I Wish I Were Far From the Madding Crowd

August 6, 2010

A chemical pot pourri

This is a real hodge-podge of items.

Bisphenol A

The Environmental Working Group (EWG) recently announced the findings of a study that found BPA in a large percentage of paper receipts it had collected.  http://ewg.org/BPA_Found_In_Receipts

Chemicals in cosmetics

Another resource EWG maintains is the Skin Deep cosmetic safety database.

http://www.cosmeticsdatabase.com/

Speaking of cosmetics, Annie Leonard (“The Story of Stuff”) has come out with “The Story of Cosmetics”, a look at chemicals in cosmetics and personal care products.  The Story of Stuff blog looks at the cosmetics industry’s reaction.

Learning and developmental disabilities and other diseases and conditions

The Collaborative on Health and the Environment (CHE) covers a wide range of topics, from learning and developmental disabilities to the CHE Toxicant and Disease Database, a searchable database that summarizes links between chemical contaminants and approximately 180 human diseases or conditions, to the Metabolic Syndrome Discussion Group.

BP (not just oil spills)

The CHE site also includes news items like:

6 Aug Thousands sign on for $10 billion BP suit. The revelation that BP’s Texas City refinery emitted toxic benzene for more than a month has ignited a furor in the port community that has suffered its share of deadly industrial accidents and toxic spills. Houston Chronicle.

Yes, before the BP oil spill there was the BP Texas City refinery explosion.  The U.S. Chemical Safety Board conducted an investigation.  I believe that they are looking into whether these incidents show that BP fostered a culture of cutting corners.

Chemicals and depression?

Was reading Peter Kramer’s Against Depression, where he argued that depression is a true illness.  (At least that’s what I’m getting out of it.)  He makes a couple of points that struck me.  One, on p. 156 he states that there is a connection between diabetes and depression.  Unfortunately, he doesn’t cite a source for that.  And if true, it’s not clear which caused which.  That is, does having diabetes make it more likely that you would be depressed?  Or does depression in some way connected to the development of diabetes.  Or could diabetes and depression be caused by the same agent?  (Or some combination of the above.)

He also talks about how long-term stress can result in increased levels of corticotropin and that such stress can lead to depression and illness.  Of course, corticotropin is but one element of the neuroendocrine system.  And with many of these things, there are feedback loops that get out of whack if enough recovery time is not available.  That’s actually why some scientists have proposed that a chronic lack of sleep can cause obesity over the long haul.  The International Agency for Research on Cancer and NIOSH are looking at whether “shift work” (along with a number of chemicals) can be considered carcinogenic.

Leptin: An example of what we didn’t know

Leptin, the appetite hormone, was not discovered until 1994 (though its effects had been observed much earlier).  (Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (December 1994). “Positional cloning of the mouse obese gene and its human homologue”. Nature 372 (6505): 425–32. doi:10.1038/372425a0. PMID 7984236.) I mention that because chemical industry apologists seem to ignore the fact that we’ve learned a lot about the human body in the last 15-20 years.  And the more we learn, the more we discover how chemicals can mess up our systems.

Regarding leptin, I found the following using the National Library of Medicine’s MedlinePlus service.

A National Cancer Institute fact sheet on physical activity and cancer states that “increasing physical activity may influence insulin and leptin levels and influence breast cancer prognosis.”

An EPA report, “A Decade of Children’s Environmental Health Research:  Highlights from EPA’s Science to Achieve Results Program,” cites an EPA-funded study that found that “autistic children showed higher levels of leptin (a hormone that affects the regulation of body weight, metabolism, and reproductive function, and influences the immune system) in their blood when compared to typically developing children (Ashwood et al. 2007; R829388C002).”

Citation: Ashwood P., Kwong C., Hansen R., Hertz-Picciotto I., Croen L., Krakowiak P., Walker W., Pessah I.N., and Van de Water J. 2007. “Brief report: Plasma leptin levels are elevated in autism: association with early onset phenotype?” J. Autism Dev. Disord. Advanced online publication (DOI 10.1007/s10803-006-0353-1).  Abstract

So our bodies are these incredibly complex systems.  Some chemical companies would have you believe that the stuff they make, even the synthetic chemicals that human beings have never been exposed to before, have absolutely NO effect on our health.

Truth is, despite the Environmental Defense Fund saying that we’re not guinea pigs, we all are.  (See previous post: “Tired of being a guinea pig?“)

“Would you like BPA with those fries?”

Advertisements

March 28, 2010

Environmental exposures and child development

Came across several articles in Current Opinion in Pediatrics because of a blog post on Autism and environmental chemicals: a call for caution. Unfortunately, only the abstracts are free to view.

But what these show is that medical science is beginning to look more closely at possible environmental causes of childhood diseases.  This  does not mean that environmental factors in and of themselves cause disease, but as Dr. Philip Landrigan notes, genetic factors account for only a small fraction of autism cases and do not explain key features of autism.

What causes autism? Exploring the environmental contribution

Landrigan, Philip J.  Current Opinion in Pediatrics. 22(2):219-225, April 2010. doi: 10.1097/MOP.0b013e328336eb9a

Excerpts from the abstract:

Autism is a biologically based disorder of brain development. Genetic factors – mutations, deletions, and copy number variants – are clearly implicated in causation of autism. However, they account for only a small fraction of cases, and do not easily explain key clinical and epidemiological features. This suggests that early environmental exposures also contribute. This review explores this hypothesis.

Expanded research is needed into environmental causation of autism. Children today are surrounded by thousands of synthetic chemicals. Two hundred of them are neurotoxic in adult humans, and 1000 more in laboratory models. Yet fewer than 20% of high-volume chemicals have been tested for neurodevelopmental toxicity.

Environmental exposures and development

Mattison, Donald R. Current Opinion in Pediatrics. 22(2):208-218, April 2010. doi: 10.1097/MOP.0b013e32833779bf

Excerpts from the abstract:

Summarizes recent studies exploring the relationship between paternal and maternal environmental exposures to chemicals before, at the time of and after conception to adverse developmental outcomes including preterm birth, death, structural and functional abnormalities and growth restriction.

Recent studies have demonstrated that human pregnancy and development are vulnerable to environmental exposures of the father and mother to chemical, biological and physical agents.

Whereas single genes and individual chemical exposures are responsible for some instances of adverse pregnancy outcome or developmental disease, gene-environment interactions are responsible for the majority.

Gene-environment interaction and children’s health and development

Wright, Robert O; Christiani, David. Current Opinion in Pediatrics. 22(2):197-201, April 2010. doi: 10.1097/MOP.0b013e328336ebf9

Excerpt from the abstract:

Purpose of review: A systematic approach to studying gene-environment interaction can have immediate impact on our understanding of how environmental factors induce developmental disease and toxicity and will provide biological insight for potential treatment and prevention measures.

Summary: Using a genome-wide approach, combined with prospective longitudinal measures of environmental exposure at critical developmental windows, is the optimal design for gene–environment interaction research. This approach would discover susceptibility variants, and then validate the findings in an independent sample of children. Designs that combine the strengths and methodologies of each field will yield data that can account for both genetic variability and the role of critical developmental windows in the etiology of childhood disease and development.

Childhood obesity and the built environment

Galvez, Maida P; Pearl, Meghan; Yen, Irene H. Current Opinion in Pediatrics. 22(2):202-207, April 2010. doi: 10.1097/MOP.0b013e328336eb6f

Create a free website or blog at WordPress.com.