Not long ago, US headlines were inundated with horror stories about the dangers of biphenol A (BPA), a chemical used to manufacture polycarbonate bottles. The articles invoked the words that would bring any American family to arms: “It could harm your children,” they read. BPA was effectively demonized. But what sources did the media use to justify the hype? Might BPA be no more a demon than a fluffy bunny?

As the saying goes, don’t believe everything you see on TV. At least, that is what is suggested by the non-profit, non-partisan investigation from STATS, Science Suppressed: How America became obsessed with BPA.

Dating back to the 1930’s, thousands of studies have heralded the safety of BPA. However, as the STATS investigation reports, the few recent dissenting studies regarding BPA failed to use sound scientific practice. Even the most prominent of them, headed by Frederick vom Saal, were rejected by foreign bodies, such as the European Union and the World Health Organization, as inherently flawed in their methods and conclusions.

However, despite their lack of recognition, those same studies were touted as evidence by the media. One newspaper, the Milwaukee Journal Sentinel, “explicitly warned by the head of the National Toxicology Program expert panel that it was relying too much on one scientist whose work and perspective had been repeatedly rejected by international risk assessments.”

Not only did small sample sizes taint the validity of the studies, but flawed methods in the administration of doses of BPA to study subjects (usually rats) further convoluted the results. In humans, 99% of BPA exposure occurs via ingestion. However, the studies that concluding BPA was harmful used primarily a subcutaneous (under the skin) injection to administer BPA. Why does this matter? Because BPA follows differing physiological pathways depending on the route of exposure:

When BPA is ingested, it is rapidly detoxified, first in the gastrointestinal tract (GI) and then in the liver by enzymes which add a sugar molecule to BPA, transforming it into a water soluble BPA-glucuronide. The sugar conjugate is easily and quickly excreted in urine. The half life of BPA-glucuronide is six hours. There is a minor metabolic pathway in which some BPA is converted to a sulfate, but this is also water soluble and quickly excreted from the body (Tsukioka et al.,2004; Völkel et al., 2002, 2005).

In both of these pathways, BPA is deactivated, meaning it loses its capacity to act like an estrogen (Matthews et al., 2001; Shimizu et al., 2002; Snyder et al., 2000). This is important to note as BPA is considered to have a weak estrogenic capacity (approximately 15,000 times weaker than the strongest naturally-occurring estrogen in humans) – one of the reasons it has been dubbed an “endocrine disruptor” by environmental activists. The way orally ingested BPA is metabolized removes that capacity.

When a rat or mouse is injected with BPA as opposed to being fed BPA different things happen. The chemical retains its estrogenic capacity as it circulates in the blood and enters cells.

Furthermore, the actual amount of BPA ingested by humans on a daily basis is 500,000 times lower than that needed to elicit adverse effects in rats: “We get vastly more estrogenic chemicals from eating nuts, cereals and bread,” says the report.

There is much more to the STATS report, but whether one is convinced of the safety of BPA or not is beside the point. The underlying point is that media outlets, as businesses, have the ultimate interest financially in selling more issues/gaining viewers. The best way to do so? Publish the most attention grabbing and emotionally driven stories possible (example: the initial hype about the killer swine flu). What’s the point in reacting to something based on anecdote or flawed data? As consumers of news media, it is important to stay skeptical.

Photo by 9ine6ix

It’s almost impossible to converse about influenza A / H1N1 without touching on the 1918 Spanish Flu. Why is that? Worry-filled observers try to draw parallels between the two. “This will be another 1918 Spanish Flu,” they say. “Wait until the fall,” they warn. But are they right?

Yes, swine flu and the Spanish flu are both of the influenza A / H1N1 subtype. And, yes, it’s true that the 1918 Spanish flu began its initial spread during spring, reaching it’s peak virulence the following fall. However, the current influenza A / H1N1 is not showing the deadliness that the 1918 Spanish flu displayed during its spring upstart.

