 1924, a Dr. Reece, about whom I know nothing more, spoke of the "remarkably large number of observations" of coincidences between influenza epidemics and "epizootics of the same character," starting in horses, then "dogs, cats, and the like." It seemed that aside from the disease itself and coincidences in timing, however, the only common element among dogs, horses, and humans was crowding. Sir William Hammer added that "epizootics may precede or follow epidemics," and they may accompany epidemics, too. Horse flu and human flu had both been troublesome in 1657-1659, 1727, 1737, 1743, 1760-1762, 1775, 1788, and 1889-1890, but a recurring question for modern epidemiologists is whether the diseases, equine or human, had been correctly identified. Creighton, a century ago, was cautious about making such judgments, as when he noted that "if Whitmore has made no mistake in his dates," the spring of 1658 and possibly the following year saw: universal coughs and catarrhs, as if a blast from the stars
Although the sequence of events in not entirely clear, this explosion of an influenza-like illness was apparently followed by "a great death of coach-horses almost in every place...and it has [now] come into our fields."
From daily experience, Creighton and all his sources had been familiar with cities in which large numbers of horses had been kept. In times past, people would have had detailed knowledge about horses in cities, knowledge that has been universally forgotten in the generations brought up in the age of the automobile. But as recently as the 1920s, annual statistics for horses were cited for places such as Omaha, Nashville, Atlanta, and Chicago, in some instances tabulated along with cause of death, somewhat as they are for humans. The problems of horses in cities had even given rise to a tongue-in-cheek warning that by such and such future date, the streets of London would be filled to the second story with horse manure.
Horses and mules -- which are less susceptible to equine flu -- had also been ubiquitous in all the world's armies. Pigeons too had been a common accompaniment of the military in World War I. (In the Paris Flea Market in the 1980s, I stopped at a stall with a stock of World War I pigeon-carriers. Pointing out details of their design and construction, the dealer assured me they were from the American army, not French, "the perfect thing for an American in Paris.")
There were also historic flu epidemics that were not associated with reports of a corresponding disease in horses or mules -- and episodes of equine flu with no flu-like illnesses among humans. But the association of the two appears to have been well known. Yet while insisting on this matter, I have avoided mentioning a key observation: people do not catch the flu from horses. Creighton's compilation of 1894 seems to contain nothing to indicate to the contrary nor, really, does A.J. Williams' "Analogies between Influenza of Horses and Influenza of Man" in the Proceedings of the Royal Society of Medicine for February 24, 1924. Williams had perhaps been too ambiguous in his original oral presentation, however, so a Professor Hobday rose to insist that there were no reports of transmission from horses to men or vice versa. This is how things then stood and pretty much as they now stand. About the best we can do is quote a statement made in 1919 by George A. Soper, a major in the United States Sanitary Corps whose conclusions were cited and emphasized by Alfred Crosby in his America's Forgotten Pandemic (first published in 1976 under the title Epidemic and Peace: 1918). In a contribution to The New York Medical Journal, Major Soper noted that despite many epidemiological and clinical similarities, horse flu and human flu were not identical, nor were they transmissible from the one species to the other, but "it would seem probable that a more thorough knowledge of the disease in horses would yield facts of great value." As concerned horses, Soper mentioned transmission via the respiratory tract, sudden onset, fever, cough, indications of muscle and joint pain, and explosive spread over whole continents on occasion, features that characterize human influenza as well. Soper also included an element I have not seen elsewhere, that horse flu was thought to be transmissible via feces and stable dust.
Dogs can catch influenza directly from horses, and humans can get it directly from pigs and vice versa. Humans can also get the flu from diverse avian species. Direct species-to-species transmission is relatively rare, however. Usually a mixing-bowl species or individual is needed, with a reassortment of viral genes taking place in a creature -- human or not -- that has become co-host for viruses originating in different species.
The Nightmare of 1918
The "Spanish Flu" wasn't Spanish at all. But at the time the flu raged through Europe, many countries were at war. Spain was neutral and did not impose press censorship, so journalists there could print the demoralizing truth, namely, that the country was going through a horrific epidemic. Elsewhere people whispered, muttered, or screamed that it was an Allied plot or that the Hun had once again let loose a poisonous gas. And what censor would pass an article saying that the enemy had been so terribly successful? In truth, the whisperings, mutterings, and screams, whether from the Allies or the Axis, seemed to have had some logic to them, for those most targeted by the 1918 flu were in the prime of their lives, military age, essentially those between the ages of twenty and forty.
