HPV associated with vaginal intraepithelial neoplasia in women exposed to DES in utero

Close follow-up is recommended for DES-exposed patients, especially those who have risk factors known to be associated with genital neoplasia

image of hpv virus
The role of human papillomavirus and herpes simplex virus in the etiology of intraepithelial neoplasia is discussed in this 1987 study.

Study Abstract

Human papillomavirus associated with vaginal intraepithelial neoplasia in women exposed to diethylstilbestrol in utero, Obstetrics and gynecology, NCBI PubMed PMID: 3037458,
1987 Jul.

Five out of 959 young women, exposed to diethylstilbestrol (DES) in utero, developed vaginal intraepithelial neoplasia while they were under follow-up in the Diethylstilbestrol-Adenosis Project at Baylor College of Medicine, Houston, Texas.

We suggest that the development of the vaginal intraepithelial neoplasia at a younger age than usual may be caused by a higher susceptibility of the DES-exposed patient to factors associated with the development of intraepithelial neoplasia. A common finding in all five women was the detection of the deoxyribonucleic acid (DNA) of human papillomavirus types 6 or 16 in their lesions, using high-stringency in situ hybridization.

The role of human papillomavirus and herpes simplex virus in the etiology of intraepithelial neoplasia is discussed.

Close follow-up is recommended for DES-exposed patients, especially those who have risk factors known to be associated with genital neoplasia.

More DES DiEthylStilbestrol Resources

80% of Cancers down to Environment and Lifestyle

Environmental and external factors such as smoking, drinking, sun exposure and air pollution account for nine in 10 cancer

image of air-pollution
Data showed people who migrated from regions of lower cancer risk to those with higher cancer risk soon developed disease at rates consistent with their new environment. University students come and go in the dense air pollution.

A team of researchers from Stony Brook University, led by Yusuf Hannun, MD, the Joel Strum Kenny Professor in Cancer Research and Director of the Stony Brook University Cancer Center, have found quantitative evidence proving that extrinsic risk factors, such as environmental exposures and behaviors weigh heavily on the development of a vast majority (approximately 70 to 90 percent) of cancers.

Study Abstract

Nature, doi:10.1038/nature16166,
CDC Early Release,
16 December 2015.

Recent research has highlighted a strong correlation between tissue-specific cancer risk and the lifetime number of tissue-specific stem-cell divisions. Whether such correlation implies a high unavoidable intrinsic cancer risk has become a key public health debate with the dissemination of the ‘bad luck’ hypothesis. Here we provide evidence that intrinsic risk factors contribute only modestly (less than ~10–30% of lifetime risk) to cancer development. First, we demonstrate that the correlation between stem-cell division and cancer risk does not distinguish between the effects of intrinsic and extrinsic factors. We then show that intrinsic risk is better estimated by the lower bound risk controlling for total stem-cell divisions. Finally, we show that the rates of endogenous mutation accumulation by intrinsic processes are not sufficient to account for the observed cancer risks. Collectively, we conclude that cancer risk is heavily influenced by extrinsic factors. These results are important for strategizing cancer prevention, research and public health.

While healthy habits like not smoking, keeping a healthy weight, eating a healthy diet and cutting back on alcohol are not a guarantee against cancer, they do dramatically reduce the risk of developing the disease.

Sources and press media releases
  • Study Reveals Environment, Behavior Contribute to Some 80 Percent of Cancers, Stony Brook University, NY, December 16, 2015.
  • Substantial contribution of extrinsic risk factors to cancer development, nature, 16 December 2015.
  • Environmental factors increase risk of some types of cancer, study finds, theguardian, 18 December 2015.
  • Cancer is not just ‘bad luck’ but down to environment, study suggests, BBC News health-35111449, 17 December 2015.
  • Nine in 10 cancers caused by lifestyle, telegraph, 17 Dec 2015.

Endocrine Disrupters and Child Health

Possible developmental early effects of endocrine disrupters on child health

This 2012 publication by WHO was supported by the National Institute of Environmental Health Sciences.

