31 October 2017
Breast cancer rates on Cape Cod are 21 percent above the state average, Silent Sprint Institute researchers reminded a 150-member audience at Barnstable Town Hall Wednesday.
Breast cancer rates on Cape Cod are 21 percent above the state average, Silent Sprint Institute researchers reminded a 150-member audience at Barnstable Town Hall Wednesday.
It's Surprisingly Hard to Ban Toxic Sex Toys, But Here's How to Protect Yourself
OCTOBER 13, 2017 3:05 PM
PHOTO: COMEDY CENTRAL
These days, most of us will carefully check ingredients lists for gluten and trans fats, demand that our water bottles be made without BPA, and seek out paraben-free, body-safe cosmetics. But the average person can’t tell you what a toxic sex toy is—or even that they exist. Unfortunately, in the unregulated sex toy industry, plenty of sex toys are potentially rife with products that can hurt you (and not even in the fun, kinky way).
Perhaps the most well-known offender in terms of toy toxicity is a group of chemicals known as phthalates, a plasticizer that can be blended with other substances to make them softer and more flexible. A spotlight’s been shone on phthalates in recent years, as publications like Bustle and Bitch, and feminist-oriented sex shops like Good Vibes and Babeland have spoken out against them.
So why all the hullabaloo? It turns out that phthalates may have side effects when they come into contact with your body that could potentially be terrible for you—and aren’t disclosed by most sex toy manufacturers. According to Amanda Morgan, D.H.S., a faculty member at the School of Community Health Sciences at the University of Nevada, Las Vegas, who wrote her master’s thesis on harmful sex toy materials, phthalates are known endocrine disruptors that can cause health problems. “[Phthalates] mess with your hormones; they can cause birth defects, or other things related to liver or kidney functioning,” Morgan told me, referencing studies that have linked phthalates to irregular fetal development, early-onset puberty, and lower sperm counts, among other issues. “They can really mess you up because they pretend to be your hormones, and so your body’s hormonal cycle gets knocked out of whack from exposure to these things.”
With the short-term effects of chlorine and the long-term effects of phthalates, PVC is, Morgan said, “definitely one of the worst sex toy materials we’ve seen.”
When you hear horror stories about sex toys, though, it’s not necessarily phthalates that are to blame. One of the most common anecdotal complaints about toxic toys is that they cause skin irritation: “I first thought [it] was a yeast infection or BV, because of extreme itching and burning on my inner labia,” reports one reader who wrote in to sex toy review blog Dangerous Lilly. “My ass suddenly felt like it was on fire. A burning sensation spread throughout my butt,” recalled sex educator Tristan Taormino about a questionable dildo she used. One Playboy story described a dildo that caused a woman “such severe pain that she could barely speak.”
I asked Emily S. Barrett, Ph.D., a professor at the Rutgers University School of Public Health who has done extensive research on the prenatal effects of endocrine disruptors like phthalates, whether these reported burning sensations fit with her understanding of the chemicals. She told me she hasn’t seen evidence that phthalates irritate the skin in this way, and that they tend to “act on a much more subtle level most of the time.”
So what is causing these health problems? According to Amanda Morgan, phthalates aren’t the only sketchy ingredient still getting into our sex toys. As part of her thesis research, Morgan tested 32 sex toys to determine their chemical makeup. What she found was pretty scary: The toys she tested typically contained 30 to 35 percent chlorine. She said PVC, a material commonly used to make inexpensive sex toys, always contains chlorine (hence the chemical name “polyvinyl chloride”). Even scarier, in 2006, BadVibes.org—an organization that, full disclosure, is linked to pro-toy-safety sex shop The Smitten Kitten—ran lab tests on four popular sex toys. They found that two of them were made of PVC and contained “very high levels of phthalate plasticizer.”
“We use chlorine to kill bacteria in things,” Morgan said. “If you are being exposed to this high level of chlorine, especially in a sensitive membrane area [like the vagina or rectum], we could definitely chalk that up to causing irritation, burning, or messing up the environment by exposing it to something that is, as we know, a sterilization product.” So with the short-term burning effects of chlorine and the long-term endocrine effects of phthalates, PVC is, Morgan said, “definitely one of the worst sex toy materials we’ve seen.”
Now, you might be thinking, “OK, great to know! I’ll just buy only safe toys from now on!” Well, it’s not so simple. Since the sex toy industry is unregulated, it doesn’t fall under the current purview of the Food and Drug Administration. According to FDA press officer Angela Stark, that’s because the agency “does not regulate devices meant purely for sexual pleasure. It does, however, regulate genital devices that have a medical purpose such as vibrators intended for therapeutic use to treat sexual dysfunction or to supplement Kegel exercises.” Of course, the vast majority of sex toys don’t fall under this “health aid” umbrella.
The current Congress likely wouldn't rush to make a bold, sex-positive statement like mandating sex toy safety.
The responsibility of regulating sex toys could potentially fall to the Consumer Product Safety Commission, but Morgan told me the understaffed CPSC is already in charge of regulating over 15,000 types of products—not to mention the products themselves. The complex issue of sex toy regulation would be a big ask on top of all that.
Add to all of this the fact that the current Congress likely wouldn’t rush to make a bold, sex-positive statement by mandating sex toy safety, and there are plenty of reasons your sex toy might not meet body-safe standards. “Our government doesn’t generally like to talk about people pleasuring themselves,” Morgan pointed out.
Beyond that, though, Morgan adds that regulating the sex toy industry might not even be the best solution to getting rid of toxic toys anyway. “If something is federally regulated, that means that the federal government—depending on where they are in their political leanings at that time—could potentially make it illegal to have these products, by saying they are ‘dangerous’ and then regulating them out of existence,” she reasoned. “You get certain types of people in power, and they may not believe in sexual health, wellness, [or] self-pleasuring. It might go against their core values, and therefore they [might] use their political agenda and the federal regulation system to regulate these products out of people’s hands.”
It’s a conclusion that Zach Biesanz, a legal assistant in the office of New York’s Attorney General, came to in his 2007 paper in the journal Law & Inequality: "Special regulation of the sex toy industry would be unreasonably burdensome from a regulatory standpoint,” he wrote. "Only banning these toxins outright will suffice to protect consumers from phthalates' harmful and even lethal effects.”
"Sniff your sex toy. That's the easiest thing you can do [to protect yourself]."
In the meantime, how do you tell if a toy is safe? Sex toy experts like Morgan, Smitten Kitten founder Jennifer Pritchett, and seasoned sex toy reviewer Epiphora all recommend buying toys made of phthalate-free, body-safe materials like pure silicone, stainless steel, glass, and hard plastic. Still, it’s difficult to know what’s what in an industry that mislabels its products so frequently. “Sniff your sex toy,” said Morgan. “That’s the easiest thing you can do. If you smell these products and they don’t smell like anything, then it most likely is a stable chemical compound like silicone.” Phthalates and PVC, however, smell “like chemicals,” according to Morgan, “like a new shower curtain,” according to Epiphora, and “like a headache,” according to Pritchett. The sex toy smell test might sound a little weird, but it’s a pretty good first line of defense.
Morgan also recommends buying toys made by “companies that take a lot of pride in making good-quality, body-safe toys,” citing Tantus and Jimmyjane as examples. Other companies that proudly declare their products body-safe include We-Vibe, Fun Factory, Vixen Creations, and Funkit Toys.
And when in doubt, find a reviewer you can trust. Sex toy review blogs abound on the internet —Epiphora, Dangerous Lilly, and Formidable Femme, to name just a few—and while you’d be wise to take claims about sex toys with a grain of salt in this unregulated industry, sometimes the preponderance of good or bad reviews about a particular company or toy can suggest conclusions about its safety (or lack thereof).
Most important, though, demand body-safe sex toys by buying only from companies you can trust. “Consumers vote with their pocketbook,” said Tantus founder Metis Black. “Support the businesses that make safe toys a priority, that use their resources to educate, that take a stand and advocate for consumers.” She added that while pure silicone toys are expensive now—especially in comparison to PVC toys, which can often be under $30 a pop versus $100+ for silicone—more consumer demand for body-safe toys will create a larger supply at lower prices, as bigger companies with more resources start making nontoxic toys in larger quantities. That’s just sex toy economics.
Bloggers, consumers, and ethical toymakers alike all dream of a future in which no sex toys will burn your junk, give you infections, or cause long-term bodily harm. It seems reasonable enough. And if we keep fighting for it, maybe one day it’ll be reality.
Two Democratic members of Congress on Thursday requested an audit of the death toll in Puerto Rico following Hurricane Maria, amid concerns that the government is undercounting the number of victims.
The request cites a Vox report published Wednesday that found a significant discrepancy between the government’s official death toll of 45 and reports from the ground. Our analysis found a total of 81 deaths linked directly or indirectly to the hurricane; another 450 reported deaths, most of causes still unknown; and reports of at least 69 people still missing.
In their letter to Department of Homeland Security Secretary Elaine Duke, Rep. Nydia Velazquez (D-NY) and Rep. Bennie Thompson (D-MS) wrote, “It would be morally reprehensible to intentionally underreport the true death toll to portray relief efforts as more successful than they are. If, on the contrary, this information has benignly been muddled due to a lack of capacity on the island, then the federal government must work hand-in-hand with Puerto Rico's government to provide a clearer assessment.”
Velazquez and Thompson went on to ask the Department of Homeland Security to do the following:
Conduct a federal examination of all death estimates provided by local authorities.
Evaluate the accuracy of such estimates and whether or not their methodology is appropriate.
Send a report of these findings to Congress within 10 days.
“The American people deserve to know what’s happening to their fellow U.S. citizens in Puerto Rico,” Velázquez said in a statement. “Given recent reports suggesting that the death toll is much higher than is being officially acknowledged, we need a swift and thorough investigation to ensure the real magnitude of this crisis is made public.”
By Ken Ward Jr. Staff writer 10 hrs ago (0)
Thousands of Kanawha Valley residents, businesses and workers now can file claims to receive their share of the $151 million settlement of the class-action lawsuit over the January 2014 water crisis.
This week, tens of thousands of notices about the settlement went out in the mail, along with separate notices that were emailed to a list of West Virginia American Water Co. customers.
Notices sent by mail include the simple claim form that most residents can use to file their claims. Claims can also be filed online and paper copies of claim forms downloaded from the settlement website, https://www.wvwaterclaims.com/. More information is available by calling 1-855-829-8121 or reading the “Frequently Asked Questions” list on the website.
Deadline for filing claims is Feb. 21, 2018, under an order issued by U.S. District Judge John Copenhaver Jr., who is overseeing the case.
“This is the only way to make sure you get any money from the settlement,” the notice mailed out this week says in encouraging claims to be filed.
Under the settlement, residential households — including homeowners and renters — can file a simple claim form and obtain $550 for the first resident and $180 for each additional resident. Residents also may file more detailed information about their losses — for things such as bottled water or replacement appliances — if they provide proof of those expenditures on a separate type of claim form.
Businesses and nonprofit organizations can likewise obtain flat payments, based on their size, or can submit documentation of specific losses to have those recouped.
The settlement also provides additional payments to women who were pregnant at the time of the chemical spill that sparked the water crisis, residents who had medical expenses and hourly-wage earners who lost money when businesses they worked in closed during the crisis. Government agencies also are eligible to submit claims.