Influenza is also an endemic seasonal disease that is always with us. In the U.S., some 35,000 flu deaths occur in non-epidemic years, primarily among children, older people, and others who lack fully-functioning immune systems. In 1918, by contrast, those in the fifteen to thirty-four age bracket who came down with influenza or pneumonia (the most common and deadly complication of the flu) were about twenty times more likely to die than had been the case in 1917, a non-epidemic year. And, of course, many, many more were catching the flu in 1918. Estimates vary. Twenty million died worldwide. Or perhaps fifty million. Or 100 million. Or some other large figure. In India, with its youthful population, mortality reached an estimated fifty per thousand. As in the U.S., the disease in India followed the railroads, and when military horses shipped from Australia to Calcutta arrived with a nasty strain of equine flu, it spread across India with the rail transport of cavalry.
The flu of 1918 was exceedingly contagious and is estimated to have affected over one fourth of the U.S. population and one fifth of the population worldwide. These estimates are not necessarily at all accurate. It is true that doctors everywhere were badly overworked and that quite a few medical personnel were dead before they could fill out and sign death certificates or other forms. But the real problem in trying to make estimates is simply that influenza was not a universally reportable disease in those days. Until 1918, it had not been considered sufficiently serious. But in 1918, the flu virus became "unlike any strain ever seen."
It was not just deadly. It was quick. According to a young woman working at the military laundry at Camp Funston, Kansas: "We'd be working with someone one day, and they'd go home because they didn't feel good, and by the next day they were gone" (Barry, 2004). Within months of the start of the epidemic, gauze face masks were being widely used and vaccines and various treatments were available. None of them actually worked, but they did much to calm nerves. Many people eventually came to terms with the fact that doctors could not do much. What was really needed was nursing care, and calls went out to anyone with the least bit of training in nursing. Many of the best were overseas with the troops, but older women and student nurses came forth. Young and old, many of these courageous volunteers caught the flu and died themselves, with mortality among the younger women commonly running exceedingly high. Another group particularly susceptible to the 1918 flu were pregnant women; one study showed an incredible 71% death rate among pregnant women who had been hospitalized with the flu.
It was an awful disease, which, due to the war and the accompanying censorship and the jolly peace that followed, was half forgotten until Crosby's book in 1976. It was also a peculiar disease. Although it eventually struck a broad portion of the population, it had seemingly started among the young and most fit, and from beginning to end it would be most efficient at killing individuals whose immune systems were the best H. sapiens can produce. There are no usable statistical measures, but here and there doctors in hospitals, nurses in wards, sailors on ships, and soldiers in barracks reported that it was the most robust, strongest, most fit, disease-free athletic sorts who suffered the worst. Post-mortem studies on such victims of the 1918 epidemic often showed enormous damage to the lungs, which could not at that time be explained. Years later, it was realized that such victims had literally drowned in the waste products of their own powerful immune reactions to the virus. As Crosby put it, "a springtide of fluids overwhelms the lungs." Thus in 1918, in contrast to other flu epidemics, many robust young people died of the influenza itself -- rather than from secondary infections of pneumonia-causing bacteria, the standard cause of death among those with weaker immune systems. They died so rapidly that pneumonia-causing bacteria had had no time to establish secondary infections.
Darkness in Kansas
Despite the name "Spanish Flu" and the endless accusations aimed at the Hun and speculations that the epidemic had started in China, the first clinically demonstrated cases were at Camp Funston, Kansas, a site established to train troops in World War I. (Funston still exists, incorporated into Fort Riley.)
A recurrent complaint at Funston in those days arose from a twofold unpleasantness. First, in common with much of the American Midwest, the camp was subject to severe dust storms. The experience at Funston was doubly unpleasant, however, due to the great concentration of horses and mules on the base and the manure they produced. I have not seen any figures for the actual number of animals, but they were sufficiently numerous to produce nine tons of manure a week.