Publisher: WHO; ISBN: 978 92 4 150376 1, 2012.

The present document is a short summary of the current knowledge of the effects of endocrine disrupters on child health. The main focus is on congenital disorders, cryptorchidism and hypospadias, which have an endocrine connection, on thyroid hormone-related problems, and on puberty. There is ample evidence of endocrine disruption in wildlife, and the mechanisms of action of endocrine disrupters have been elucidated in experimental animals, but there is limited knowledge of the association of human disorders with exposure to endocrine disrupters. Accumulating data suggest that many adult diseases have fetal origins, but the causes have remained unexplained. Improving fetal and child health will influence the whole life of an individual and improve the wellbeing of our society.

Sources and more information

The Full Xmas Moon 21st FullMoonEngageMe Social Media Event on EmpireKred

For the first time since 1977, the full moon will be exactly on Christmas day

image of full-Christmas-moon
Between Wednesday the 23rd and Sunday the 27th of December 2015, join our free social media event taking place at each Full Moon – via #EmpireKred – and give a boost to your social networking!. earthsky.

December Full Moon

The Metonic cycle
and Christmas Day…

The full moon that appears in December is usually called the Cold Moon : because the winter cold fastens its grip and the nights become long and dark. For the first time since 1977, the full moon will be exactly on Christmas day (at 11:11 UT) in 2015! Since this won’t happen again before 2034 – learn more here – let’s call it the Full Xmas Moon

21st #FullMoonEngageMe Schedule

full moon icons
Join us to have fun, “get bought”, connect, super charge your social networking!

Our free event will start on Wednesday the 23rd of December 2015 at +/- 07:00 UTC and will last until Sunday the 27th at +/- 24:00 in HERE.

More Information

Our first #FullMoonEngageMe event launched in May 2014 ; it’s about networking and having fun. By meeting and connecting with top social media engagers, you may grab a unique opportunity to super charge your social networking – on #EmpireKred and beyond.

You must know that Empire Avenue became Empire.Kred including a new domain and new look. Two years ago I said that we all had kred somewhere, and now Kred says that the score was just the tip of the iceberg

The Full Pink Moon saw some extravaganza – such as special achievements, moon pies, and daily drawings… so let’s see what happens this time! Recent joiners can expect to receive some extra support during the five days.

If you are confused, please read our FAQs page. And is you are not familiar with the platform – yet – you can join for FREE Empire.Kred at anytime – before and after any social media event.  Use the comment section to ask any question about the event.

Time for some “serious buzz” and serious FUN!
See you soon 😉

Market Share Liability in DES Cases: The Unwarranted Erosion of Causation in Fact

In the final analysis, the legislature, and not the court, is the appropriate forum for determining whether to adopt or reject market share liability

image of Hand-of-Justice
The Article concludes that market share liability is an unsound concept, that it represents too wide a leap in our tort principles, and that the abrogation of such a fundamental tort requirement is unwarranted. Hand of Justice.


DePaul Law Review,
David M. Schultz,
Volume 40, Article 5,
Issue 3 Spring 1991.

As our society progresses in complexity, theories of tort law have evolved in order to provide redress for the harms caused in a changing world. Tort law evolution has resulted in the creation of new remedies and, in many instances, the erosion of certain preconditions for recovery in tort. Nevertheless, with limited exceptions, there has not been significant erosion of the requirement that a plaintiff must first be able to identify the person or entity that caused her injury before she can recover in tort. In the past decade, however, a small number of courts have abrogated this principle, which is referred to as “causation in fact.” In the place of causation of fact, these courts have adopted the concept of “market share liability.