Residents, businesses and others don’t have to have previously hired a lawyer or signed up for a lawsuit to be eligible, but they do have to file claims.
Anyone who falls within the definition of the “class” covered by the settlement can file a claim for compensation. The class covered by the case includes 224,000 residents and 7,300 businesses. It includes basically any business or resident who received tap water from the Elk River intake plant and any hourly-wage earner whose employer closed because of the spill and resulting water system contamination.
In the case, lawyers for residents and businesses had alleged that West Virginia American did not adequately prepare for or respond to the spill and that MCHM-maker Eastman did not properly warn Freedom of the dangers of its chemical or take any action when Eastman officials learned that the Freedom facility was in disrepair. West Virginia American and Eastman continue to deny any liability. They say the blame for the crisis rests with Freedom Industries, which admitted to criminal pollution violations related to the spill.
Distribution of the settlement funds will not start until the settlement receives final approval from Copenhaver, following a hearing scheduled for Jan. 9, and until after the Feb. 21 deadline for filing claims.
Members of the class have the right to “opt-out” of the settlement or to object to certain terms of the deal. The deadline for opting out or filing objections is Dec. 8. Class members also may ask for permission to speak during the Jan. 9 hearing on the settlement.
Reach Ken Ward Jr. at
or follow @kenwardjr on Twitter.
By Lynn Desjardins | email@example.com
Tuesday 10 October, 2017 , No Comments ↓
Five environmental groups say Canada’s law governing toxic chemicals is outdated and they urge the government to amend soon it to protect children and the general population. Muhannad Malas of Environmental Defence uses the example of a class of chemicals called phthalates to highlight the need to change the law.
Europe, some U.S. states have acted
“The Canadian government assessment of phthalates concluded, surprisingly, that none of that phthalates that were in the assessment…pose a risk to the health of Canadians,” he said. “And this is really not consistent with what we have seen in other jurisdictions like in Europe and in the United States where several states have designated a number of phthalates as harmful to health.”
These chemicals are used in plastic toys, personal care products, and food packaging. They are also used in fragrances and other scented products and there is no obligation for them to be mentioned on the labels of these products.
Phthalates may be in fragrances and other scented products. © iStock/Getty Images
Links to reproductive abnormalities
Environmental Defence says this group of chemicals has been linked to many health impacts including reproductive abnormalities and infertility.
Malas says the law governing toxics, the Canadian Environmental Protection Act (CEPA) was passed in 1999 and science has discovered much since then about the effects of hormone disruptors on the human body.
Environmental groups call for better protection for pregnant women, children and other vulnerable groups.
Groups call for proof chemicals are safe
He and other environmentalists would like the law to be amended to better protect vulnerable populations like children and pregnant women and to require proof chemicals are safe before they are used in consumer products.
“What we need to see here is…the idea of reversing the burden of proof onto industry when it comes to these substances of very high concern, like some phthalates like BPA, to make sure that they’re only used when their use is proven to be safe,” says Malas.
Government committee called for law changes
He says a House of Commons committee recently reviewed the CEPA and listed this burden of proof issue as one of 87 recommendations it made to update and reform the law. The environment minister has promised to consider the recommendations but the groups are calling on her to act soon. They are Environmental Defence, Ecojustice, David Suzuki Foundation, Equiterre, and the Canadian Association of Physicians for the Environment (CAPE).
Tagged with: CEPA, health, phthalates, toxic chemicals
Posted in Environment, Health
In our news wrap Tuesday, the confirmed death toll in Puerto Rico rose to 43 nearly three weeks after Hurricane Maria wrecked the island. Authorities blamed infections and bad road conditions, among other factors. Also, President Trump denied he was undercutting Secretary of State Tillerson, despite proposing to Forbes magazine they compare IQ tests after Tillerson reportedly called him a “moron.”
SUPPORT FOR PBS NEWSHOUR PROVIDED BY
Did a culture of complicity protect Harvey Weinstein?
How Sinclair Broadcasting puts a partisan tilt on local news
What revoking the Clean Power Plan means, from both sides
JUDY WOODRUFF: And in the day’s other news: The confirmed death toll in Puerto Rico rose to 43, nearly three weeks after Hurricane Maria wrecked the U.S. territory. Authorities blamed infections and bad road conditions, among other factors.
At the same time, local officials said power has been restored to just 16 percent of the island’s customers. Maria knocked out electricity to all of Puerto Rico.
President Trump today denied that he is undercutting his secretary of state, Rex Tillerson. The president spoke as he met with former Secretary of State Henry Kissinger. He told reporters, “I don’t believe in undercutting people.”
Earlier, in a “Forbes” magazine interview, Mr. Trump reacted to reports that Tillerson had called him — quote — “a moron.” He said — quote — “If he did that, I guess we will have to compare I.Q. tests. And I can tell you who is going to win.”
This afternoon, White House spokeswoman Sarah Sanders dismissed questions about the president’s quip.
SARAH SANDERS, White House Press Secretary: He wasn’t questioning the secretary of state’s intelligence. He made a joke. Maybe you guys should get a sense of humor and try it some time. But he simply made a joke.
He’s been extremely clear, time and time again, despite the fact that you guys want to continue to bring this up and create a story. He’s got 100 percent confidence in the secretary of state.
JUDY WOODRUFF: All of this came on a day when President Trump had lunch with Secretary Tillerson, and with Defense Secretary Jim Mattis.
The president also went after Democrats today over immigration reform. In a morning tweet, he charged, “The Democrats don’t want secure borders,” and he said, “They don’t care about safety for USA.”
Last month, Mr. Trump met with Democratic leaders about protecting young undocumented immigrants. He now says that a border wall and other measures must be included in any deal.
U.N. humanitarian agencies say they are on full alert, as a new exodus of refugees from Myanmar floods into Bangladesh. Some 11,000 Rohingya Muslims have made the crossing yesterday alone. Today, UNICEF said it’s working to give 900,000 doses of cholera vaccines to the refugees. They are crowded into makeshift camps, where the disease is spreading.
A diplomatic row between Turkey and the United States heated up today. Overnight, the U.S. ambassador to Ankara condemned the arrest of a Turkish man employed at the U.S. Consulate in Istanbul. Today, Turkey’s President Recep Tayyip Erdogan charged that the man was a spy. He also criticized the ambassador and the U.S. decision to halt visa services.
In Spain, the president of Catalonia stopped short today of declaring the region’s independence. He called instead for negotiations. The region’s government says that Catalans voted overwhelmingly to secede in a referendum on October 1.
The Catalan president addressed his parliament today and urged calm, after Madrid flatly rejected the outcome.
CARLES PUIGDEMONT, Catalan Regional President (through interpreter): We propose that parliament suspend the effects of a declaration of independence, so that in the next few weeks, we start a dialogue, without which it is not possible to get to a concerted solution. We firmly believe that, at this moment, a de-escalation of tensions is necessary.
JUDY WOODRUFF: Spain’s central government has warned that it will sternly oppose any attempt to secede.
Kenya’s opposition leader, Raila Odinga, declared today he will not compete in a rerun of the presidential election. That leaves President Uhuru Kenyatta without a challenger. Odinga says the election commission has — quote — “stonewalled reforms” that are needed to ensure the vote is fair. Kenyatta won an August election, but the Kenyan Supreme Court overturned it.
Back in this country, owners of the National Football League’s teams will consider making it mandatory for players to stand during the national anthem. Commissioner Roger Goodell told the executives in a memo today that the issue is dividing the league from many fans. The owners meet next week.
And on Wall Street, the Dow Jones industrial average gained nearly 70 points to close at 22830. The Nasdaq rose seven, and the S&P; 500 added almost six.
Francis Koster: We can reduce breast cancer by reducing pollution
By Francis Koster
Email the author
Published 12:21 am Sunday, October 8, 2017
By Francis Koster
This is Breast Cancer Awareness Month.
Here are some facts about breast cancer you may not know.
Sadly, around 40,000 women die from breast cancer each year. Of these, only about 30 percent of cases can be explained by known risk factors like genetics. Research now tells us that pollution accounts for a large number of the rest.
As our nation recoils in horror from the scenes of the massacre in Las Vegas, we will be reminded over and over that (not counting suicides) around 14,000 Americans were killed annually by guns fired by other people. We will all hear cries for various forms of gun control.
You are not likely to be reminded that almost three times that many woman die annually as a result of breast cancer — and you are not likely to hear cries for pollution control to prevent more senseless death.
October is national breast cancer month, full of fund-raising marches of people noting their concern by wearing pink ribbons.
Shouldn’t we also be asking why we march for a cure, and not for prevention?
When pollution and contamination are discussed, they are frequently illustrated with images of polar bears on shrinking icebergs, or references to dying forests or fish kills. We do not talk about the reality that pollution kills and maims everyday people.
Studies from all over the world show that women who live in areas of high air pollution develop twice as much breast cancer as women who live in areas with clean air. As China has become more industrialized, its air and water pollution have become legendary — and its breast cancer rates are skyrocketing.
The key suspect in the polluted air is nitrogen dioxide — created by burning fossil fuels, mostly automobile gasoline. Several Canadian studies have found that the chances of developing breast cancer at a relatively young age increased by 20 percent if a woman lives in an area with high nitrogen dioxide. The higher the amount in the air, and/or the longer the woman lives in areas with high pollution, the more her chances of developing breast cancer rise.
They found an increased risk of developing breast cancer for approximately 25 percent for every increase of 5 parts per billion in exposure.
There is another factor associated with air pollution that increases the risk of breast cancer. Doctors know that women who have what is called “dense breast tissue” are at higher risk for breast cancer than other women. In studies done around the world, dense breast tissue has been found to be caused in part by air pollution.
A lot of this research has been done in countries with national health insurance, because the governments are searching hard for ways to invest in the prevention of disease, instead of just healing it. America is not behaving this way.
In 2017, U.S. government spending on cancer research, adjusted for inflation, is at its lowest rate since 2001. On top of that, the current administration has submitted a 2018 budget calling for an additional $1 billion in cuts. If that is not bad enough, that same budget calls for a 30 percent cut in funding for the Environmental Protection Agency.
When we talk about pollution, in addition to pictures of polar bears on melting icebergs, or fish kills, we must also display the images of the bare chest of a woman with the scars of a breast removed — because that is also a problem that must be solved. If we control the pollution, not only will the polar bear and fish be saved, so will our loved ones.
Maybe the horror of those images would make people ask why the North Carolina legislature ordered the removal of half of all bought and paid for air quality monitors in the state over the last three years.
It is time to recognize that the cost of prevention is far cheaper than the cost of curing — and that if our society regulated pollution more, we would spend less on healthcare.
Do you want to fix the federal deficit by lowering health care spending? Stop pollution. One in eight American women (the number who get breast cancer) will thank you.
And we will need fewer pink ribbons.
Francis P. Koster of Kannapolis is a member of the Society of Environmental Journalists and the Association of Health Care Journalists.
Julia R. Barrett
PDF Version (532 KB)
About This Article
Published: 04 October 2017
Note to readers with disabilities: EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact firstname.lastname@example.org. Our staff will work with you to assess and meet your accessibility needs within 3 working days.
