Mandating science advice
The new EU Science Advice Mechanism, convening for its inaugural meeting in January 2016.
In July, Science reminded its readers of the existence of the European Commission’s new Science Advice Mechanism (SAM), a panel of internationally-recognised scientists tasked with providing scientific advice, in a mechanism intended to address the shortcomings of the ill-fated, single-headed role of Chief Scientific Adviser abandoned in 2014.
In fact, the SAM has already held its first two panel meetings, on 29 January and 16-17 March this year, at which it was agreed its first two questions would relate to “improving the measurements of CO2 emissions so they more closely resemble real-world emissions” and (more vaguely) cybersecurity and “the single digital market”.
A number of the problems with the initial Chief Scientific Adviser position appear, at least to some extent, to have been resolved: there is now a panel of advisers representing diverse interests and backgrounds; they have a reasonable budget; and they have a much larger team of support staff to do the research on which their advice will be based (see the legislative mandate here).
Problems of budget and staffing are relatively trivial, however, compared to the challenge of giving the SAM appropriate mandate and oversight, to ensure that it complements rather than supplants the political process.
This is important because, while it is intuitive to say that policy should in some way follow the evidence, it is in fact only in some very specific circumstances (sometimes described as “tornado politics”) possible or appropriate for “the evidence” to play a decisive role in what the appropriate policy outcome is (and even then, with certain important caveats).
This is because when people disagree it is very often due to their wanting different outcomes, not because they interpret “the evidence” in different ways. Resolving disagreement and defining a mutually acceptable course of action is what politics is for; if the job is handed over to scientists (or handed over further still, to some dictat of “the evidence”), the political solution is short-circuited and there is a deficit of democracy.
Keeping politics separate from science is therefore important. Political processes should be transparent, not masked behind a supposedly scientific debate which is in reality determining a political outcome. Conversely, if science is a proxy battleground for politics, its value in understanding our factual environment, the consequences of our actions, and the mechanisms by which we can most likely expect to achieve our desired goals, becomes diminished.
However, only so much can be done in defining how the SAM should function; it is as much up to the recipients of advice from the SAM as it is up to the SAM itself that its pronouncements are not taken as determining outcomes when politics is required instead. As to whether and how that happens, only time will tell.
August news bulletin: identifying “bad actors”; asking why cancer prevention is not more of a priorityAugust 8, 2016 at 5:34 pm | Posted in News and Science Bulletins | Leave a comment
August 2016 News Bulletin
Commentary: Identifying the “bad actors”— new challenges for the evaluation of endocrine disrupting chemicals. “We encourage decision makers around the world to adopt a new chemical evaluation tool that could save lives and money.” (Environmental Health News)
Why Isn’t Cancer Prevention a Priority? “Research shows that more than half of all cancers are preventable. Yet, why isn’t prevention a priority? More precisely, why aren’t environmental chemicals a focus of prevention research? When researchers talk about prevention, more often than not, they’re referring to things like diet, exercise, tobacco, and other lifestyle factors. Given the mounting evidence linking environmental chemicals with cancer, however, and the fact that toxic chemicals are so widespread, it’s hard to understand why there is so little research focused on environmental carcinogens.” (Silent Spring)
A Call for Action on Toxic Chemicals. Every day, children and adults are exposed to a variety of chemicals found in common household items. Now a growing body of research suggests that many of these chemicals — which are used to make plastic more flexible, fruits and vegetables more abundant and upholstery less flammable — may also pose a threat to the developing brain. (New York Times)
PFOA, PFOS Likely Hazardous to Immune System: Scientists. A panel of epidemiologists, toxicologists, microbiologists and other scientists have critiqued and then supported the National Toxicology Program’s draft analysis that concluded perfluorooctanoic acid, more commonly known as PFOA, and perfluorooctane sulfonate, or PFOS, are presumed to be immune hazards to humans. “The systematic approach helped readers to clearly understand what science the program considered and the reasons some scientific studies provided higher levels of confidence while others were graded more moderate or lower priority in the program’s final conclusions,” the commenters and panel members said. (Bloomberg BNA)
Wal-Mart Asks Its Suppliers to Stop Using Eight Chemicals. Wal-Mart Stores Inc. is asking suppliers to remove formaldehyde, triclosan and six other substances from their products, part of an effort to eliminate controversial chemicals from household goods. (Bloomberg)
August science bulletin: PFCs affect thyroid hormone levels in newborn girls; metabolic changes from environmental chemicalsAugust 8, 2016 at 5:22 pm | Posted in News and Science Bulletins | Leave a comment
August 2016 Science Bulletin
Thyroid disruption, PFCs | Prenatal exposure to perfluorinated compounds affects thyroid hormone levels in newborn girls. Thus, prenatal PFC exposure may disrupt thyroid hormone homeostasis. Thyroid hormones play a crucial role in fetal development and may have gender specific action. Hence, these results are of utmost importance in high-risk groups, such as pregnant women and children.
Metabolic changes, environmental chemicals | Developmental Exposure to Environmental Chemicals and Metabolic Changes in Children. Prenatal exposure to EDCs, particularly the persistent organic pollutant DDT and its metabolite DDE, may influence growth patterns during infancy and childhood. The altered growth patterns associated with EDCs vary according to exposure level, sex, exposure timing, pubertal status, and age at which growth is measured. Early exposure to air pollutants also is linked to impaired metabolism in infants and children. As a result of these and other studies, professional health provider societies have called for a reduction in environmental chemical exposures. We summarize the resources available to health care providers to counsel patients on how to reduce chemical exposures.
Fetal growth, pesticides | Prenatal Exposure to Organophosphorous Pesticides and Fetal Growth: Pooled Results from Four Longitudinal Birth Cohort Studies. This study confirms previously reported associations of prenatal OP exposure among black women with decreased infant size at birth, but finds no evidence of smaller birth weight, length, or head circumference among whites or Hispanics.
Food contact materials, chemical exposure | Printed paper and board food contact materials as a potential source of food contamination. 613 of 1,095 substances in the FACET food contact materials database are registered under REACH, and up to 59 of these are found in the European Chemicals Agency’s (ECHA) Community Rolling Action Plan (CoRAP) list. 18 of the registered substances are present in the Candidate List of substances of very high concern (SVHCs), and 2 are included in Annex XIV (intended for phase-out) due to their toxic effects on reproduction. One has been restricted since June 2010.
Obesity, flame retardants | Perinatal triphenyl phosphate exposure accelerates type 2 diabetes onset and increases adipose accumulation in UCD-type 2 diabetes mellitus rats. Perinatal TPhP exposure increased body and fat mass in 3.5 month old male and female rats, while leptin and cumulative energy intake were elevated in males and females, respectively. Independent of body mass, perinatal TPhP exposure accelerated T2DM onset in males and increased plasma non-esterified- fasting fatty acids. These observations suggest that perinatal exposure to TPhP exacerbates the development of obesity in male and female UCDavis-T2DM rats and accelerates T2DM onset in male UCD-T2DM rats.
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