The market share liability theory has developed mainly through lawsuits filed by women who claim to suffer injuries resulting from their mothers ingestion of the drug Diethylstilbestrol (DES) while pregnant. These plaintiffs are commonly referred to as the “DES daughters.” The time that passes between the maternal ingestion of DES and the diagnosis of the injuries is generally twenty or more years because the injuries do not manifest themselves until sometime after the daughter has reached puberty. A DES daughter is often unable to identify the specific manufacturer of the drug her mother took for two key reasons: the long passage of time and the fungible nature of DES. Faced with the possibility of leaving these plaintiffs without a remedy as a result of their inability to identify the manufacturer, some courts have instead abolished the traditional requirement of establishing causation in fact. In place of causation in fact, these courts have adopted a theory that imposes liability upon any defendant who participated in the manufacturing or marketing of DES in the relevant market. Under this “market share liability” theory, each defendant is liable for the proportion of the judgment that its share of the market represented during the relevant time period.

Market share liability is a flawed concept that likely will apply only to a narrow class of plaintiffs and defendants.

Market share liability has been controversial since its inception. The concept has been adopted with varying modifications by a handful of courts and promoted by a larger number of legal commentators. At the same time, other courts have denounced the theory of market share liability when faced with the opportunity to adopt the proposition in either DES cases or cases involving other products. Currently, only nine state supreme courts have addressed the market share liability issue in a DES case. Most likely, however, other jurisdictions will eventually be forced to face this issue, especially in light of the fact that DES was used nationwide, some plaintiffs have achieved success with the theory, and there is the potential for large recoveries.

Most legal commentary on the issue of market share liability has supported the adoption of the theory. Commentators and courts that support the market share liability theory correctly argue that there is a need to adapt our existing tort law in the face of progress. They also argue that there is strong emotional appeal to insure a remedy for all plaintiffs, especially plaintiffs who are innocent of any wrongdoing. However, this Article contends that courts should not develop a market share liability concept.

  1. This Article begins with a brief history of the development of the drug DES.
  2. In the next section, this Article reviews the tort requirement of causation in fact.
  3. The third section outlines the DES cases in which state supreme courts have adopted market share liability,
  4. and the fourth section addresses cases where courts have rejected the theory in the DES context and in other actions.

Some DES plaintiffs have been able to establish the identity of the specific manufacturer, while others will be able to establish enough evidence to proceed to trial on the issues of causation in fact or negligence.

The Article concludes that market share liability is an unsound concept, that it represents too wide a leap in our tort principles, and that the abrogation of such a fundamental tort requirement is unwarranted. Two ideas are presented to support this conclusion.

  1. First, there is insufficient data to accurately develop the required market shares for each of the hundreds of pharmaceutical companies that produced DES. This lack of data precludes the fair allocation of liability for DES related injuries among all DES manufacturers.
  2. Second, upon close scrutiny, the underlying policies offered to justify adoption of the market share liability theory are either not achieved by the theory, and even if they can be achieved, they do not provide sufficient reasons to adopt it.

This Article proposes that the judicial development of market share liability involves making public policy determinations that more appropriately should be left for state legislatures. A legislative response, similar to the federal legislation established to compensate persons injured by childhood vaccines such as the diphtheria, pertussis, and tetanus (“DPT”) vaccine is a proper method of compensation, and one that will not require a radical change in a state’s tort law.

More DES DiEthylStilbestrol Resources

Environmental Impacts on Reproductive Health and Fertility

Focusing on exposures to environmental contaminants, this book provided the first comprehensive source of information in this field

This is a leading book in the exploding field of the study of environmental impacts. Physicians, scientists, policy makers, and epidemiologists interested in this topic should read this book, not only because of the number of experts who contribute, but also because of the vast amount of information they provide. While other books may focus on animal studies and the search for a mechanism of toxicity, this one focuses more on evidence from human studies, which makes it a standout book for its audience.