Related EHP Article
Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6–12 Years of Age in Mexico
Morteza Bashash, Deena Thomas, Howard Hu, E. Angeles Martinez-Mier, Brisa N. Sanchez, Niladri Basu, Karen E. Peterson, Adrienne S. Ettinger, Robert Wright, Zhenzhen Zhang, Yun Liu, Lourdes Schnaas, Adriana Mercado-García, Martha María Téllez-Rojo, and Mauricio Hernández-Avila
As a trace element, fluoride can help ward off dental cavities. Exceptionally high pre- and postnatal exposures, as seen in populations whose drinking water supplies are contaminated by natural fluoride sources, have been implicated in a number of adverse health effects.1,2,3,4 However, less is known about fluoride’s neurotoxic risks at lower levels of exposure. A new study in Environmental Health Perspectives examines risks of exposure to prenatal fluoride at concentrations typical of the general population.5
In many countries, small amounts of fluoride are added to drinking water, salt, or milk to reduce the incidence of tooth decay.6,7,8 The U.S. Public Health Service recommends an optimal level of 0.7 mg/L fluoride in drinking water for caries prevention.2 Fluoride can also occur naturally in water, with concentrations exceeding 4.0 mg/L in some areas of the United States1; this is the maximum contaminant level for fluoride set by the U.S. Environmental Protection Agency.6
There is some debate regarding whether fluoridation is still needed for drinking water. Fluoridation of public water supplies was started in 1945 in the United States as a preventive measure to reduce the incidence of tooth decay.9 Most of the evidence for the benefits of fluoridation was collected prior to 1975, before widespread use of fluoride toothpastes and dental treatments1,9 and before modern assessments of dietary sources of fluoride.1,10 However, for people who do not have access to proper dental care, cutting off water fluoridation could cause them to get too little fluoride.
With high exposure—typically exceeding the maximum contaminant level—fluoride can accumulate in teeth and bones, causing tooth discoloration and weakness as well as bone pain and increased fracture risk.1 An additional concern is potential neurotoxicity, particularly during fetal development and early childhood.1,4,11 In a 2012 review of studies conducted in China and Iran,3 children living in regions with very high levels of naturally occurring fluoride in drinking water had lower scores on intelligence tests than children living in regions with low water levels of fluoride.
Philippe Grandjean, a professor of environmental health at the Harvard T.H. Chan School of Public Health who coauthored the 2012 review, notes that the advantage of the studies in China is that they were primarily conducted in rural areas where families remained in the same place for an extended time. Therefore, when a child was examined at school age, his or her current exposure to fluoride in water likely matched his or her prenatal exposures. “However, we do not have that kind of a setting in other parts of the world, necessarily, and particularly not in the United States,” says Grandjean, who was not involved in the present study.
The authors of the new study5 used data on 299 mother–child pairs collected through the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) Project. Pregnant women recruited at three Mexico City hospitals provided urine samples during gestation, and information was collected regarding their demographics, lifestyle, and medical history. Their children’s cognitive ability was evaluated at 4 years of age using the McCarthy Scales of Children’s Abilities, and at 6–12 years of age, the children completed an IQ assessment (Wechsler Abbreviated Scale of Intelligence) and provided urine samples.
Higher levels of fluoride in mothers’ urine during pregnancy were associated with lower cognitive and IQ scores in their children, but no association was found between the scores and the children’s own fluoride levels at 6–12 years of age. Maternal and child urinary levels of fluoride averaged 0.90 and 0.82 mg/L, respectively. The authors estimated that each 0.5-mg/L increase in maternal urinary concentration was associated with an average decrease of 3.15 and 2.50 points in cognitive and IQ scores, respectively. The researchers recommend greater scrutiny of potential adverse effects of fluoride, particularly in pregnant women and in children.
For people who get enough fluoride from toothpastes and dental treatments, fluoridated drinking water could result in overexposure. However, for people without access to proper dental care, fluoridated water is an important preventive measure. Image: © Ian Cartwright parenting/Alamy Stock Photo.
The study’s strengths include its longitudinal design, its large sample size, and the assessment of children’s neurocognitive development using validated tests. However, the researchers could not rule out the impact of unmeasured variables, including total exposure to other neurotoxicants.
“So little research has been done on the effects of prenatal fluoride on neurodevelopment that it is difficult to know how to interpret the implications of this study,” says study coauthor Howard Hu, a professor at the Dalla Lana School of Public Health, University of Toronto. “There are gaps that need to be addressed in order for the scientific world to better interpret the implications of our study. And, of course, it is just one study, and these results need to be addressed with additional studies of its kind.”
Julia R.Barrett, MS, ELS, a Madison, Wisconsin–based science writer and editor, is a member of the National Association of Science Writers and the Board of Editors in the Life Sciences.
The Gaza Strip was a month into this summer’s suffocating electricity crisis when Thair Salah Mortaja became a father for the first time. He had spent thousands of dollars to overcome infertility – first paying for drugs, then a futile operation, and finally for costly in vitro fertilisation (IVF) – but the struggle for parenthood did not end there.
His wife, Fatima, went into labour when she was just seven months pregnant, partly because of poor prenatal care. Their doctor wanted to get her to a specialist in Nablus, but the hard-to-procure permit to exit blockaded Gaza into Israel and proceed to the West Bank city didn’t come through. After a tense labour, she gave birth prematurely to triplets (multiple births are common with IVF). But the intensive baby care unit at Gaza’s largest hospital, Shifa, was already over capacity.
Facebook Twitter Pinterest
Thair Salah Mortaja, left, with his uncle, centre, and father, right, and his uncle’s children. Photograph: Miriam Berger
So they waited hours until an incubator became available. The doctors decided to put the son and one daughter together in the incubator, run by generators amid the power shortages. The third child remained on oxygen in a little bed beside her siblings. The overstressed intensive care unit frequently makes such arrangements for IVF twins and triplets, a doctor explained.
The war-torn and impoverished coastal enclave – which the UN has declared “unlivable” – is a surprising place to find widespread access to IVF treatment. But it is accepted by Palestinians in Gaza, for whom having children is a source of social respect, national strength and religious duty – feelings only heightened by the death and destruction around them. Amid socio-economic pressure to conceive, IVF has also been a politically expedient tool to garner goodwill: this summer, Gaza’s extremist Hamas government provided free treatment for chosen couples, as did the NGO run by the wife of another major Palestinian political player, Mohammed Dahlan.
A week on, Fatima was back home recovering while the couple’s babies remained hospitalised. Mortaja’s heart was still racing constantly. In the weeks before, and since, several babies have died waiting for the rival Palestinian Authority and Israel to approve exit permits for people to receive urgent care unavailable in resource-limited Gaza. One day that week in July at Shifa’s intensive care unit, a baby who had just died lay in an incubator, his body withered and still, before doctors removed him to make way for another.
Israel and Hamas have fought three wars since 2007, while Israel and Egypt have kept Gaza blockaded on security grounds. Now Gaza’s 2 million people are faced with unemployment and population density that is among the highest in the world, stuck in what they often describe as an open-air prison.
Facebook Twitter Pinterest
Palestinian boys stand beside Hamas militants as they take part in a military show against Israel’s newly installed security measures at the entrance to the al-Aqsa mosque compound in Khan Younis, in the Gaza Strip. Photograph: Ibraheem Abu Mustafa/Reuters
The dire situation worsened in June when the Palestinian Authority, which runs the West Bank, stopped paying Israel for Gaza’s electricity in an attempt to squeeze Hamas out. In response, in the dead heat of summer, Israel cut electricity and Gazans went from having eight hours of power to just three or four. Anger against the authority, its Fatah party, and Hamas, along with Israel, only grew.
In these circumstances, IVF comes with a host of complications. The fertility rate in Gaza is among the highest in the Arab region, with 4.5 children a couple, compared with the West Bank’s 3.6, according to a 2017 UN Population Fund report. Dr Bakr Qaoud, of the Gaza City Helow Centre, says more than 1,000 couples annually try the treatment in Gaza through private clinics, at a cost of $2,000-$2,500 (£1,500-£1,900) a round. He says thousands more would like it, but can’t pay.
Dr Mohamed Jouda, who runs the Hala Centre in Gaza City, says that over the years he’s been working in the field he has seen a decline in male fertility rates, which he attributes to the stresses of war and environmental factors such as the use of herbicides and other toxins.
There are, however, no formal studies of infertility rates in Gaza. Neither is there research into the impact of pesticides used by Israelis and Palestinians, although rumours in Gaza persist that the Israelis use pesticides on food imported into Gaza that contribute to male infertility.
While some conservative communities object to IVF, Hamas has supported and subsidised the treatment, funding couples during the yearly Ramadan holiday. Gaza is also politically polarised – right down to which clinics people use, says Qaoud, explaining that some are known to be Hamas funded.
Facebook Twitter Pinterest
Palestinian children do their homework during a power cut in Gaza. Residents of Gaza, home to 2 million people, have been experiencing long hours of electricity outage. Photograph: Mahmud Hams/AFP/Getty Images
Mortaja didn’t have any political connections to pay for IVF treatment. In the five years since his marriage, he has spent about $10,000 on hospital visits, operations and IVF. They have sold Fatima’s gold dowry and got into debt with friends and family.
Others are luckier: Ziad Khader, 35, an actor, was among 600 couples to receive free treatment from a charity run by Dahlan’s wife.
For nine years, Khader and his wife failed to conceive. Then he saw an advertisement for funding from Jaleela Dahlan’s group. His wife is now three months pregnant with twins.
Khader is from a Fatah family, and he says he is thankful for the support from Dahlan, who is also Fatah. But he loathes being indebted to anyone. He would rather support his family, he says, but there are no jobs.
“It’s a siege of ideas,” says Khader of the political and economic repression. For now, though, he can’t see beyond the excitement of his wife expecting twins.
Industry and government officials say PFOA, the toxic chemical blamed for contaminating drinking water supplies in Hoosick Falls and several other area communities, is no longer used in manufacturing in the United States.
But if PFOA has been phased out, what are industries using in its place?
People like Silvia Potter would like to know the answer to that question for the two Saint-Gobain Performance Plastics plants that still operate in Hoosick Falls.
Potter said people in her community know “absolutely nothing” about the identity of the chemical or chemicals the company is using as a replacement for PFOA. The lack of information has been frustrating for Potter and other members of the local advocacy group NY Water Project.
“We only know what the company volunteers,” she explained.
Perfluorooctanoic acid, widely used for decades in the making of nonstick coatings like Teflon and a variety of other consumer products, is considered toxic even in tiny amounts. PFOA has been linked to cancer, birth defects and immune system dysfunction.
In 2006, eight major chemical companies, including 3M and DuPont, entered into a “voluntary stewardship agreement” with the U.S. Environmental Protection Agency to phase out the production and use of PFOA by 2015.
In its place, the industry switched to other chemicals in the same family that were deemed less hazardous by the EPA. But lately a variety of experts have begun to believe that these new chemicals also pose grave threats to human health.
Remarkably, it’s not clear whether government regulators – or even companies like Saint-Gobain – know the specific chemical identities of the substances being substituted for PFOA. In response to questions for this story, Saint-Gobain issued a statement saying it has relied on its suppliers to provide replacement chemicals for PFOA and that the composition of these chemicals “in the case of some suppliers may be proprietary.”
At public meetings, Potter said she and other members of NY Water Project have asked questions “at every appropriate moment” about what substances have replaced PFOA. But the information they have sought hasn’t been forthcoming.
