My latest in the Washington Times.
My latest in the Washington Times.
Does a new study link “pollution” with cancer — or the just junkiest of statistics with opponents of EPA budget cuts?
The New York Times weeps this morning for the NINE jobs in EPA’s endocrine disruption program that President Trump has put on the chopping block. JunkScience.com readers will recall the fraudulent origin of these jobs.
Lead hysteria was borne out of “science” that the University of Pittsburgh found was “difficult to explain as honest error.” Nothing has changed.
The baby mice weren’t reported to be overweight or otherwise unhealthy. Mere biological effects (if even true) do not necessarily equate to adverse health effects. Also… mice are NOT little people.
The media release is below.
Prenatal bisphenol A exposure weakens body’s fullness cues
Mouse study sheds light on how endocrine-disrupting chemical increases obesity risk
THE ENDOCRINE SOCIETY
WASHINGTON — An expectant mother’s exposure to the endocrine-disrupting chemical bisphenol A (BPA) can raise her offspring’s risk of obesity by reducing sensitivity to a hormone responsible for controlling appetite, according to a mouse study published in the Endocrine Society’s journal Endocrinology.
BPA is a chemical found in a variety of food containers, including polycarbonate plastic water bottles and can linings. BPA can interfere with the endocrine system by mimicking estrogen, one of the main sex hormones found in women. Research indicates BPA exposure is nearly universal. More than 90 percent of people tested in population studies had detectable levels of BPA and compounds produced when it is metabolized by the body in their urine.
As of 2014, nearly 100 epidemiological studies had been published tying BPA to various health problems, according to the Society and IPEN’s Introduction to Endocrine-Disrupting Chemicals.
The new study found mice born to mothers exposed to BPA were less responsive to the hormone leptin, which is sometimes called the satiety hormone. Leptin helps inhibit the appetite by reducing hunger pangs when the body does not need energy. The hormone sends signals to the hypothalamus region of the brain to suppress the appetite.
“Our findings show that bisphenol A can promote obesity in mice by altering the hypothalamic circuits in the brain that regulate feeding behavior and energy balance,” said the study’s senior author, Alfonso Abizaid, Ph.D., of the Department of Neuroscience at Carleton University in Ottawa, Canada. “Low level prenatal exposure to BPA delays a surge of leptin after birth that allows mice to develop the proper response to the hormone. BPA exposure permanently alters the neurobiology in the affected mice, making them prone to obesity as adults.”
To examine how BPA can encourage the development of obesity, the researchers fed pregnant mice BPA in their food. The mice were exposed to doses of BPA that are lower than levels deemed safe by the U.S. Food and Drug Administration and Health Canada. Once the mice gave birth, the researchers gave their offspring injections of leptin at various intervals and then examined their brain tissue and analyzed their blood to gauge the response to the hormone.
Other pregnant mice were not exposed to any chemicals or were exposed to an estrogen chemical called diethylstilbestrol (DES), so their young could be compared to those born to mice that were exposed to BPA. All the mice were fed a control diet to eliminate differences in food intake.
Newborn mice typically exhibit a surge of leptin when they are eight days old that programs the hypothalamus circuits to respond to fullness cues. The study found that animals exposed to BPA experienced this surge two days late, and mice exposed to DES never had a surge of leptin. When they were treated with leptin over the course of two days, control animals that weren’t exposed to either chemical lost more weight than BPA- or DES-exposed mice.
In addition, researchers found that mice exposed to BPA before birth had reduced fiber density and brain activity in the hypothalamus circuits involved in regulating energy expenditure.
“This study improves our understanding of how BPA can disrupt the endocrine system in a manner that raises the risk of obesity in animals,” Abizaid said. “Since BPA has also been linked to obesity in humans, people need to be aware that environmental factors can lead to increased susceptibility to obesity and cardio-metabolic disorders.”
Other authors of the study include: Harry MacKay of Baylor College of Medicine in Houston, Texas, and Zachary R. Patterson of Carleton University in Ottawa, Canada.
The research was supported by a Carleton University Research Award given to Abizaid, a Canadian Institutes for Health Research Graduate Scholarship and Ontario Graduate Scholarship awarded to Patterson, and an Ontario Graduate Scholarship given to MacKay.
The study, “Perinatal Exposure to Bisphenol-A (BPA) Delays the Postnatal Leptin Surge in Male and Female CD-1 Mice,” will be published online at https://academic.oup.com/endo/article-lookup/doi/10.1210/en.2016.1718, ahead of print.
Ridiculous for several reasons.