But some still contest that as influenza A / H1N1 didn’t have the opportunity to reach its deadly potential–it didn’t appear until the tail end of flu season. Influenza has little ability to spread during the summer months, so influenza A / H1N1 will likely lie dormant until next fall. But most experts suggest that future infections will continue to be relatively mild.

However, with so little observational data available, completely refuting the doomsayer theory of a deadly fall outbreak proves difficult. So should we err on the side of caution, stockpile anti-virals, and hunker down until it all blows over? Just in case?

In the norther hemisphere, with little collateral damage, influenza A / H1N1’s spread is slowly dropping off as summer approaches. But fearfully waiting until fall to see if it has any unknown deadly potential wont be necessary. Influenza A / H1N1 has already been confirmed in New Zealand and Brazil.

The flu season in the southern hemisphere is just beginning, and swine flu already has a running start. If the doomsayers are correct, they’ll be all over the media in the next few weeks. For those living in the northern hemisphere, don’t worry about canceling any spring or summer plans. Take out the sun shades, hit the beach, and relax.

Photo by hesenrre

Egypt decided to slaughter all of their nation’s 300,000 pigs, President Obama asked Congress for $1.5 billion for flu preparedness, and China herded and quarantined 70 healthy Mexican nationals. But why? Is all the fear and preparation justifiable?

The initial numbers seemed to suggest so as reports highlighted the deaths in relation to the relatively few confirmed cases. But we now know that this new influenza A/H1N1 strain is currently no more deadly than the normal seasonal flu. As the hype is starting to wear down the focus in the media is switching from new infections to speculations regarding how the virus could change.

Influenza is a volatile virus. Its genes change rapidly through regular mutations. And when two different influenza strains infect the same host, they can swap and borrow bits of genetic material. This process, known as reassortment, compounds influenza’s unpredictability.

Sometimes reassortments led to new pandemics. It is possible that reassortment enables flu viruses to escape the immune system so well that they can make people sicker and spread faster to new hosts.

Reassortment also played a big role in the emergence of the current swine flu. Its genes come from several ancestors, which mainly infected pigs.

-New York Times, “10 Genes, Furiously Evolving”

When the reassortment occurs between two strains already endemic in the human population, the results tend to be less than extraordinary. But when unlike strains come together, just as bird, pig, and human strains formed the 1918 Spanish flu, the result can be extremely virulent.

So it’s a fair question to ask: what if this new strain of influenza A/H1N1 becomes more deadly? Even though there have only been 1490 confirmed cases and 30 deaths globally (WHO, 5 May 2009), governments continue preparations as if a deadly outbreak were imminent.

Should the outbreak take a turn for the worse, any government taking a more conservative stand would be hard pressed to justify any inaction. Erring on the side of caution, governments more readily hedge their bets.

Will this new influenza A/H1N1 virus become more deadly? It seems unlikely, but certainty tends to be a luxury of hindsight.

Photo by Eneas

More swine flu news (I know, it’s been a hot topic these last few days). The number of deaths in Mexico attributable to swine flu are up, but there have still been no deaths or hospitalizations in the US.

Also, the World Health Organization raised its pandemic alert level to 4 in response spreading of swine flu. While “alert level” may sound intimidating, level 4 only signifies that the virus is capable of sustained transmission at the community level. It doesn’t measure the lethality of the strain.

Below is a summary of the relevant WHO alert phases:

Level 2:

• Predominantly animal infections.
• Few reports of animal-to-human infection.
• No human-human transmission.
• Potential pandemic threat.

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The news is flooded with headlines like “Mexico City on alert over swine flu outbreak” and “Mexico Swine Flu Epidemic Worries World”. So far, there have been 42 deaths from 1112 confirmed cases of A/H1N1 subtype influenza in Mexico (May 7, 2009, WHO).

Photo by be_khe

H1N1 is endemic to pig and bird populations and has been compared to the Spanish flu pandemic of 1918 (which killed up to 100 million people worldwide). But the spanish flu only exists today in a few isolated lab samples, and the bird and pig H1N1 strains are usually only transmittable through animal to human contact. However, the recent swine flu cases have shown that the new H1N1 strain is capable of human to human transmission.

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