“We’re just assured that everything is safe,” she said. “This concerns us, because things went wrong once. We wouldn’t even know about PFOA if it weren’t for Michael Hickey and his determination to get to the bottom of these mysterious illnesses. I believe the town owes Michael a debt of gratitude.”
Hickey’s father, who for many years worked at one of the local Saint-Gobain plants, died of kidney cancer. It was Hickey who thought to test Hoosick Falls’ water for PFOA in 2014, revealing the village’s water contamination problem for the first time.
Change for the better?
PFOA is sometimes called C-8, for its chain of eight carbon atoms, each bonded to fluorine. The carbon-fluorine bond is extremely strong, making PFOA virtually indestructible. So it stays in the environment essentially forever: It doesn’t degrade in water or soil, and plants and animals don’t metabolize it.
By 2014, long after PFOA’s hazards to the environment and human health were first documented, the EPA classified the chemical and its cousin PFOS, which was widely used in firefighting foam, as “emergent contaminants.”
But to this day, the federal government still doesn’t regulate them. And PFOA and PFOS, despite their notoriety, are only two of an estimated 3,000 to 6,000 other unique, highly fluorinated compounds.
The chemicals fall within the EPA’s purview under the federal Toxic Substances Control Act of 1976. But in the four decades since that law was enacted, the EPA has formally assessed only a tiny fraction of the more than 80,000 manmade chemicals on the market.
PFOA is part of a family of highly fluorinated chemicals known as polyfluoroalkyl substances, or PFAS. The chemicals are used to make consumer products resistant to water, grease or stains, such as Gore-Tex rain gear, Teflon no-stick cookware and Scotchgard stain-repellent for carpets and furniture fabrics.
The EPA agreement that phased out PFOA and PFOS by 2015 didn’t stop the production and use of other highly fluorinated chemicals. Instead, the chemical industry has shifted from PFAS compounds with long chains of carbon and fluorine atoms, like PFOA, to shorter-chain compounds in the same family.
The industry had persuaded the EPA that short-chain PFAS chemicals are less persistent in the environment and less harmful to human health than their longer-chain predecessors.
But experts who gathered at a conference this summer in Boston said the supposition that short-chain compounds are inherently safer is not warranted, even though the EPA has enshrined a distinction between short- and long-chain compounds in its policies.
“Every perfluorinated compound studied is causing problems,” said Linda Birnbaum, a toxicologist who serves as the director of the National Institute of Environmental Health Sciences and the National Toxicology Program.
A new generation of toxins
Birnbaum outlined the adverse effects of PFAS compounds in her keynote address at a June conference focused on these chemicals. The conference at Northeastern University brought together research scientists, government officials, lawyers, journalists, environmentalists and people from communities affected by PFAS contamination.
Birnbaum said even minuscule concentrations of perfluorinated compounds can pose risks.
According to conventional wisdom and principles of toxicology, she explained, poison is a function of dosage. So if a substance doesn’t pose risks at high doses, it’s considered unlikely to do so at low exposure.
But with this class of chemicals, Birnbaum said, low levels of exposure may induce biological effects even if high levels of exposure do not. This same dynamic also occurs with other endocrine-disrupting substances.
Andrew Lindstrom, an EPA research scientist who studies trace contaminants for the National Exposure Research Laboratory, told those attending the conference that industry is using short-chain substitutes in place of long-chain compounds like PFOA and PFOS. But he said the replacement compounds present multiple challenges.
First, he said, regulators and the public generally don’t know the specific identities of these chemicals, the quantities in which they’re being produced, their health effects or how long they’re retained in the human body.
There is some data, though, on one short-chain PFAS compound produced under the product name GenX. DuPont introduced GenX in 2009 specifically as a safer replacement for PFOA for use in making Teflon and the stain-resistant and water-repellant coatings found in many consumer products.
In her series “The Teflon Toxin,” investigative journalist Sharon Lerner of the online magazine The Intercept details the numerous health and environmental hazards with this short-chain PFAS compound.
She wrote that DuPont “submitted 16 reports [to EPA] of adverse incidents related to GenX between 2006 and 2013, describing experiments in which lab animals exposed to the chemical developed cancers of the liver, pancreas, and testicles as well as benign tumors. The industry research also tied GenX to reproductive problems, including low birth weight and shortened pregnancies in rats, and changes in immune responses.”
Local companies stay mum
The question of what chemicals have replaced PFOA is moot in North Bennington, Vt., where a former Saint-Gobain plant -- now blamed for contaminating the private wells of more than 200 homes -- has been closed since 2002.
But the issue remains a pressing one for neighbors of the Saint-Gobain plants in Hoosick Falls and the Taconic Plastics factory in Petersburgh, which has been blamed for PFOA contamination discovered last year that affected about 70 local water users.
Neither Saint-Gobain nor Taconic have revealed what chemicals they’re using in place of PFOA.
A call to Saint-Gobain did not yield a direct answer. The response came via Peppercomm, a New York City public relations firm. The firm provided a written statement attributed to Dina Pokedoff, Saint-Gobain’s director of branding and communication.
The statement said Saint-Gobain officials “reasonably rely on our suppliers” to provide replacement chemical for PFOA.
“As part of the U.S. EPA’s Stewardship Program that major raw material producers participated in, a primary goal was to eliminate PFOA from producers’ production processes and to identify replacements for PFOA,” the statement said.
But Saint-Gobain would not characterize those replacement chemicals more specifically. Instead it simply stated, “It is our understanding that the compounds that eventually replaced PFOA are reviewed by the U.S. EPA and in the case of some suppliers may be proprietary.”
A query to Taconic Plastics, which used PFOA for years at its Petersburgh plant, brought a response from corporate counsel Laurie Mason. She declined to provide any information for this report, citing a Superfund investigation and pending civil litigation.
Company records detail hazards
Rob Bilott, a lawyer who brought a class-action suit against DuPont on behalf of people exposed to PFOA near the company’s plant in Parkersburg, W.Va., said the company has a history of professing the safety of highly fluorinated compounds to the public and government regulators -- despite its own research demonstrating serious hazards.
DuPont settled the Parkersburg suit for $235 million in 2004. But Bilott told participants in the June conference how the lawsuit opened a rare window into the normally secret world of an industrial corporation grappling with responsibility and liability for a nightmare chemical.
Through the legal process of discovery, DuPont handed over more than 100,000 pages of internal documents, which Bilott said he then submitted to the EPA with the goal of putting them into the public record.
In that trove of papers, Bilott said he discovered that DuPont had been aware of PFOA’s dangers for several decades. The company studied the chemical in its laboratory program and also collected evidence by monitoring its workers. As a result, DuPont had internally concluded in 1988 that PFOA was a human carcinogen, Bilott said.
By the 1970s, DuPont already knew that PFOA was bio-persistent. In 1984, the company surreptitiously collected samples to test public drinking water for contamination and determined that PFOA was getting into public water supplies, Bilott said.
More than 35 years ago, 3M’s rodent studies had linked PFAS with birth defects. When DuPont repeated the studies, it dismissed any association. But then it monitored a small number of pregnant employees exposed to PFOA. Two women out of a sample of eight or ten gave birth to babies with the same type of unusual birth defects, Bilott said.
In the late 1980s DuPont established its own action level of 500 parts per trillion for PFOA in drinking water. That’s 100 times lower than the threshold of 50 parts per billion that New York was using as a fallback when PFOA was first found in Hoosick Falls’ drinking water in 2014, prior to EPA’s intervention in late 2015 to warn the public not to drink the village water.
The EPA first set a guidance level of 400 ppt for short-term exposure to PFOA in drinking water in 2009. In 2016, the agency established 70 ppt as a guideline upper level for long-term exposure, and New York followed suit.
Last year, after PFOA was detected in North Bennington wells, Vermont established a drinking water enforcement standard of 20 ppt.
Contamination spread widely
Jason Galloway, an Ohio State University graduate student who grew up along the Ohio River, told conference participants he became interested in determining the geographic extent of PFAS contamination from DuPont’s Parkersburg plant, now operated by DuPont spinoff company Chemours. Galloway teamed up with Lindstrom, the EPA scientist, who has sensitive analytic equipment for detecting PFAS, and went out in a kayak to collect water samples.
The plant’s air emissions are only monitored within a 2-mile radius, but some of Galloway’s samples taken much further away contained PFOA. In the direction of prevailing wind, to the northeast, he found PFOA at 100 ppt 15 miles from the plant. At a distance of more than 25 miles, PFOA was still detected, though concentrations dropped to 10 ppt.
Twenty miles north of the plant, Galloway also found GenX, though the short-chain PFOA replacement had only been used for a short time.
Lindstrom and his collaborators also detected GenX at a concentration of 661 ppt in the drinking water supply of Wilmington, N.C., where they collected samples downstream of another DuPont-owned factory operated by Chemours.
The EPA has estimated, based on its monitoring of large public water systems, that PFOA and other long-chain perfluorinated compounds are in the drinking water of 6 million Americans.
But Harvard environmental engineering professor Elsie Sunderland told participants in the Boston conference that this number seriously underestimates the magnitude of the problem, because about 90 million people rely on private wells or small public water systems that aren’t subject to EPA monitoring.
Sunderland also questioned whether the testing methodologies used by water systems to comply with EPA’s requirements are sensitive enough to find these chemicals. PFAS compounds can cause health effects at levels as low as 1 ppt, she said.
Pushing for a phase-out
Arlene Blum, an environmental chemist who founded the Green Science Policy Institute, said a body of research now contradicts DuPont’s claim that short-chain PFAS compounds are safe and environmentally preferable to longer-chain compounds like PFOA.
Using a science-based approach – convening scientific experts, motivating needed studies, and publishing research findings in peer-reviewed journals -- the Green Science Policy Institute has embarked on a new campaign to eliminate six classes of harmful chemicals. PFAS is the first class the group is targeting.
The institute’s approach builds on the Madrid statement, which calls for limiting PFAS as a class because the chemicals pose numerous serious hazards that make them unsuitable for production and use. In 2015, 230 scientists from 38 nations signed the Madrid statement, which was published with references in the peer-reviewed journal Environmental Health Perspectives.
This class-wide strategy would prevent “regrettable substitutions” like those that scientists fear are occurring with the new short-chain PFAS compounds, Blum explained.
So far, at least 40 companies have been persuaded to stop using all PFAS compounds – both long- and short-chain – in clothing and textiles, Blum said.
“Our big hope is that the military will do the same,” she added.
Despite widespread water and soil contamination on military bases from the use of PFOS-containing firefighting foam, the Pentagon has continued to procure highly fluorinated products for this purpose, she said.
Detailing health risks
The most definitive information on how PFOA exposure can affect human health comes from studies of 70,000 people living near a DuPont chemical plant in Parkersburg, W.Va. As part of the settlement in the large class-action lawsuit brought by Bilott against DuPont, three epidemiologists approved by both sides studied this population, which also received free health monitoring. DuPont agreed not to fight personal injury suits from area residents who experienced these health problems.
The data indicated a probable association between PFOA exposure and kidney cancer, testicular cancer, ulcerative colitis, thyroid disease, high cholesterol, and pregnancy-induced hypertension. Although other effects may occur, they were not statistically significant in this population.