Publisher: Cambridge University Press; 1 edition (March 15, 2010)

Many reproductive and developmental health problems are caused by exposure to chemicals that are widely dispersed in our environment. These problems include infertility, miscarriage, poor pregnancy outcomes, abnormal fetal development, early puberty, endometriosis, and diseases and cancers of reproductive organs. The compelling nature of the collective science has resulted in recognition of a new field of environmental reproductive health. Focusing on exposures to environmental contaminants, particularly during critical periods in development and their potential effects on all aspects of future reproductive life-course, this book provides the first comprehensive source of information bringing together the arguments that are spread out among various scientific disciplines in environmental health, clinical and public health fields. It provides a review of the science in key areas of the relationship between environmental contaminants and reproductive health outcomes, and recommendations on efforts toward prevention in clinical care and public policy.

Sources and more information

Promising new screening test for ovarian cancer needs more study

It may soon be possible to screen for ovarian cancer

image of woman-and-sky
There is no reliable way to detect ovarian cancer, which may explain why most women who are diagnosed already have advanced disease. But a new test may change that. Look II.
2015 Study Summary

The exciting thing about this paper is that it’s the first evidence that suggests if you catch the cancer early enough, perhaps it can save lives

Ovarian cancer has a poor prognosis, with just 40% of patients surviving 5 years. We designed this trial to establish the effect of early detection by screening on ovarian cancer mortality.

In this randomised controlled trial, we recruited postmenopausal women aged 50–74 years from 13 centres in National Health Service Trusts in England, Wales, and Northern Ireland. Exclusion criteria were previous bilateral oophorectomy or ovarian malignancy, increased risk of familial ovarian cancer, and active non-ovarian malignancy. The trial management system confirmed eligibility and randomly allocated participants in blocks of 32 using computer-generated random numbers to annual multimodal screening (MMS) with serum CA125 interpreted with use of the risk of ovarian cancer algorithm, annual transvaginal ultrasound screening (USS), or no screening, in a 1:1:2 ratio. The primary outcome was death due to ovarian cancer by Dec 31, 2014, comparing MMS and USS separately with no screening, ascertained by an outcomes committee masked to randomisation group. All analyses were by modified intention to screen, excluding the small number of women we discovered after randomisation to have a bilateral oophorectomy, have ovarian cancer, or had exited the registry before recruitment. Investigators and participants were aware of screening type. This trial is registered with ClinicalTrials.gov, number NCT00058032.

Between June 1, 2001, and Oct 21, 2005, we randomly allocated 202 638 women: 50 640 (25·0%) to MMS, 50 639 (25·0%) to USS, and 101 359 (50·0%) to no screening. 202 546 (>99·9%) women were eligible for analysis: 50 624 (>99·9%) women in the MMS group, 50 623 (>99·9%) in the USS group, and 101 299 (>99·9%) in the no screening group. Screening ended on Dec 31, 2011, and included 345 570 MMS and 327 775 USS annual screening episodes. At a median follow-up of 11·1 years (IQR 10·0–12·0), we diagnosed ovarian cancer in 1282 (0·6%) women: 338 (0·7%) in the MMS group, 314 (0·6%) in the USS group, and 630 (0·6%) in the no screening group. Of these women, 148 (0·29%) women in the MMS group, 154 (0·30%) in the USS group, and 347 (0·34%) in the no screening group had died of ovarian cancer. The primary analysis using a Cox proportional hazards model gave a mortality reduction over years 0–14 of 15% (95% CI −3 to 30; p=0·10) with MMS and 11% (−7 to 27; p=0·21) with USS. The Royston-Parmar flexible parametric model showed that in the MMS group, this mortality effect was made up of 8% (−20 to 31) in years 0–7 and 23% (1–46) in years 7–14, and in the USS group, of 2% (−27 to 26) in years 0–7 and 21% (−2 to 42) in years 7–14. A prespecified analysis of death from ovarian cancer of MMS versus no screening with exclusion of prevalent cases showed significantly different death rates (p=0·021), with an overall average mortality reduction of 20% (−2 to 40) and a reduction of 8% (−27 to 43) in years 0–7 and 28% (−3 to 49) in years 7–14 in favour of MMS.