Not really a victory for the rats since they won’t be bred to start with. In any event, computer modeling and cell tests are hardly substitutes. Continue reading A big victory for lab rats: Congress moves to limit chemical testing on animals
Hard to believe the endocrine disruption scare is still alive. Continue reading Claim: Exposure to common flame retardant chemicals may increase thyroid problems in women
This law will not enhance public health since typical exposures to chemicals in the environment and consumer products are not known to cause any harm in the first place. Continue reading Congress reaches deal to overhaul chemical regulation
How would this work? More likely a socio-economic effect — if even an actual effect. Continue reading Claim: PFOA causes early termination of breastfeeding
Call me skeptical about a claim whose authors admit, among assorted problems: “These wells may contain arsenic.” [Emphasis added]
The media release is below.
Elevated bladder cancer risk in New England and arsenic in drinking water
NIH/NATIONAL CANCER INSTITUTE
A new study has found that drinking water from private wells, particularly dug wells established during the first half of the 20th century, may have contributed to the elevated risk of bladder cancer that has been observed in Maine, New Hampshire, and Vermont for over 50 years. Other risk factors for bladder cancer, such as smoking and occupational exposures, did not explain the excess risk in this region. The study, by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, and colleagues at the Geisel School of Medicine at Dartmouth, Hanover, New Hampshire; the departments of health for Maine, New Hampshire, and Vermont; and the U.S. Geological Survey, appeared May 2, 2016, in the Journal of the National Cancer Institute.
Bladder cancer mortality rates have been elevated in northern New England for over half a century. The incidence of bladder cancer in Maine, New Hampshire, and Vermont has been about 20 percent higher than that in the United States overall. Rates are elevated among both men and women. A unique feature of this region is the high proportion of the population using private wells for their drinking water, which are not maintained by municipalities and are not subject to federal regulations. These wells may contain arsenic, generally at low to moderate levels. Previous studies have shown that consumption of water containing high concentrations of arsenic increases the risk of bladder cancer.
There are two possible sources of arsenic in the well water in northern New England. Arsenic can occur naturally, releasing from rock deep in the earth, and arsenic-based pesticides that were used extensively on crops such as blueberries, apples, and potatoes in the 1920s through the 1950s.
“Arsenic is an established cause of bladder cancer, largely based on observations from earlier studies in highly exposed populations,” said Debra Silverman, Sc.D., chief of the Occupational and Environmental Epidemiology Branch, NCI, and senior author on the study. “However, emerging evidence suggests that low to moderate levels of exposure may also increase risk.”
To explore the reasons for the higher rates of bladder cancer in northern New England, the researchers conducted a large study in Maine, New Hampshire, and Vermont. They compared 1,213 people newly diagnosed with bladder cancer with 1,418 people without bladder cancer who lived in the same geographic areas as those who developed the disease. The researchers obtained information on known and suspected bladder cancer risk factors, including smoking, occupation, ancestry, use of wood-burning stoves, and consumption of various foods.
“Although smoking and employment in high-risk occupations both showed their expected associations with bladder cancer risk in this population, they were similar to those found in other populations,” said Silverman. “This suggests that neither risk factor explains the excess occurrence of bladder cancer in northern New England.”
Researchers estimated the total amount of arsenic each person had ingested through drinking water based on current levels and historical information. They found that increasing cumulative exposure was associated with an increasing risk of bladder cancer. When investigators focused on participants who had used private wells, they saw that people who drank the most water had almost twice the risk of those who drank the least. This association was stronger if dug wells had been used. Dug wells are shallow, less than 50 feet deep, and potentially susceptible to contamination from manmade sources. Most of the dug well use occurred a long time ago, during an era when arsenic concentrations in private well water were largely unknown. However, the risk was substantially higher if the dug well use began before 1960 (when application of arsenic-based pesticides was commonplace in this region) than if dug well use started later.
The major limitation of the study was the inability to precisely measure arsenic exposure in the water consumed by people over their entire lifetime, which made it challenging to accurately quantify the contribution of arsenic exposure to the excess risk of bladder cancer. In particular, there were no known measurement data on arsenic levels in well water in the region prior to the 1960s, when arsenic-based pesticides were in widespread use.
The likelihood of exposure to arsenic from dug wells has diminished in recent years because arsenic-based pesticides are no longer used. Also, dug well use is much less common now than in the past. However, possible current exposure to arsenic in drinking water through use of private wells drilled deeply into fractured bedrock is a potential public health concern. For reference, the U.S. Environmental Protection Agency has established 10 micrograms per liter as the regulatory standard for arsenic in drinking water supplied by municipalities.
“There are effective interventions to lower arsenic concentrations in water,” said Silverman. “New England has active public health education campaigns instructing residents to test their water supply and to install and maintain filters if levels are above the EPA threshold. But we should emphasize that smoking remains the most common and strongest risk factor for bladder cancer, and therefore smoking cessation is the best method for reducing bladder cancer risk.”
The authors offer no evidence of any harm caused despite consumption of much fish containing POPs. Continue reading Claim: Pollutants in fish inhibit human’s natural defense system