As endocrine disruptors, PFAS compounds affect hormonal systems. This can cause of a cascade of effects, because hormones act as signals to start, stop and otherwise regulate many physiological processes.
Courtney Carignan, a reproductive environmental epidemiologist at Harvard, noted that PFAS compounds affect thyroid function. Adequate thyroid levels are critical for brain development and maturation in the developing fetus and during childhood, she said.
PFAS compounds also are associated with an autoimmune hypothyroid marker. PFOA also disrupts sex hormones, for example by depressing testosterone levels.
At the blood concentrations found in children in the Ohio River valley where DuPont’s Parkersburg’s plant contaminated drinking water, PFOA exposure affects mammary gland development in the developing fetus. Later in life, prenatal exposure may impair a woman’s capacity to breast feed and predispose her to breast cancer.
Alan Ducatman, a professor of medicine and public health at West Virginia University, suggested other mechanisms through which PFOA can cause developmental problems. He said studies show PFOA induces problems with fat metabolism in rodents and disrupts cholesterol metabolism in humans. Cholesterol is a sterol, and the disruption of sterol metabolism is associated with developmental abnormalities, he said.
Highly fluorinated compounds also affect the immune system in complex ways. Birnbaum cited a long-term study of mother-child pairs in the Faroe Islands, which are part of Denmark. In that study, children whose mothers were in the top 20 percent for exposure to PFAS compounds couldn’t mount a normal immune response to vaccination.
In pregnant women, perfluorinated compounds are carried from the placenta to the fetus, and breast milk is a source of exposure for children.
Cathy Dawson, an operating room nurse who’s lived in Hoosick Falls for 30 years, brings a health orientation to the NY Water Project. When she first “heard the rumblings” about PFOA and saw a notice about it in her village water bill, she said she didn’t pay much attention.
But then she messaged Michael Hickey. As a boy, he and his parents and siblings were her next-door neighbors when Dawson first moved to Hoosick Falls. Hickey’s response propelled her into action.
“Michael filled me in on everything that was going on, and told me about his research,” she recalled.
Picking up where he left off, she did her own research. What she learned left her outraged.
“A lot of people are afraid of the cancers” associated with PFOA, Dawson said. “But something like arthritis impacts people day to day with pain and disfigurement. PFOA is also known to cause cranial-facial abnormalities, and there are all the endocrine disorders. Studies have also linked PFOA to seizures. From a health-care perspective, it’s awful.”
NY Water Project’s big push now is to get the village a new water supply. Although state officials say a new filtration system is now keeping PFOA out of tap water, the village’s water comes from underground wells near the Saint-Gobain plant on McCaffrey Street, and the wells remain heavily contaminated.
But water isn’t the only part of Hoosick Falls’ environment affected by industrial pollution. Portions of the village that were contaminated by Saint-Gobain’s plants are on track to be designated a Superfund site – they made it onto EPA’s National Priorities List in late July -- and thus become eligible for federal cleanup funds.
For the people being affected, local pollution isn’t just a legacy issue. Dawson said she believes Saint-Gobain is still releasing industrial toxins into the air, and air deposition is one way that highly fluorinated compounds get into ground and surface water.
“The air still stinks, though it’s not as bad as it used to be,” she said, adding that odors from the plant are intermittent. “It smells like burning plastic, like if you left a Teflon pan on the stove.”
Workplace exposure to carcinogens such as diesel exhaust, asbestos and silica are together causing thousands of cancer cases in Ontario each year, says a new study that reveals the toll of on-the-job hazardous substances.
Asbestos leads them all, causing an estimated annual burden (cases that could be prevented) of 630 cases of occupational lung cancer and 140 of mesothelioma in the province, says the paper formally released on Wednesday by the Occupational Cancer Research Centre and Cancer Care Ontario.
Estimates on numbers of workers exposed to carcinogens have been produced before in Canada. This study is the first to estimate the number of cancer cases from workplace exposure in Ontario and is part of a four-year national project, OCRC director Paul Demers said.
"I can't count the number of times that I have talked about how important it is to prevent exposure to carcinogens, but raising awareness doesn't always lead to action," said Dr. Demers, who is leading the study. "I think the numbers are important to make this real and push action towards preventing exposure to these causes of cancer."
This is the first publication in the project; a national picture is expected within about a year.
Workers in Ontario spend on average a third of their waking hours on the job, although little research has been done until now on the impact of cancer-causing exposure in the workplace, the paper said.
The study examined a range of known or suspected carcinogens, including radon, wood dust and shift work. It identified four key carcinogens: Asbestos, diesel-engine exhaust, silica and solar ultraviolet radiation, or outdoor sun exposure.
These four "should be prioritized for exposure prevention and control because they present the best opportunity for making a large health impact," the paper said.
Asbestos also causes an estimated 15 laryngeal cancers in Ontario each year, as well as some ovarian cancers. By industry, most workplace exposure to asbestos is in construction, largely through maintenance and renovations of homes and buildings, as well as in manufacturing.
"Asbestos is still our worst carcinogen, or nightmare, depending upon your choice of words," Dr. Demers said. "It's one that has had such a big impact that we're going to be living with it for a while."
Canada will ban asbestos in 2018. However, it is still in products such as insulation, tiles and brake pads and was widely used in construction of homes and public buildings such as schools and universities.
Other substances also hurt workers' health. Exposure to fine crystalline silica dust – the most common form of which is quartz – causes an estimated nearly 200 work-related lung cancer cases each year. Workers in construction and manufacturing are most exposed.
Exposure to diesel exhaust accounts for an estimated 170 lung cancer cases and 45 bladder cancer cases each year. Workers in mining and transportation have the highest level of exposure.
Solar radiation causes an estimated 1,400 non-melanoma skin cancer cases a year, with workers in agriculture and construction most exposed.
The paper also examined shift work that disrupts circadian rhythms as a potential carcinogen, saying studies since 2007 have found this type of work may be associated with breast cancer. Although cautioning that additional research is needed, the paper said shift work "may be responsible" for 180 to 460 new cases of breast cancer in Ontario a year.
These cancers are almost entirely preventable, Dr. Demers said. The study recommended strengthening rules on workplace exposure limits, reducing or eliminating the use of toxic substances on the job, and creating registries of worker exposures to occupational carcinogens.
Researchers in Britain and at the World Health Organization have done similar studies. The Canadian study estimated the cancer burden using data from Carex Canada (a research project) on the prevalence of workplace exposure to different carcinogens, along with Statistics Canada labour force survey data. Funding was from the Canadian Cancer Society.
FOLLOW TAVIA GRANT ON TWITTER @TAVIAGRANT
Breathing dirty air and living in stress combine to increase the likelihood NYC kids will have a behavior disorder.
That's the message from a new study that found black and Dominican children who suffer from high prenatal air pollution exposure and a lack of food, clothing and shelter have significantly higher rates of ADHD.
The study, published today in the journal Environmental Research, is the first to suggest that polycyclic aromatic hydrocarbons (PAHs)—common contaminants in city air from burning fuels such as diesel, coal, gas, oil—combined with a hard home life may bring about behavioral problems.
“A lot of people in the most polluted communities already talk about this, how pollution stresses pile on top of life stress," said Molly Rauch, public health policy director at Moms Clean Air Force, a national nonprofit organization focused on air pollution, climate change and kids' health.
However “showing that interaction is really important to get a better handle on how low income communities are impacted," said Rauch, who was not involved in the study.
Not a “single trigger"
ADHD is increasingly common: about 11 percent of U.S. children between 4 and 17 years old have been diagnosed with the disorder, which has a range of symptoms including impulsiveness, inattention and hyperactivity.
It's not entirely clear why some children get ADHD. Some potential culprits include mothers' smoking or drinking alcohol, problems during pregnancy, stress and genetics.
There isn't a “single trigger" for attention deficit/hyperactivity disorder (ADHD), said the lead author of the new study, Frederica Perera, director of the Columbia Center for Children's Environmental Health. But some environmental contaminants, such as PAHs or lead, may play an important role, she added.
Following 351 kids from New York City since their mothers' pregnancy, she and colleagues previously reported that children exposed to PAHs while still in the womb were more likely to get ADHD. Knowing that social suffering can also spur behavioral problems, in the new study, using the same children, they examined the combined effect of the pollution and mothers' struggles to have enough food, provide a warm home and clothing.
Children with higher exposure to PAHs and whose mothers experienced "persistent hardships" during both pregnancy and the early childhood years were most likely to have ADHD symptoms.
Perera said the mothers enrolled in the study were all nonsmokers, non drug users, and healthy at the time of enrollment, which means the findings can't be generalized for the entire population.
However, a “healthy population could also lead to an underestimation of the risk," she said.
PAHs are in the fine particles and gases from burning fuels and are easily inhaled by people.
Perera and colleagues tested PAHs directly from the mothers' blood at delivery. This gives a much more accurate picture of fetal exposure, she said, as PAHs are known to cross the placenta and, some studies suggest, the blood brain barrier.
Fetuses, and growing children, are particularly vulnerable to toxics such as PAHs since their bodies and brains are still developing. The compounds can cause DNA damage and inflammation, which hurts the brain.
Suffering from a lack of basic needs can cause stress on children, too, which also promotes inflammation and can alter development.
This combination of chemical and social stress may “amplify" each other and spur the behavioral problems, Perera said. A 2015 study found a similar link—showing that PAH exposure and hardships at home were linked to a lower IQ for kids at age 7.
Rauch said Perera's research highlights why it's important for parents to recognize that air pollution “goes beyond asthma impacts."
“People in the most polluted communities often understand it's a total body experience, and that air pollution can affect every organ system of the body including the brain," she said. “But many people, especially those lucky enough to have clean air, are often surprised to hear it."
The study can't prove the pollution and stress at home is causing behavior disorders and was limited in that it was a small sample of children and the researchers don't have information on the children's fathers.
But the study is just the latest evidence that there is “growing recognition" of the combined effects of pollution and social stress, the authors wrote.
“The goal of this work is prevention," Perera said. “To protect mothers and children we need to combine stronger policies and initiatives to reduce exposure to pollution in urban areas and also intervene on economic hardship during pregnancy."
It remains one of the great mysteries of the Zika epidemic: Why did a virus that existed for decades elsewhere in the world suddenly seem to become more destructive when it landed in Latin America?
Why did the Zika virus cause thousands of babies to be born with microcephaly, unusually small and damaged brains, when previous outbreaks in Africa and Asia seemed to cause much less harm?
An intriguing study in mice, which has prompted some skepticism among experts, suggests that a single genetic mutation helped transform the Zika virus into a devastating force in Latin America. The report was published on Thursday in the journal Science.
The mutation, called S139N, first arose in an Asian strain of the Zika virus in 2013, just before a small outbreak in French Polynesia — the first linked to an increase in babies born with microcephaly.
Zika is believed to have first appeared in Latin America later in 2013, possibly introduced by soccer players from French Polynesia competing in a tournament in northeastern Brazil. The mutation has appeared in every strain of the virus in the Latin American outbreak, the researchers said.
The study, by scientists in China, found that strains of Zika with the S139N mutation caused substantially more death and microcephaly in mice than other strains. And in a laboratory dish, the S139N strain killed many more human cells important to early brain development than an earlier strain without the mutation.