Although the mortality reduction was not significant in the primary analysis, we noted a significant mortality reduction with MMS when prevalent cases were excluded. We noted encouraging evidence of a mortality reduction in years 7–14, but further follow-up is needed before firm conclusions can be reached on the efficacy and cost-effectiveness of ovarian cancer screening.

Sources and more information
  • Ovarian cancer screening and mortality in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial, The Lancet, doi.org/10.1016/S0140-6736(15)01224-6, 17 December 2015.
  • Early Detection of Ovarian Cancer May Become Possible, NY Times, DEC. 17, 2015.
  • It May Soon Be Possible to Screen for Ovarian Cancer, time, Dec. 17, 2015.

“Intersex” male bass found throughout protected Northeast US waters

Evidence of estrogenic endocrine disruption in smallmouth and largemouth bass inhabiting Northeast U.S. national wildlife refuge waters

image of Rappahannock-River
The Rappahannock River Valley National Wildlife Refuge was one of 19 refuges where intersex bass were found (USFWS).

By Brian Bienkowski,
Environmental Health News,
December 17, 2015

Eighty-five percent of male smallmouth bass tested in or nearby 19 National Wildlife Refuges in the U.S. Northeast had signs of female reproductive parts, according to a new federal study.

The study, led by the U.S. Geological Survey and U.S. Fish and Wildlife Service, also reported that 27 percent of male largemouth bass in the testing sites were intersex.

The study is the first of its kind in National Wildlife Refuges and adds to growing evidence that endocrine disrupting chemicals are getting into U.S. lakes, rivers, streams and reservoirs—no matter how protected the waters seem. And such contamination seems to affect the reproductive development of some fish species, which can lead to threatened populations.

For the bass in this study, those considered “intersex” either had a protein that is used to make egg yolk typically found in females, or immature egg cells in their testes, said co author Fred Pinkney, a biologist with the U.S. Fisheries and Wildlife.

The eggs were in the very, very early stages

But any change to fish reproductive systems could possibly threaten overall fish populations and ability to properly reproduce.

During the fall seasons of 2008 to 2010, the researchers tested a total of 118 male smallmouth bass from 12 locations and 85 percent were intersex. They tested an additional 173 male largemouth bass from 27 sampling sites and 27 percent were intersex.

It’s not entirely clear why the bass were intersex as the researchers did not test the waters for specific chemicals, said lead author Luke Iwanowicz, a research biologist with the U.S. Geological Survey.

However, the suspected culprits of the sex changes are endocrine disrupting compounds.

This includes hormones, industrial chemicals and pesticides that are or mimic estrogen hormones. These compounds enter rivers and streams via permitted effluents, stormwater and agricultural runoff, and wastewater treatment plants, where excreted birth control and natural estrogens pass through relatively un-altered.

The study is just the latest to find intersex fish in U.S. waterways and builds on a U.S. Geological Survey study in 2009 that showed intersex male fish in nine U.S. river basins, though that study didn’t include Northeast basins. The bass tested in the Northeast waterways had a higher prevalence of intersex than the fish in the 2009 study.

It seems that certain fish species may be more sensitive to estrogenic compounds than others, as evidenced by the disparity between largemouth and smallmouth bass in this study. Previous studies also have reported that smallmouth bass seem more susceptible to intersex changes.

However it’s not clear if this is actual physical sensitivity to the chemicals or if it’s due to some species spending more time in more contaminated habitats.

National Wildlife Refuges are areas protected by the U.S. Fish and Wildlife Service. There are more than 560 such refuges nationally.

The U.S. Fish and Wildlife Service encourages management actions that reduce runoff into streams, ponds and lakes—both on and off of refuge lands

The national refuges tested spanned from eastern Ohio up to Maine and included: the Patuxent Research, Susquehanna, Montezuma, Great Swamp, Wallkill River, Great Meadows, Assabet River, Rappahannock River Valley, Mason Neck, Back Bay, John Heinz, Erie, Cherry Valley, Great Bay, Lake Umbagog, Sunkhaze Meadows, Missisquoi, Moosehorn and Ohio River Islands refuges.