On March 9, 1918, despite an impending dust storm, standard practice at Camp Funston was followed and the manure was burnt. The result was a stinging yellow haze with the sun going "dead black." Or so it is said. There had been similar days at Funston in the past and presumably elsewhere, but this event (if it actually occurred as related) was remembered as particularly severe, and the clean-up that night supposedly involved a hundred men and many hours of raking and sweeping.
According to some websites, it was two days later, "shortly before breakfast March 11th," that Company cook Albert Gitchell reported to the infirmary with a "bad cold." The March 11th date is most probably incorrect, however, and is perhaps a storyteller's concoction intended to tie in with the account of the manure-burning. Better sources give March 4th as the date of Gitchell's illness. In any case, Corporal Lee W. Drake was right behind Gitchell with similar symptoms, and by noon the Camp Surgeon had a 107 flu patients on his hands. Within three weeks, the number of sick and dead at Funston was above a thousand. In the next two months, over 500 prisoners at San Quentin penitentiary also came down with the illness, followed by comparable outbreaks at Camps Hancock, Lewis, Sherman, and Fremont. It is said that there were few incidences of the flu within the general population during these months, and although self-censorship at the newspapers has to be taken into account, later investigators have concluded that there had been nothing special to report. Civilians had remained healthy that summer.
In September the disease reached Boston, first affecting sailors and shipyard workers, then soldiers, and then moving into the general population and overseas. Some of the most awful-sounding accounts are those of outbreaks on the badly overcrowded troop transports on their way across the Atlantic. An often-cited sailor's diary reads, "October 5 -- fifteen more bodies have just been buried from the President Grant." During the last two months of the war, over 4,000 American servicemen died at sea or after being put ashore for hospitalization at Halifax. There were also those who died the first few days after arriving in Europe. Troopships disembarking large numbers of sick and dying men in French ports hindered the Allied effort, but such things were only written about after the war.
Some people have associated the flu outbreak at Camp Funston with episodes of manure burning, whatever the exact dates. But in his The Great Influenza: The Epic Story of the Deadliest Plague in History (2004), John M. Barry suggests that the ultimate origin of the 1918 pandemic is to be found elsewhere. Barry went back to original sources, always the best procedure if time is available, and in doing so, he identified a Dr. Loring Miner who in 1918 had had a decades-old medical practice in sparsely-populated Haskell County, Kansas, some 300 miles west of Camp Funston. Doing his rounds from town to town in "late January and early February 1918," Miner encountered a new ailment that he diagnosed as influenza, signaling the U.S. Public Health Service to warn of "influenza of severe type."
Newspapers across the U.S. in 1918, whether large or small, had been reluctant to publish items that might hurt morale. Nevertheless, on February 14, 1918, the Santa Fe Monitor in Haskell County (as cited by Barry in 2004), reported: "Mrs. Eva Van Alstine is sick with pneumonia. Her little son Roy is now able to get up...Ralph Lindeman is still quite sick...Goldie Wolgehagen is working at the Beeman store during her sister Eva's sickness...Homer Moody has been reported quite sick...Mertin, the young son of Ernest Elliot, is sick with pneumonia...Pete Hesser's children are recovering nicely...Ralph McConnell has been quite sick this week." A week later, the same paper reported, "Most everybody over the country is having la grippe or pneumonia."
In 1918 the population of Haskell County was 1,720, including many fit military-age men, all of whom trained at Camp Funston along with some 50,000 others before being shipped overseas or being buried as flu victims. The issue of the Santa Fe Monitor with the news that "most everybody over the country is having la grippe or pneumonia" also reported that "Dean Nilson surprised his friends by arriving at home from Camp Funston on a five days furlough" and that Ernest Elliot left "to visit his brother at Funston just as his child fell ill" (Barry, 2004). The February 28th issue recorded the departure of John Bottom for Funston, and it is clear that there must have been very many other comings and goings between the camp and parts of rural Kansas, of suppliers of fodder, for example. It is also clear that there must have been comings and goings of horses.
Tracing the Spread
The incubation period for influenza is very rapid, just one to three days, which partially explains how and why the flu is able to spread so rapidly. Another reason is that individuals about to come down with the flu may spread the virus before they develop symptoms. (These same properties characterize most epidemic diseases.) Influenza subsides once it runs out of susceptible people to infect, but after an estimated ten to thirty passages through humans, the virus may change and adapt to a different sub-population.