Some experts voiced doubts, saying the findings were too preliminary to establish that a single mutation was the critical factor. At least, they said (and the study authors agree), the results must be replicated in primates, because laboratory experiments with mice and even human brain cells cannot fully capture how the virus functions in nature.
“It’s potentially important, and it’s provocative,” said David H. O’Connor, head of global infectious diseases at the University of Wisconsin-Madison’s primate center, which has tested the Zika virus in monkeys.
“But it will require a lot of additional work to show that it can be reproduced in multiple settings, to show that it isn’t simply a coincidence.”
Other experts found the study persuasive.
“They showed this mutation is both sufficient and necessary to make the virus worse,” said Hongjun Song, a neuroscientist at the University of Pennsylvania who helped discover how Zika attacks the fetal brain. “I would say this is one of the smoking guns.”
“The scary part, maybe the take-home message, is that it doesn’t take that much — just one mutation — to make something really, really bad,” he added.
The researchers do not claim the S139N mutation is solely responsible for the birth defects among children born to women infected by mosquitoes during pregnancy. Other causes could involve differences in the population in Latin America, including the possibilities that their genetic makeup or exposure to previous mosquito-borne viruses made them more susceptible to harm from Zika.
It is also possible that Zika previously caused microcephaly, but cases simply went unnoticed when the virus reached Asia around the 1960s.
Microcephaly has many causes, many mothers gave birth at home, and newborns with severe brain damage might have died without immediate intensive care. The surge in microcephaly in northeast Brazil in late 2015 was noticed by doctors in hospital neonatal units.
The researchers noted that strains of the virus without the S139N mutation caused some mice to develop mild microcephaly, meaning that the mutation, which occurs on a protein involved in making the virus’s protective coating, is likely only a piece of the puzzle.
But it seems to be an important piece, the scientists said.
“In the beginning, we thought we may need multiple mutations” to create a viral strain that causes severe microcephaly, said Dr. Zhiheng Xu, a principal investigator with the Institute of Genetics and Developmental Biology at the Chinese Academy of Sciences, who led the study with Cheng-Feng Qin, a virologist at the Beijing Institute of Microbiology and Epidemiology.
“That was a surprise to us, that it was just one mutation.”
The researchers first compared a strain of the Zika virus from an outbreak in 2010 in Cambodia with three strains from the recent Latin American outbreak. The viruses were injected into brains of one-day-old mice whose development, the researchers said, approximates that of third-trimester human fetuses.
About 17 percent of mice infected with the Cambodian strain died, compared to 100 percent of mice infected with the Latin American strains.
Next, the researchers created a Zika virus with several of the seven mutations that have appeared since 2013 and found that it caused greater mortality in newborn mice than the Cambodian strain. Then the team made seven strains of the Zika virus, each with one mutation.
Six caused comparatively mild damage, similar to the Cambodian strain. But the virus with the S139N mutation — in which only one nucleotide differs from the Cambodian version — killed more mice and caused more brain damage. In mouse embryos, the S139N mutation caused more severe microcephaly and dead brain cells.
To double-check the finding, the researchers created yet another strain, this one with a reversed version of the mutation: N139S. Its effect on mice was mild, like the Cambodian strain.
Even then, Dr. Qin was “not quite confident about the significance of our finding,” he said. “Honestly, we are also asking ourselves, ‘Can these results directly translate to humans?’”
So they tested the strains on human neural progenitor cells, which act as scaffolding upon which the fetal brain forms and are the virus’s main target. The S139N strain reproduced faster than the Cambodian strain and killed more cells.
The authors and other experts said they did not know why the mutation might have such a profound effect.
The viral coating protein that contains the S139N mutation is “used in viral assembly” before part of the protein degrades, said Genhong Cheng, a microbiologist at the University of California, Los Angeles, who was not involved in the study.
So S139N may make the coating more protective or help the virus assemble more effectively, he said. “It certainly seems like this particular mutation is able to at least make a contribution to making it more virulent,” Dr. Cheng added.
Still, recent microcephaly cases in Thailand were caused by an Asian strain without S139N, he noted, so it is unlikely to be the only villain.
Kristian G. Andersen, director of infectious disease genomics at the Scripps Research Institute, said the study had several important limitations, including that it did not explain why, in the recent outbreak, microcephaly rates varied widely across the Americas.
Microcephaly cases were heavily concentrated in northeastern Brazil, for example, but the mutated Zika strain was found everywhere.
“This is an interesting study, but I’m skeptical of their findings, and I don’t believe their hypotheses are well supported,” he said.
Dr. O’Connor noted that injecting the virus directly into mouse brains did not mimic infection in nature, where the virus must infect a mother, cross the placenta and reach the fetus.
The researchers also did not try to address why this mutation might have persisted. Did it confer a survival advantage to the Zika virus or just incidentally increase the virus’s ability to cause microcephaly?
“That’s a very good question,” Dr. Xu said. “You got me.”
Walking by the side of her house, Rimiko Yoshinaga points at the broad, vine-encrusted tree her grandfather used to climb. During one of the most famous environmental disasters in history, this tree stood over the calm, clear waters of the Shiranui Sea. He would perch up there and call down to say whether the fish were coming, Rimiko says.
The view today is jarringly different. Now the steep edge of Myojin Point in Minamata, Japan, doesn’t overlook the water. Standing there now, you see roads, athletics fields, three separate museum facilities, a seaside memorial park and a scenic bamboo garden – because bamboo roots grow sideways instead of down. Under all this new land is a plastic seal. And under that are millions of tonnes of mercury sludge.
Reclaimed after a long, expensive construction project, this was ground zero for a mystery illness known first as ‘strange disease’ or ‘sauntering disease’ or, ominously, ‘dancing cat disease’. Now it’s just called Minamata disease. The cause? From 1932 to 1968, the Chisso chemical factory discharged up to 600 tonnes of mercury into what was then a harbour. The factory was using the mercury to speed along a reaction that produced acetaldehyde, an ingredient in many plastics. But the company lost so much mercury in the process that it later established a subsidiary to mine it back from polluted sediment nearby.
After flowing out of the factory’s drainage channel, some of the mercury was taken in by plankton, which were then eaten by bigger things like horse mackerel, sardines and shellfish, which in turn were eaten by still bigger creatures like cutlass fish and black porgy. At every step, the mercury – a potent neurotoxin – became more and more concentrated, until it ended up between a pair of chopsticks.
In her living room, Rimiko brings out green tea and local pastries, sits down with her mother and husband, and starts talking. Like almost everyone else in Minamata, and especially like the three other families living in their small hamlet close to the pollution’s source, they ate a lot of seafood in the early 1950s. They didn’t know. Rimiko’s grandfather was a fisherman – every day he brought some of his catch home. Her father had a job at the factory that caused the pollution, but he himself would go fishing after coming home at night. Her elder brother gathered shellfish and crabs.
When she gives public talks, Rimiko pauses at this point of the story to show a black-and-white picture of her and her three siblings in formal clothes. Then she asks audiences to pick her out of the line-up. It’s easy – she still has the same round, open face and high eyebrows. While her siblings sport bowl cuts, her short brown hair parts in the same place today as it did then. Born in 1951, she is the youngest. She smiles during this part of the story.
The mass poisoning that happened next is famous in Japan and around the globe. It acts as a sort of first cause for mercury researchers and policy makers, many of whom have made pilgrimages to Minamata or who have met survivors like Rimiko at international conferences. The tragedy has also given them a prime directive. Literally. With a UN treaty that governs the use of mercury, called the Minamata Convention on Mercury, they aim to prevent something like this from ever happening anywhere again.
Since it was signed in 2013, 74 countries have ratified the Minamata Convention. It entered into legal force in August 2017. Just this week, the arrangements for its implementation are being negotiated at the first Conference of the Parties in Geneva. That’s good news, made possible because finding alternatives to mercury in industrial processes is not too difficult, says Susan Keane of the National Resources Defense Council. “It’s not climate change,” she says. “Here’s a problem where most of the world agrees we can do something.”
Some six decades on, you could argue that the story of Minamata is on its way to a neat resolution. But the town’s legacy split into different branches a long time ago. It’s part parable: the research Minamata inspired on mercury has helped identify other poisoning episodes, and is now culminating in an attempt to solve a thorny environmental problem. Of course, Minamata is also a real place, saddled with an immense burden and filled with reminders: memorials, old trees that used to stand over the sea, and a large population of activists and ageing victims, many of whom report that their health is now deteriorating.
To get to Minamata from Kagoshima airport in Kyushu, Japan’s southernmost major island, I take a bus and then a train that hugs the coast. Summer is the wrong time to go. It’s so hot and humid that the green islands out in the Shiranui Sea fade into a grey mist of water vapour. In the city itself, mountains prickled with narrow cedars run almost straight into the water – there’s a small downtown and a few scattered communities crammed into a network of valleys.
Right across from the central train station is the front entrance of the same sprawling factory as in the history books. Today, with a slight makeover, the sign reads JNC – standing for Japan New Chisso – which is the entity that took over the chemical business in 2011. Chisso itself now exists mainly to administer settlements. Modern Minamata, mindful of its history, has embraced an eco-friendly identity. In the 1950s, though, Minamata resembled feudal Japan, with the entire community in orbit around the company’s castle.
Before anyone in Rimiko’s family fell ill, they started seeing what are now recognised as omens of environmental catastrophe. Fish floated to the surface, struggling, and could be caught by hand; they still tasted fine, though. Then the family cat was racked with convulsions, fell into the sea and died. Hundreds of other cats, valued because they protected Minamata’s fishing nets from being chewed on by rodents, died after similar dancing fits all over town. The mouse population boomed. Crows dropped from the sky.
Rimiko was too young to remember much about when the neighbours got sick, or when her father fell ill, or when he eventually died – shivering and crying in bed – in 1956. But her mother, Mitsuko Oya, a sprightly if reserved 92-year-old, does. After her husband returned from a stay at the hospital, Mitsuko tried to help him recover the best way she or anyone knew how: by feeding him more nutritious fish from the bay. Her father-in-law, the fisherman, died the same year.
To feed her children, Mitsuko took up part-time fishing and construction work. She says her most vivid memories from that whole period are not her husband’s final days but the very beginning, when he started discussing his symptoms. “He complained about [how] he cannot talk properly,” she says, through an interpreter. “He wants to talk, but the words will not come out.”
Numbness in the mouth and in other extremities, along with difficulty speaking, are some of the hallmarks of mercury poisoning. But, by now in this story, saying just “mercury poisoning” is too vague. Mercury, element number 80 in the periodic table, occurs in a variety of chemical forms. Each has its own particular character.
The mercury you might find as a silvery liquid in a thermometer is dangerous but not the worst form. In 2014, doctors in India treated a teenage boy months after he had secretly injected his forearm with liquid mercury in an attempt to transform his bones into metal like the X-Men character Wolverine. He recovered. When the same liquid mercury vaporises into an odourless gas, it’s worse: it can be absorbed through the lungs and go on to cause tremors, behavioural changes and kidney damage.
These forms are inorganic, which means that they have no carbon to tempt carbon-rich biological molecules into ill-advised interactions.
But the mercury that spilled into the Shiranui Sea and infiltrated Minamata’s main sources of protein was methylmercury, an organic form with one carbon and three hydrogen atoms attached.