Pinkney said the bass indicate that many aquatic species in Northeast U.S. refuges may be exposed to estrogenic chemicals.

200% increase in the rate of overdose deaths involving opioids in the U.S. since 2000

Deaths from drug overdoses have hit an alarming record high in the US

image of opioids-benzodiazepines
Benzodiazepines are subject to legal restrictions in the UK both under medicines regulation and by the Home Office under the Misuse of Drugs Act. However, considerable activity takes place online, outside UK jurisdiction. To Sleep Forevermore.

Increases in Drug and Opioid Overdose Deaths — United States, 2000–2014,
CDC Early Release,
December 18, 2015. PDF.

The United States is experiencing an epidemic of drug overdose (poisoning) deaths. Since 2000, the rate of deaths from drug overdoses has increased 137%, including a 200% increase in the rate of overdose deaths involving opioids (opioid pain relievers and heroin). CDC analyzed recent multiple cause-of-death mortality data to examine current trends and characteristics of drug overdose deaths, including the types of opioids associated with drug overdose deaths. During 2014, a total of 47,055 drug overdose deaths occurred in the United States, representing a 1-year increase of 6.5%, from 13.8 per 100,000 persons in 2013 to 14.7 per 100,000 persons in 2014. The rate of drug overdose deaths increased significantly for both sexes, persons aged 25–44 years and ≥55 years, non-Hispanic whites and non-Hispanic blacks, and in the Northeastern, Midwestern, and Southern regions of the United States. Rates of opioid overdose deaths also increased significantly, from 7.9 per 100,000 in 2013 to 9.0 per 100,000 in 2014, a 14% increase. Historically, CDC has programmatically characterized all opioid pain reliever deaths (natural and semisynthetic opioids, methadone, and other synthetic opioids) as “prescription” opioid overdoses. Between 2013 and 2014, the age-adjusted rate of death involving methadone remained unchanged; however, the age-adjusted rate of death involving natural and semisynthetic opioid pain relievers, heroin, and synthetic opioids, other than methadone (e.g., fentanyl) increased 9%, 26%, and 80%, respectively. The sharp increase in deaths involving synthetic opioids, other than methadone, in 2014 coincided with law enforcement reports of increased availability of illicitly manufactured fentanyl, a synthetic opioid; however, illicitly manufactured fentanyl cannot be distinguished from prescription fentanyl in death certificate data. These findings indicate that the opioid overdose epidemic is worsening. There is a need for continued action to prevent opioid abuse, dependence, and death, improve treatment capacity for opioid use disorders, and reduce the supply of illicit opioids, particularly heroin and illicit fentanyl.

image of opioids-death-rate
Opioids, which are primarily prescription pain relief drugs and heroine, counted for 28,647 deaths in 2014, according to the report released by the Centres for Disease Control and Prevention (CDC) .

The National Vital Statistics System multiple cause-of-death mortality files were used to identify drug overdose deaths.* Drug overdose deaths were classified using the International Classification of Disease, Tenth Revision (ICD-10), based on the ICD-10 underlying cause-of-death codes X40–44 (unintentional), X60–64 (suicide), X85 (homicide), or Y10–Y14 (undetermined intent) (2). Among the deaths with drug overdose as the underlying cause, the type of opioid involved is indicated by the following ICD-10 multiple cause-of-death codes: opioids (T40.0, T40.1, T40.2, T40.3, T40.4, or T40.6); natural and semisynthetic opioids (T40.2); methadone (T40.3); synthetic opioids, other than methadone (T40.4); and heroin (T40.1). Some deaths involve more than one type of opioid; these deaths were included in the rates for each category (e.g., a death involving both a synthetic opioid and heroin would be included in the rates for synthetic opioid deaths and in the rates for heroin deaths). Age-adjusted death rates were calculated by applying age-specific death rates to the 2000 U.S standard population age distribution (3). Significance testing was based on the z-test at a significance level of 0.05.