The flu virus in the fall of 1918 was not identical to that of the spring disease, and toward the very end of 1918 additional mutations gave rise to a third wave. This was less deadly than the second but still a truly terrible disease to which individuals who had survived infection during one of the earlier waves had only partial immunity. The flu was still present through 1919, and in 1920 the reported death rate by influenza among young adults was still well above normal. "Just-married" couples were mourned throughout the epidemic, and the parents of young children sometimes died within days of each other. During the second wave, feverish, newly-orphaned children were found dazedly wandering city streets.
Differing by a week with the sources mentioned above, Crosby and Barry give March 4th as the day the first soldier at Camp Funston reported ill with symptoms of influenza. This fits Barry's claim that the epidemic may have originated in Haskell County in January or early February 1918. If so, as Barry writes, it might readily have died out for lack of susceptible human hosts in sparsely-populated Haskell, where the epidemic was so short-lived that school had reopened with healthy children by mid-March. But, Barry writes, the war then brought the flu to Funston.
There is nothing obviously wrong with Barry's belief that the epidemic started in Haskell County, but it is of limited value because it leaves so many important questions unanswered. Why Haskell County? Why Funston? Why the virulence of the disease? Why was it especially severe among individuals who were fit? Was the disposal of horse manure crucial? Valid answers would also have to be consistent with the very recent claim that the human virus of 1918 had an avian source.
The Santa Fe Monitor mentioned two-way traffic between Haskell County and Camp Funston, but there seems to be nothing special about Haskell County aside from the presence of the flu-like disease somewhat before March 1918. Camp Funston, on the other hand, was special. First of all, there was the crowding. Then there were the horses and mules and their weekly output of nine tons of manure. And then there was the select presence of fit young men and women to the near exclusion of anyone else. (There were enough young women at Funston for weekend dances but, I would guess, few babies, children, or older people other than some senior officers and their wives.) So if a weak or "standard strength" flu virus had been brought to Funston, perhaps by birds feeding on undigested seeds in the manure, it would have found itself in proximity to an unreceptive human population whose members all possessed well-functioning immune systems. A soldier who caught this flu prior to March 1918 would have presumably been subject to a few coughs and perhaps some aches in his joints. He might well have avoided a visit to the camp hospital, since in the wartime society of the U.S. during this period, the very worst thing to be was a "slacker." (Following a disappointment in love, my grandfather's brother Jake left home as a very young man and joined the U.S. Customs Service in the Philippines. There, around the turn of the century, he caught a tropical disease and had to be repatriated. He was later exempted from military duty. When the draft was again activated in the 1940s, Uncle Jake was at pains to explain to anyone who would listen that he had not been "a slacker" during The Great War.)
Weak or standard-strength versions of avian or avian-equine or equine-avian influenza may have passed from soldier to soldier at Funston without necessarily exhibiting consequences severe enough to be preserved in military records or memories. And those who carried the virus might have included men belonging to the prime-of-life cohort, such as Dean Nilson, who had made a round trip between Funston and Haskell County while on furlough. In Haskell they would have encountered people whose immune systems were far weaker, some whose identities are known to us: "Pete Hesser's children," "Mrs. Eva Van Alstine's little son Roy," and "Mertin, the young son of Ernest Elliot," who had been "sick with pneumonia."
In these children and anyone who may have picked up the virus from them, the particular viral strain would have undergone changes that could then have been brought back to Camp Funston. While this is hypothetical and will perhaps forever remain so, we know that while the children of Haskell County were recovering and heading back to school, a highly contagious version of the flu began to run its course through the soldiers in training at Camp Funston. At this stage, the illness gave few signs of becoming the horrific thing Barry calls "the deadliest plague in history." According to Crosby, the flu at this stage usually meant "two or three days of misery" and in any case the epidemic at Funston waned rapidly, "bobbing up only now and then as new lots of draftees arrived." It was much the same story throughout March and April 1918 as the disease spread through Camps Oglethorpe, Gordon, Grant, Lewis, Sherman, Doniphan, Fremont, Hancock, Kearney, Logan, McClellan, Sevier, and Shelby, an unpleasant countrywide epidemic in the military that at this stage had still not spread into the civilian population. Some unfortunate soldiers at Funston and other camps had indeed died, but the cause of their deaths generally appears to have been pneumonia and other secondary complications. For although it was highly contagious, the Funston-style version of the 1918 flu -- "the first wave" -- was not itself a great killer. The second wave, which was the dreadful pandemic itself, would not come until the autumn when it would break out from the military camps on the East Coast.