In living flesh, organic mercury binds with certain biological molecules and stops them from working. In some situations this also allows it to masquerade as one of the many types of amino acid in the body, the building blocks of proteins. Because of this, organic mercury can smuggle its way through erstwhile protective walls like the placenta and the blood–brain barrier. And it sticks around in a body for months, long enough to get concentrated into higher and higher doses through the food chain.
With an efficiency you might admire under different circumstances, the human gut can pull out up to 95 per cent of the methylmercury contained in each bite of fish. It enters blood cells, where it binds with haemoglobin, and some of it goes to the liver. But the real damage comes from the sizeable amount of methylmercury that makes it into the brain, where it wreaks neurological havoc in various regions. There, it slowly changes back to inorganic mercury, which can stay in the brain for years.
The same year that Rimiko’s father died and grandfather fell ill, doctors at the Chisso factory hospital began seeing the same constellation of symptoms again and again. Numbness. Loss of motor control. A narrowing of the visual field that one victim described as like looking through a bamboo pipe. In parallel, methylmercury also caused cerebral palsy-like symptoms in children born during this period, like in the Kaneko household next door.
The mothers of children affected in this way were possessed by a haunting notion: that their babies had absorbed the toxin, sacrificing themselves to save their mothers. “I saw these babies with severe neurological symptoms, and at first I couldn’t believe [this was] why the mother was so safe,” says Mineshi Sakamoto, a researcher at Japan’s National Institute for Minamata Disease. Medically, this painful belief turned out to be right: in 2004, Sakamoto showed, with rats and later with people, that methylmercury flows out of pregnant mothers and into fetuses.
This all took a while to figure out, but court proceedings ultimately found Chisso responsible in 1973, charging it with negligence for not foreseeing the risk posed by its wastewater. Long beforehand, in the summer of 1959, factory hospital doctor Hajime Hosokawa had been conducting his own experiment by giving Chisso wastewater to cats. When one of these – the now infamous cat 400 – developed signs of Minamata disease, he reported it to management.
They ordered him to keep further experiments secret, then spent years denying responsibility as Minamata’s disease outbreak drew media attention. Backed by the national government and scientists in Tokyo, Chisso criticised researchers who blamed the disease on mercury from the factory and supported research that hunted for other potential causes, like the victim-blaming theory that Minamata residents had eaten already-spoiled fish. The corporation even staged a misleading photo-op to prove the wastewater was being safely treated.
A strong argument in the company’s favour was that similar factories didn’t seem to be linked to the same problems. Then, almost a decade after the Minamata outbreak, the strange disease popped up again along the Agano river in faraway Niigata in northern Japan, next to another factory that used mercury in the production of acetaldehyde. It took until September 1968 for Japan’s Ministry of Health and Welfare to make a formal announcement on both cases. Yes, the cause was methylmercury. Yes, it was from the factories.
The following years brought Minamata even more national and then global attention. Sympathetic outsiders moved into town from other parts of the country. In 1972, a Life magazine article by photojournalists Eugene and Aileen Smith brought chiaroscuro images of Minamata’s victims to many for the first time. Activists and patients made trips to Tokyo to press the government and Chisso for compensation, leading up to the pivotal 1973 court case, subsequent negotiations and other trials.
But for many families with one or more probable victims at home, Minamata disease was something to hide. Once meaningful settlements started to come into play after the 1973 court ruling, successful claimants were afraid of what jealous neighbours would say behind their backs. And the town’s economic fortunes still depended on Chisso. These tensions even played out in individual people: Rimiko’s mother Mitsuko had taken on construction work for Chisso, then felt torn when she found herself attending a sit-in at the factory’s gates.
Even today, patients are cautious and deliberate about the decision to come out publically with a connection to Minamata disease. Mitsuko, who won’t complain about any possible symptoms of neurological harm even now, attended a meeting or two at an activist’s house. She was out; her daughter wasn’t. “I wanted to live without Minamata disease,” Rimiko says. “I wanted to forget about the fact, even though my father, mother – they are all patients.”
Once the Ministry of Health and Welfare made its announcement, with social tensions in Minamata coming to a boil, the basic science of preventing methylmercury poisoning seemed like an easy solve by comparison. You just needed to prevent methylmercury pollution. But a young scientist at the same ministry was about to help muddy the waters.
It seems fair to describe Hirokatsu Akagi, now 75, as a Dumbledorean figure in the world of mercury science and among people with Minamata disease, who view him as a sympathetic ally. He has style: usually white or tan pants, a tucked-in shirt in a similar colour and a signature stingy brim hat, out from which pokes a ring of white hair. “Everybody knows Dr Akagi,” says Laurie Chan, a toxicologist and environmental scientist at the University of Ottawa. “Everyone calls him Akagi-sensei: a teacher.”
Growing up south of Minamata in Kinzancho, meaning literally ‘gold-mine town’, Akagi first encountered mercury as a child. “Mercury is very good play material. If you push it down, it spreads,” he says, before laughing and extending a half-serious invitation: “I have [it] here.”
A retired government researcher, Akagi now maintains his own lab in Fukuro, a neighbourhood of Minamata struck hard by the disease. Stacks of old papers have precipitated out over available surfaces. The walls of his side-room office are plastered with photos of scientists in conference rooms next to pictures of wedding parties next to CVs of international researchers he considers peers and friends. One such person, Swedish scientist Arne Jernelöv, has particularly high billing above his desk.
In 1969, Jernelöv published a scientific paper in the journal Nature, which Akagi, fresh out of pharmaceutical school and newly hired at the Ministry of Health and Welfare, read with interest. Strangely, Swedish pike had been measured with high levels of methylmercury, even though nearby factories were releasing only other forms of mercury. Jernelöv and his coauthor hypothesised that mercury could be methylated inside living organisms, setting in motion the discovery that, for evolutionary reasons that remain fuzzy even today, bacteria can convert other kinds of mercury into methylmercury under the right conditions.
Curious, Akagi started digging through the ministry’s own archive of chemical samples. He found a piece of mercury acetate, yet another toxic variety of mercury. It was so old that the label was barely legible. The substance should have been a white crystal, he says, absentmindedly sketching out its chemical formula on a sheet of paper.
But Akagi noticed a yellow layer on the surface that he scraped off and tested. Methylmercury, again. Not produced by humans, not converted by bacteria, but made in yet another new way – by light. Not only could other kinds of mercury waste be transformed into methylmercury, but they had more than one path to get there.
In 1972, Akagi first wrote up his findings in Japanese. “People working at companies like Chisso, and [other] chemical companies, they attack me,” he says. Industry had a major stake in inorganic mercury being safe. “They call me to discuss. So many come. Old people, like they are president or something, vice-president in the company.” Only 30 years old at the time, embedded in a more hierarchical culture than his Western peers, he says he continued out of a sense of moral obligation. He resolved to publish future work in English instead.
What really mattered, Akagi thought, was not the specific way methylmercury came into being, but how much was flowing through an ecosystem. And so he set out – and succeeded – at developing a chemical method to measure mercury better than anyone else.
After a stint in Canada honing his technique in the polluted Ottawa river, and more time at Japan’s Ministry of Health and Welfare, Akagi finally came to Minamata in 1981 to join the newly established National Institute for Minamata Disease, or NIMD. Ten careful, cautious years later he published his mercury measurement bible: a cookbook to count up the amount of methylmercury in a sample of water, soil, blood, hair, fish, whatever. At long last, he could use the method to map out the full rhythms of mercury in history’s most famously exposed place, Minamata Bay.
At least that was the plan. Then the world’s mercury researchers came knocking, and a much larger picture of mercury around our planet started coming into focus. First it was the Brazilians, concerned about mercury in the Amazon. “There is no reliable data at the time,” Akagi says. “Not only in the Amazon but everywhere.”
He started travelling to help assess sites of mercury pollution – Brazil and then Indonesia, the Philippines, Tanzania. At the same time, dozens of researchers from all over the world started making pilgrimages to Minamata to learn the technique. They were young and sometimes poor, and they almost always slept at Akagi’s house. His wife and children liked it, he says.
Armed with Akagi’s method, researchers have shown that the mercury problem is multifaceted. Besides Minamata, there have been other severe and concentrated mercury poisonings. The indigenous Grassy Narrows people in Ontario, Canada, developed their own cases of Minamata disease thanks to discharges from a paper and pulp mill that created mercury waste, and rural Iraqis died by the hundreds in 1971 after eating imported grain intended for planting that had been dressed with methylmercury fungicide.
Much larger populations are exposed to lower but still harmful concentrations. Inorganic mercury also comes into the world from sources like volcanoes, and in the last few centuries human industry has accelerated its release – it’s also emitted by burning coal. The atmosphere is now laden with five times more mercury than in pre-industrial times. This pollution doesn’t respect borders. Once in the air it can settle all over the globe, even in supposedly pristine locations like the Arctic, and can be converted to methylmercury in environments ranging from the guts of insects to thawing permafrost to the water column of the open ocean.
For most of the developed world, the health effects are subtle, with adverse effects being largely avoidable. Food webs and biochemistry alike focus mercury into the muscle tissue of large, sleek ocean animals that humans like to eat – so don’t consume lots of athletic predators like swordfish and tuna, especially when you’re pregnant. But this advice is harder to follow, and the risk of poisoning more immediate, for communities like Minamata with deep cultural ties to the water and no other accessible, affordable protein.
Overall, the world’s coastal indigenous groups fill their plates with 15 times more seafood than the average for their country, a 2016 study found. Faroe Islanders traditionally eat pilot whales, which build up high levels of methylmercury, for example. Many of Canada’s indigenous First Nations depend on fish and seals.
Many of the sites Akagi has visited in South America, Africa and Asia are small gold mines, as cavalier with mercury today as Akagi’s hometown was in the 1940s. Right now, this is the world’s largest source of mercury pollution. If you mix mercury with gold-rich sediment, the two metals form an amalgam, and you can then cook off the mercury as vapour. It’s all very convenient for miners ignorant of the risks or resigned to living with hazards. Some 10 to 15 million people are involved in this enterprise, about a third of them women and children, spread over 70 countries. But that mercury then gets into soil and rivers, is converted to methylmercury, and builds up in fish and fish eaters.
“You see people passing around old Coke bottles of mercury, pouring them out haphazardly,” says Keane from the National Resources Defense Council, who has also visited many of these small communities. “Often kids are hanging around, and women with babies balanced on their hips.” Afterward, mercury in the miners’ breath has been measured to exceed the occupational standards for air, she says, adding wryly that the miners themselves might qualify as toxic mercury sources.
It’s not a pretty picture. But Akagi’s chemical analyses have helped reveal a world where the dangers of mercury still persist, even after decades of better regulations. In person, he seems to prefer talking through the pure chemistry. His scientific progeny, many now big names in the research world, are the ones smiling down from the walls of his office. He comes to the lab to keep chiselling away at – what else – the same old problem of helping people measure mercury, stopping for lunch most days at the roadside noodle restaurant next door.
Another of those CVs up on the wall belongs to Milena Horvat, a chemist who came to visit him several times from Slovenia. She now heads up the Department of Environmental Sciences at the Jožef Stefan Institute in Ljubljana. The institute is about an hour’s drive from a town called Idrija – home to a 500-year-old mercury mine, the second biggest in the world, recently active and now a UNESCO World Heritage Site. With Horvat and her colleagues, Akagi is now working on a method for measuring mercury that uses cheaper chemical ingredients, for developing countries. He thinks it will be his last major project. He doesn’t know how many years he’ll need.
