Wednesday, December 12, 2012

Meningitis link to smoking in pregnancy: Cigarettes can treble child’s chance of developing the disease

Boring rubbish:  Working class people are more likely to smoke and they are less healthy anyway.  Connection between smoking and meningitis just assertion

Smoking during pregnancy can treble the baby’s chance of developing meningitis, researchers warn, and children exposed to smoke from a parent’s cigarettes at home are twice as likely to have the deadly illness.

Scientists estimate that more than 600 children a year in Britain develop meningitis as a result of their parents’ second-hand smoke.

They think that passive smoking gradually weakens children’s immune system making them more susceptible to the illness.

Researchers from the University of Nottingham analysed 18 studies which looked at the link between passive smoking and meningitis.

They found that children exposed to second hand smoke in the home were more than twice as likely to get the illness.

The under-fives were even more vulnerable - they were found to be two and a half times more at risk.

And children whose mothers smoked during pregnancy were three times more likely to get meningitis, the study published in BMC Public Health found.

Lead researcher Dr Rachael Murray, from the UK Centre for Tobacco Studies at the University of Nottingham, said: ‘We estimate that an extra 630 cases of childhood invasive meningococcal disease every year are directly attributable to second-hand smoke in the UK alone.

'While we cannot be sure exactly how tobacco smoke is affecting these children, the findings from this study highlight consistent evidence of the further harms of smoking around children and during pregnancy, and thus parents and family members should be encouraged to not smoke in the home or around children.’

In recent years a number of studies have shown passive smoking increases a child’s risk of meningitis.

But this is one of the first to show the link between a mother smoking during pregnancy.

The findings of this latest study imply this process begins while the baby is still in the womb.


Researchers repudiate BPA junk science

The chemical bisphenol A (BPA) — which is used to make hard, clear plastics and resins that line food containers — regularly appears in news headlines claiming the substance causes everything from heart disease to obesity. But a new study on the topic shows that much of this “research” is little more than junk science.

Many of the alarming BPA studies suffer from a common flaw: they rely on National Health and Nutrition Examination Survey (NHANES) data. NHANES data are produced via a Centers for Disease Control and Prevention (CDC) program to assess national health trends. As I noted in a prior blog post, CDC collects health data from a different group of volunteers every year via physical exams and interviews. In addition to recording health aliments of the volunteers, the data also measure BPA in urine and blood. Numerous BPA studies pull the data from various years to see if there are correlations between certain illnesses and levels of BPA in the volunteers’ urine or blood.

There are myriad ways to manipulate these data to generate an array of results, such as excluding certain participants as “outliers” or pulling out select subsets of data from the larger database; therefore, findings and conclusions can vary between studies. In addition, we can expect some associations to emerge by mere chance. Meanwhile, studies that don’t find associations, unfortunately, don’t get published as often and don’t grab headlines because they are not as interesting. Hence, those studies that are published create false impressions about the state of the research.

A key problem with using these data to draw any conclusion is the fact that NHANES data only includes “spot sampling” of BPA — measuring exposure via one (or a couple) urine sample per subject. But BPA levels in urine change practically hourly, which means that one-time measurements tell us nothing about actual exposure. Specifically, a person might have high levels in their urine at one moment simply because he or she just drank a soda from a can lined with BPA resins. But if researchers test this same person just a few hours later, the results may indicate very low BPA exposure. Thus, data from “spot sampling” of BPA are largely meaningless because they don’t measure long-term exposure.

Second, all these studies largely ignore the fact that the human body quickly metabolizes BPA before it can have any health impacts. For more background on these two issues, see my blog posts on BPA and coronary heart disease and BPA’s alleged impacts on obesity.

Higher quality and more comprehensive studies and scientific reviews of the full body of research find that BPA risks are low and its benefits outweigh any such risks.

Today, a new study shows that NHANES data can be manipulated to provide a variety of conflicting results. But more importantly, it explains why NHANES data is inappropriate for drawing any conclusions about BPA risks. Specifically, it notes:
    Our objectives were to analyze four NHANES datasets using consistent a priori selected methods to address the following questions: Is there a consistent association between urinary bisphenol A (BPA) measures and diabetes, coronary heart disease (CHD), and/or heart attack across surveys? Is NHANES an appropriate dataset for investigating associations between chemicals with short physiologic half-lives such as BPA and chronic diseases with multi-factorial etiologies?…

    Using scientifically and clinically supportable exclusion criteria and outcome definitions, we consistently found no associations between urinary BPA and heart disease or diabetes. These results do not support associations and causal inferences reported in previous studies that used different criteria and definitions. We are not drawing conclusions regarding whether BPA is a risk factor for these diseases. We are stating the opposite–that using cross-sectional datasets like NHANES to draw such conclusions about short-lived environmental chemicals and chronic complex diseases is inappropriate. We need to expend resources on appropriately designed epidemiologic studies and toxicological explorations to understand whether these types of chemicals play a causal role in chronic diseases. …

    To be clear, we are not drawing conclusions as to whether BPA is a risk factor for any of the chronic diseases discussed in this paper. In fact, we are stating the opposite – that using the NHANES surveys to draw such conclusions about short-lived environmental chemicals and chronic complex diseases is inappropriate.


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