The sequence of events described above depends on mutations of the 1918 flu virus. These produced a sequence of events that could not and cannot be predicted in advance. Simultaneously, a different sort of disease pattern was being traced out within particular populations, military camps, towns, and cities (and perhaps ships). This pattern depended on the number of local person-to-person passages of the virus, and the pattern produced by the sequential passages was always the same: those struck in the first ten days were far more likely to become severely ill than those affected after the virus had undergone a number of person-to-person passages. By October 1918, mutational changes to the virus had rendered it especially deadly. It then weakened everywhere with passages from person to person, and by late November conditions were briefly very much better. But additional mutations then set off a third wave in December. In common with the second, it was worldwide. Crosby, who touched on such matters at many points in his study, concluded that a patient's outcome depended primarily on the virus rather than the care he received.
It looks as though the human version of the "1918" epidemic had started at Camp Funston at the end of 1917 or toward the beginning of 1918 with birds, horses, manure, and the burning of manure all perhaps implicated. It was not then able to cause human illness sufficiently severe to be recorded or remembered. Yet it had enormous potential for harm because it was by then already adapted to people with first-class immune systems, passing among them and perhaps producing the occasional cough or touch of fever, if that. Its ecological niche was strictly among the healthy. It knew no other type of host environment. In February and perhaps January 1918, carriers of this flu variant had mixed with the general population in Haskell County where, as is typical, the virus passed from person to person, undergoing unknown changes. When it returned to Funston in late February or very early March, it spread, causing considerable short-term miseries, but not as an especially deadly disease. The virus at this stage was active, contagious, and disease-causing but it was confined to an inhabitual ecological niche characterized by host-individuals with strong immune systems: army nurses, men in military training camps, troops moving about on trains, dockers, miners, and men in prisons. And as luck and the Kaiser would have it, these individuals were frequently forced into crowded circumstances, tightly packed among others with similar immune profiles and then shipped from one camp to another and then overseas.
As a consequence of its passage through the general population in Haskell County, some of the early strains of the 1918 influenza virus were capable of surviving and multiplying outside their preferred niche and eventually more or less thriving in other environments. Still, it would always remain a disease of the robust, one Swiss doctor recording that he had never seen a severe case in anyone over fifty.
The virus might be compared to a Wall Street employee who could readily thrive if transferred to a high-stress environment in Washington or London but might or might not be able to adapt to a low-stress job as a pool cleaner. In general, it is only the individual creature itself -- human, animal, or microbial -- who determines whether a new environment is a good one. That's why zookeepers have so much trouble keeping certain animals. It is much the same with medical researchers, who can do little better than trial and error in selecting a suitable medium on which to try to culture unfamiliar bacteria.
Lessons from 1918
Some potentially useful lessons emerged while researching this material. One involved the immense danger of crowding and insufficient ventilation. Men in wind-blown trenches had far less flu -- or perhaps it was less flu with pneumonia -- than those living in crowded barracks behind the lines. The risk of the flu was far higher in the spic-and-span military camps on the East Coast of North America than in Europe's muddy trenches, and this was not something it took a statistician to detect. French soldiers who left the crowded barracks for the front reduced their chances of getting the flu by a factor as much as twelve (Crosby, 2003, p. 153). The dangers of crowding were apparently double, a greatly increased risk of catching the flu -- and, it seems, a similarly greatly increased risk of dying from it. Sailors on ships came down with the flu just as frequently as the tightly-packed troops they were transporting. But their onboard living conditions and daily routines -- which presumably excluded playing cards for long hours below decks -- provided them with a systematically lower mortality rate, lower by a factor of three to five.