Almost 12,000 kilometres from Minamata, Rimiko Yoshinaga, seated next to an interpreter at a desk at the front of the room, picks up a microphone and begins. She is tired from jetlag, and it is cold here compared to Kyushu. The seafood available pales in comparison to what she is used to from Minamata Bay, which was finally declared safe in 1997. “This is my first time in the United States,” she says. “I have been here four days, and I am starting to yearn for the fish in Minamata.”
She is speaking to a room of researchers in Providence, Rhode Island, gathered for the 13th International Conference on Mercury as a Global Pollutant. Organised by a volunteer committee, the meeting is a get-together that happens every two years. This summer, roughly a thousand researchers are in attendance from some 50 countries, many of them buzzing about the Minamata Convention coming into force. Akagi hosted the sixth such meeting in Minamata in 2001, and he is here too, to present his work with the Slovenians.
Rimiko has come to Providence as a kataribe, a storyteller. People with Minamata disease have been fulfilling this role in official and unofficial capacities at international conferences for 45 years. In her presentation, she shows a picture of her father, breaking down in tears while quoting her mother Mitsuko. She weaves her family story back and forth into the wider history. It’s hard but it comes with catharsis, she says later. “Every time I give a talk, I feel like I am releasing whatever things I hide in myself,” she says. “That makes me little by little more comfortable.”
For years Rimiko kept her status a secret. Unlike many other victims, whatever neurological harm she suffered as a child isn’t obvious from the outside – excepting the occasional muscle cramps she worries about – even though she ate the same fish as everyone else. Before she married her first husband, she didn’t mention the disease until his parents, snooping on their son’s prospective bride, unearthed the connection. Her fiancé asked her point-blank and she had to admit to being a sufferer. But she stayed silent in public until 1994, during a period of official apology and reconciliation called moyainaoshi, a local term that alludes to fisherman connecting their boats to work together.
When she did speak out, a delegation of city officials showed up at her door. Long-time Minamata activist Toshio Yoshinaga, the man who is now her husband, accompanied them. They asked her to give a speech in front of several hundred people. At first, she balked. “It was that time when I started to think about my father,” she says. “I felt I had to do it.”
Rimiko, who makes and sells small ornaments of recycled glass from a small shed behind her home, is the current vice-president of the storytellers’ group. She is a charismatic, emotional speaker, and as one of the youngest, healthiest people in the Minamata disease community, she can still travel widely. Over the years, she has also spoken in the Philippines and in Johannesburg. But given the timing, the conference this summer in Providence is particularly special. “I am relieved to hear that the Minamata Convention on Mercury will come into force,” she tells her audience. “I truly hope that no more people suffer health damage caused by mercury.”
The experts in Providence express cautious hope as well. “All of the pieces are in place for the international community to be able to move forward if they want to,” says Boston University’s Henrik Selin, a professor of international relations who visited Minamata and nearby Kumamoto City in 2013, when the convention was first opened for signatures.
The convention comes with a long checklist of deadlines. Nations must immediately give up building new mercury mines and, within three years, they need to submit a plan of action to come to grips with small-time gold miners. By 2018, they need to have phased out using mercury in the production of acetaldehyde – the process that poisoned Minamata is still in use. By 2020, they need to have begun phasing out products that contain mercury.
But beyond that, the actual decision-making power on mercury control comes from those Conferences of the Parties, starting in Geneva. It isn’t yet clear which countries will pony up the cash to pay for campaigns to raise awareness about the dangers of mercury, for example, Selin says. Nor is it clear whether countries like China, and especially India – who were dragging their feet in 2013 with the argument that stricter mercury standards would be prohibitively expensive – can be convinced to beat the deadlines.
Rimiko won’t be in Geneva, so Providence is her last chance for a while to get her specific message out. At the end of her story, she launches into a plea to the assembled scientists. “We, the ones who live by the sea, are the first ones to realise the strange phenomena,” she says. “Always listen to the voices of nameless persons.
“What you are protecting are the irreplaceable lives of human beings. This is the wish of Minamata, Japan, where many lives were sacrificed, and [where] some 10,000 people with health damages are still living.”
Three times a week, a support group of about a dozen people living with the lingering effects of Minamata’s poisoning gathers. It’s Monday morning and they trickle into a room at a community centre and sit on chairs or on the floor around a low table. Patients and activists chat, glancing at nonstop coverage of the latest Kim Jong-un provocation on the news. Two attendees bring their cats in carriers, and the organisers let the cats out in an adjacent room. People take shifts to go play with them.
Yoichi Tani, a long-time Minamata activist who first recruited Rimiko’s now-husband Toshio Yoshinaga to the cause in 1972, hosts this informal meeting. It draws a diverse crowd. There are a few high-profile storytellers, several patients who were poisoned in the womb, a couple who recently came out and were covered in the newspapers, and two sisters who spend most of their time with the cats and ask to not have their picture taken.
Hunched over by the wall, her arm bent and held close to her chest, is Shinobu Sakamoto, who was affected in the womb and is maybe the most ‘famous’ living Minamata victim. In 1972, she travelled to an international environmental conference in Stockholm with her mother to talk to scientists about Minamata. Her haircut today is the same as in the pictures, and she’s still flanked by her mother, a tiny, determined-looking woman. Shinobu has never quite abdicated that role: Tani’s group is paying to bring her to Geneva. Hovering in the background is a journalist who quit his newspaper gig last year to write a book about her, and who now serves as an expert in understanding her slurred speech.
Another patient, Hideo Ikoma, shares his own version of the story many victims have spent their lives telling. He lived by the sea and caught fish, but nothing happened until he was on summer vacation aged 15. He was hanging out with friends up in the mountains as they gathered vines to make crafts. They stopped for a cold treat of shaved ice, and after a few scoops the spoon jumped out of his hand. His friends, thinking he was overheated, suggested he go home and take a nap.
Hideo’s own speech is slurred, and as he talks through an interpreter he occasionally pauses, bends his face down, and brings a mug of green tea to his mouth in jerky steps. “I don’t know how long I slept, but when I woke up, from my head to the toe I felt the hairy worms all around my body,” he says. “I wanted to tell my father but I realised I can’t. I couldn’t talk properly at that time, having numbness.”
Hideo, like Rimiko, has travelled internationally to present Minamata to a wider audience. He’s 74, though, and his health is worsening. About five years ago, he still had the dexterity in his hands to make the wooden dolls and crafts that many Minamata disease victims sell to raise money. Now he doesn’t. He says he would go to Geneva himself, but his back hurts too much on long flights.
Although methylmercury lingers in the body, its half-life is short compared to human memory: just 50 days. Mercury levels in Minamata’s food long ago returned to normal, so Hideo’s current symptoms are the tangled product of his severe exposure as a child and everything since.
Other patients report similar recent experiences. In the span of a few years, their health and motor skills can deteriorate quickly. “We see delayed effects,” says Chan, the toxicologist from the University of Ottawa. “We know that it is possible, but exactly how we don’t know yet.”
Hideo’s worsening health has left him thinking about the legacy of Minamata’s storytellers. “The adults who got affected are now already passed away,” he says. People who were affected as children and actually remember the onset of their symptoms are now in their 70s. Those in his generation, he says, “are kind of the last people to talk about these things.”
To some of these patients and their advocates, long at odds with the Japanese government, the Minamata Convention is only a partial resolution. “I will say what no one will say,” says Masanori Hanada of nearby Kumamoto Gakuen University, speaking through an interpreter. Hanada, head of a group called the Open Research Center for Minamata Studies, also leads efforts to study and advocate for victims of mercury poisoning in Grassy Narrows, Canada. “The members of this research centre, we would not say Minamata Convention. We say ‘mercury convention’,” he says. “[The negotiators] understood the lesson of Minamata disease, but not the real fact or the real situation of Minamata.”
One gripe goes back to the beginning and is still being contested in lawsuits today: Who exactly qualifies as a sufferer? Who deserves compensation? There have only been about 2,000 certified patients, most of them already dead. It’s a strict certification process – you are examined for neurological symptoms by a medical panel and need to prove you lived in Minamata around the right time. In recent years, very few names have been added.
Even Rimiko, one of the most visible Minamata ambassadors, says that she and her siblings have not applied for fear of rejection. Instead, Rimiko is part of a complex, tiered system that pays at least some compensation or healthcare expenses to tens of thousands more. To Tani, the activist, tens of thousands is still too small: he argues a comprehensive approach should be taken that considers historic methylmercury exposure in fish eaters around the full Shiranui Sea.
Another point of conflict is all that untreated mercury under the park, athletics fields and waterfront memorial – which was the site of a ceremony during the Minamata Convention signing. “We think here the Japanese way is just [to] bury mercury underneath the land. It’s not safe at all,” Hanada says. In 2016, the Kumamoto region containing Minamata experienced a 7.3 magnitude earthquake. Rimiko worries that a subsequent disaster could free the buried mercury back into the bay.
That isn’t as serious a concern as it might seem, says Sakamoto at NIMD, where he is head of the Department of Environmental Science and Epidemiology. According to Sakamoto, over the years the mercury has transformed to mercury sulfide, a stable and safer form. But to Hanada and others, ‘mercury sulfide’ is an old chestnut. “Nobody has checked,” says Sakamoto’s former boss Akagi, who speaks ruefully of an unused chemical process he once developed to treat the sludge before it was buried.
For Hideo Ikoma, wrapping up his story at the community centre, Minamata’s still-simmering conflicts are worth fighting but are stressful on a personal level. He says he finds solace somewhere both unexpected and blindingly obvious: a small boat with a safety railing that he takes out on the Shiranui Sea.
It’s harder to get out there now that he has to visit the hospital every day. And until two or three years ago, he loved to fish, but since then it’s become almost impossible to bait a hook. Thinking about it, he lights up. Earlier this week he let a bare line hang in the water, he says, and caught a few octopuses. There’s also a social component. “Whenever I go out into the sea, I see an acquaintance or my old friends doing something” – almost all of them Minamata disease ‘patients’, or ‘sufferers’, or otherwise connected.
He’ll go over and chat, or sometimes just manoeuvre his boat with one hand on the engine, his head clear. “While I am at the sea I don’t need to think about anything,” he says. “I can be so quiet and peaceful.”
Chisso Corporation did not respond to Mosaic’s requests for comment in relation to this article.
With thanks to Hiroko Saisho for interpreting.
Author: Joshua Sokol
Editor: Chrissie Giles
Editor: Rob Reddick
Fact checker: Lowri Daniels
Copyeditor: Rob Reddick
Photographer: Joss McKinley
Art director: Charlie Hall
As western wildfires become bigger and more intense, state and federal fire agencies are using more and more aerial fire retardant, prompting concerns over fish kills, aquatic life, and water quality.
The chemicals, known as PFAS, are linked to health effects including cancer, thyroid disease, high cholesterol, pregnancy-induced hypertension, asthma, and ulcerative colitis.
The painkiller, taken by half of pregnant women worldwide, could be contributing to rising rates of reproductive system problems and neurodevelopmental disorders like ADHD and autism.
"If we look at the rate of carbon emissions, most is emitted by the developed and industrialized countries, but the problem is poor countries like Bangladesh are the main sufferers."