The opioid epidemic is devastating American families and communities.
To curb these trends and save lives, we must help prevent addiction and provide support and treatment to those who suffer from opioid use discords.
CDC Director, Dr. Tom Frieden

During 2014, 47,055 drug overdose deaths occurred in the United States. Since 2000, the age-adjusted drug overdose death rate has more than doubled, from 6.2 per 100,000 persons in 2000 to 14.7 per 100,000 in 2014 . The overall number and rate of drug overdose deaths increased significantly from 2013 to 2014, with an additional 3,073 deaths occurring in 2014, resulting in a 6.5% increase in the age-adjusted rate. From 2013 to 2014, statistically significant increases in drug overdose death rates were seen for both males and females, persons aged 25–34 years, 35–44 years, 55–64 years, and ≥65 years; non-Hispanic whites and non-Hispanic blacks; and residents in the Northeast, Midwest and South Census Regions . In 2014, the five states with the highest rates of drug overdose deaths were West Virginia (35.5 deaths per 100,000), New Mexico (27.3), New Hampshire (26.2), Kentucky (24.7) and Ohio (24.6). States with statistically significant increases in the rate of drug overdose deaths from 2013 to 2014 included Alabama, Georgia, Illinois, Indiana, Maine, Maryland, Massachusetts, Michigan, New Hampshire, New Mexico, North Dakota, Ohio, Pennsylvania, and Virginia.

In 2014, 61% (28,647, data not shown) of drug overdose deaths involved some type of opioid, including heroin. The age-adjusted rate of drug overdose deaths involving opioids increased significantly from 2000 to 2014, increasing 14% from 2013 (7.9 per 100,000) to 2014 (9.0). From 2013 to 2014, the largest increase in the rate of drug overdose deaths involved synthetic opioids, other than methadone (e.g., fentanyl and tramadol), which nearly doubled from 1.0 per 100,000 to 1.8 per 100,000. Heroin overdose death rates increased by 26% from 2013 to 2014 and have more than tripled since 2010, from 1.0 per 100,000 in 2010 to 3.4 per 100,000 in 2014. In 2014, the rate of drug overdose deaths involving natural and semisynthetic opioids (e.g., morphine, oxycodone, and hydrocodone), 3.8 per 100,000, was the highest among opioid overdose deaths, and increased 9% from 3.5 per 100,000 in 2013. The rate of drug overdose deaths involving methadone, a synthetic opioid classified separately from other synthetic opioids, was similar in 2013 and 2014.

Relates Press Releases

  • Bold bid to rein in painkiller prescriptions hits roadblocks, cnbc, 19 Dec 2015.


Reproductive Health and the Environment Symposium 2015

International Federation of Gynecology and Obstetrics (FIGO) XXI 2015 World Congress

Video Overview

The video mentions the Diethylstilbestrol and Thalidomide tragedies…

  • 00:40 Introduction: Reproductive Health, OBGYNs and the Environment, Jeanne A. Conry, MD, PhD, Past president, American College of Obstetricians and Gynecologists, Assistant Physician-in-Chief North Valley, Kaiser Permanente.
  • 08:40 From Silent Spring to Silent Night, Tyrone B. Hayes, PhD, Professor, Integrative Biology, University of California, Berkeley.
  • 28:40 Environmental Reproductive Health in Developing Countries, Katsi Cook, Program Director for Indigenous Communities, NoVo Foundation.
  • 54:40 Global Reproductive Health and the Environment: What Does the Evidence Say? Tracey J. Woodruff, PhD, MPH, Professor and Director, University of California, San Francisco, Program on Reproductive Health and the Environment.
  • 01:18:10 Vision for the Future. Dr. Jennifer Blake, CEO, The Society of Obstetricians and Gynaecologists of Canada.
More information