Another potentially useful lesson relates to what have (inexactly) been called "relapses." Deaths among recovered patients were not necessarily caused by the flu itself, nor its secondary complications. The risk for newly recovered patients was that their immune systems were so exhausted that exposure to most any infectious agent at all in the four to six weeks following recovery from the flu could be fatal. The cause of death could be a tertiary factor, such as the sniffles.
There are other lessons, too, though they do not always apply to today's world. It is clear, for example, that the flu could be avoided by total isolation. Eskimos were so severely affected by the epidemic that there had been talk of the possible disappearance of the entire people, but at least one Eskimo family who were living by themselves with no contact with others had had no incidences of disease.
One symptom of the pandemic of 1918-1920 may not have been given sufficient attention. In diverse countries around the world, flu patients complained of diarrhea (see Crosby, 2003, Ch. 9). Diarrhea is not "supposed" to accompany human flu -- yet when stool tests for the usual bacterial culprits and for amoebas were carried out on U.S. military personnel, the results were systematically negative. Whether or not there is a useful lesson here, this anomaly should not be ignored, and it should be noted that in birds the flu virus normally infects the intestinal tract.
Another highly troubling issue was the impaired judgement and mental stability of many after recovering from severe cases of influenza -- a matter which may not be specifically limited to the flu of 1918-1920. "Toxic involvement of the nervous system" was one term and " slowed cerebration" was another. Individuals who were touched appear have included Woodrow Wilson who, according to one aide, had "manifested peculiarities" after coming down with typical symptoms of influenza plus severe diarrhea in early April 1919.
The good news is that the conditions in 1918 were a product of the times
and are unlikely ever to be repeated. Although Creighton's survey of historic
epidemics shows that the flu can be very unpleasant indeed, a strain of
influenza will probably never again be offered such a highly specific
and frightfully dangerous niche within the human population. Barring bad
luck, the 1918 epidemic will permanently retain its title as "The
Deadliest Plague in History."
California state legislator Lori Saldana and a California recycling advocacy group are expected to introduce legislation to expand soon-to-be released restrictions on the presence of toxic compounds in electronic equipment sold in California. The proposed legislation, which would expand California's electronic waste recycling law of 2003 that targets consumer electronics, is likely to be modeled after the Restriction of Hazardous Substances (RoHS) Directive adopted by the European Union, according to a legislative source who spoke to Risk Policy Alert. The EU Directive, which takes effect July 1, restricts the use of six hazardous materials in the manufacture of various types of electronic and electrical equipment, including lead, mercury, cadmium and chromium. The proposed legislation could cover all electronic equipment, including industrial equipment, tools and many electronic components, basically anything with a plug.
Sen. Pete V. Domenici and Sen. Jeff Bingaman, February 2006
The purpose of this document is to lay out some of the key questions
and design elements of a national greenhouse gas program in order to facilitate
discussion and the development of consensus around a specific bill. We
recognize that there are many ways to structure such a regulatory program
and that there are entirely different approaches that might include a
carbon tax, technology incentives and voluntary programs, but we have
limited our consideration here to mandatory market-based systems contemplated
by the Sense of the Senate Resolution.
A new model of Russia has taken shape. The state has become, essentially, a corporate enterprise that the nominal owners, Russian citizens, no longer control. Indeed, changes in legislation and limitations on political freedoms have effectively devalued the shares in this company - call it Russian State - that ordinary Russians hold, while an elite class of investors enjoys ever increasing privileges.
State-owned companies have become the assault weapons of this corporate state. Having mastered the main principle of state-corporatism - "privatize profit, nationalize loss" - they have turned to taking over private-sector companies, sometimes at cut-rate prices. Their victims include major industrial companies like Yuganskneftegaz, Sibneft, Silovye Mashiny, Kamov, OMZ, and Avtovaz.
Companies that are still in private hands resemble ever more closely their state-owned siblings. Any request from the state - whether it's a donation to a project or the sale of the company itself to "correct" buyers - is fulfilled. The fate of Mikhail Khodorkovsky, the chief executive of the Yukos oil company who is now in a penal colony after falling out with the Kremlin, is known to all.
Meanwhile, a guiding principle of Russia's new economic model is selectivity. One company is confronted with the maximum possible (and sometimes impossible) tax bill; another gets unique exemptions. One company is forbidden to sell shares to foreigners; another gets overwhelming state support for such a move (along with financing beyond any limits set by law). One company is not allowed to hire foreign workers; another is encouraged to do so. One set of buyers pays one price; another, five times as much.
It is not only economic freedom that has disappeared in Russia. Political freedom is also gone. The human-rights monitor Freedom House last year moved Russia from the group of "partly free" countries to the "not free" group, which includes Cambodia, Rwanda and Sudan.
Politically, the corporate ideology may seem unclear: it does not look communist, or liberal, or nationalistic, or imperial. Instead, it is an ideology of "nash-ism," or in English, "ours-ism," in which subsidies, credits and powers are handed out to those who are "nashy."
This ours-ism does not know national or ethnic boundaries. The former chancellor of a foreign country is made a member of the corporation and becomes "our man in Europe." Meanwhile, a Russian businessman who created a company that brought billions into the national treasury turns out to be an "other" and is exiled to the depths of Siberia.
The entire might of the Russian State is thrown behind "our" members of the corporation, whether this means refusing to allow Kazakhoil to travel to Lithuania via a Russian pipeline, switching off electricity to Moldova or waging a "gas war" against Ukraine. Russian imperialism has taken a distinctly corporate image.
The point of the new model is to redistribute resources to "our own." The rule of law is only for civilized countries. Fair business practices are only for countries that want to catch up with the developed world. Good relations with foreign neighbors are necessary only if Russia is interested in long-term development. The corporation has other goals.
Is it only in Russia that this model exists? No, there are other countries like this: Libya and Venezuela, Angola and Chad, Iran and Saudi Arabia. Russia is one of them now. And yes, this politico-economic model can last for quite some time. In some OPEC countries it has survived for a third of a century; in Venezuela, for half a century. It can survive even without high prices for energy. Cuba and North Korea have even more impressive models, and they don't even have oil. And then, of course, there was the Soviet version of this model.
So from a historical point of view, there's nothing particularly novel about the new Russian model. But choosing it today, at the outset of the 21st century, is nothing other than deliberately choosing the third-world model. More precisely, the model of a very specific group of countries in the third world whose long-term prospects are well known no matter how much money they get from oil, no matter how many pipelines they control at home and abroad, and no matter what saccharine stories they tell on TV.
It is a historical dead end. No country that has set off on this road has become richer or stronger or more developed. Nor will Russia. It will fall farther behind. And the price will be paid, as usual, by Russian citizens.
In a democracy, political change is linked to a change of rulers, which occurs regularly and at minimal social cost. In countries with limited freedom, a change of rulers also occurs - as with the "velvet revolution" in Czechoslovakia and the "orange revolution" in Ukraine - but the social costs are much higher.
Measures that the corporation has taken to prevent a similar revolution make change highly unlikely in Russia in the short term. But power will shift - sooner or later. When it does happen, it may not be as velvet. In this case, the cost to the country will be incomparably higher.
It is difficult to say when or how this change of power will occur. For those who cannot accept a corporate state, or the Venezuelization of the economy, or the degradation of social life, the current situation seems nauseating: Before there can be a deed, there must be a word, and the most important mass media are under the corporation's control.
But one can start one's own separation from such a state through a campaign of non-participation. In this way, working from below, one can begin to restore civil, political and economic freedoms, freedoms that were offered to Russian citizens in 1905, 1917 and again in 1991, but squandered. If we succeed, we may get a new Russia - free, open and tolerant. A dynamic, developed and steady country, standing on its own feet, genuinely respected by its neighbors. A country with a future. Another country.
Andrei Illarionov was an economic adviser to President Vladimir Putin
of Russia until resigning in protest in December. The article, a version
of which originally appeared in the Russian newspaper Kommersant, was
translated by The International Herald Tribune from the Russian.
"Obviously I do not think the government has the right to silence a scientist for stating his scientific view. However I have rather mixed feelings about this case, and find I am sympathizing more with the government.
For a scientist in the civil service, the rules really are not the same as they are at, say, a university. I spent 33 years as a scientist [at the Naval Research Laboratory] in the civil service, and ended up either on Hansen's level or one level below. The things he did, I would never have contemplated doing. My instinct was always to avoid publicity in the outer world, but speak my mind in scientific meetings.
In a sense, I was in a similar position to him with my advocacy of the fusion-fission hybrid [for nuclear energy generation]. It is an idea that I think can save civilization, but really it has not caught on in the larger world. When I had support on it, articles I wrote on it had to be cleared by NRL, at least one level above me, before they could submitted. This was true of any article anyone at NRL writes. Usually it is no big deal. I did write one fission-fusion article while at NRL, but with no NRL support. I did not use an NRL affiliation on the article.
But Hansen went way beyond that. He went to Iowa, gave his scientific talk and then said that global warming was so important and since Kerry appreciated his brilliance and Bush did not, he advocated voting for Kerry. If, when I was at the lab, by some fluke, Kerry had latched onto the fusion hybrid, and then I went and gave a talk on it, and advocated that my audience vote for Kerry because he understood the importance of the hybrid, I hate to think what my lab would have done to me. I also think I would have deserved it. Doing something like using your government science position to advocate a vote for a particular candidate based on his liking of your science, would be for me unthinkable. It is the elected policymakers who make the decisions we have to live with, and the science, even if it is non-controversial, is only one aspect of what they have to deal with.
The thing I do not understand is why Hansen does not just retire. Apparently,
he has 39 years in the civil service, he is working almost for nothing.
If he retires, he can say whatever he wants. I do this. On any hybrid
article I write, I just say "retired from NRL." This way, if
there is anything to what I say, NRL can bask in my glory, if not, no
blame goes to the lab.
Roy Spencer points out "that climate scientists aren't always
unbiased keepers of truth. The arena of global warming overflows with
more strongly held opinions than it does unbiased or scientific truths.
Fred Singer comments:
My view is that Hansen makes scientific claims that are NOT "consistent with best available science" -- or at least are questionable -- and then exploits these for political purposes. I am quite prepared to demonstrate this -- with Hansen present or without him. I would choose two recent examples:
1. His June 3, 2005 paper in Science is fundamentally flawed (see attached critique). In a news release, he claimed that he has found the "smoking gun" for anthropogenic global warming. That's sheer bunk (even though he may really believe it).
2. More recently he claimed that 2005 is the warmest year on record. This claim is not exactly wrong; but it is a consequence of his idiosyncratic method for calculating a global average temperature. His result thus disagrees with both of the well-established records of temperature trends: the Global Historic Climate Network (GHCN of NOAA) and Jones-East Anglia Univ (Hadley Centre, UK) . Both show 2002 warmer than 2005 -- and 1998 much warmer.
I think that Hansen is losing his good scientific judgement as he gets
caught up in the political aspects of Global Warming. It's a real shame;
I used to have a lot of respect for him.
Last year's cloning fraud case of South Korean scientist Hwang Wook-suk -- and last month's less-reported protest resignation of a British university scientist after an unrelated cloning report -- should prompt many to be more cautious of accepting scientific claims that await greater scrutiny of the scientific community. According to Wendy McElroy, a research fellow at the Independent Institute, the media and the public should routinely raise the following questions when new scientific findings are published:
**Is the report, including all data and methodology, available for examination?
If not, then the researcher is asking you to accept his word for the findings....
Asking the above five question isn't always sufficient -- -- but such questions are necessary, McElroy notes. Hwang's cloning fraud was heralded by the prestigious magazine SCIENCE. Scientific authority should receive the same skepticism that usually greets similarly bold claims of political authority. Both impact your life and are your business."
See "Questions to Ask Scientific Authority," by Wendy McElroy
Nature 439, 660 (9 February 2006) | doi:10.1038/439660a
We have analysed a suite of 12 state-of-the-art climate models and show
that ocean warming and sea-level rise in the twentieth century were substantially
reduced by the colossal eruption in 1883 of the volcano Krakatoa in the
Sunda strait, Indonesia. Volcanically induced cooling of the ocean surface
penetrated into deeper layers, where it persisted for decades after the
event. This remarkable effect on oceanic thermal structure is longer lasting
than has previously been suspected1 and is sufficient to offset a large
fraction of ocean warming and sea-level rise caused by anthropogenic influences.