Life is a ballet : we don’t dance once.


La vie est un ballet : on ne le danse qu’une fois.

Life is a ballet : we don’t dance once.

Dancer – Darian Volkova

20161229-d-012-darian-volkova

WHO Year in Review


WHO Year in Review
March 2016:
Environmental risk factors such as air, water and soil pollution, chemical exposures, climate change and UV radiation contribute to more than 100 diseases and injuries

20161229-t-003-who

19 HOUSEHOLD ITEMS YOU DIDN’T REALIZE HAD EXPIRATION DATES


http://www.themagicoflife.info/other/19-household-items-you-didnt-realize-had-expiration-dates/

19 HOUSEHOLD ITEMS YOU DIDN’T REALIZE HAD EXPIRATION DATES

You should start checking expiration dates…and not just the stuff in your fridge!

 

 

 

 

The Boucquillon house in the rock by Michel Boucquillon & Donia Maaoui


http://www.caandesign.com/the-house-in-the-rock-by-michel-boucquillon-donia-maaoui/

The Boucquillon house in the rock by Michel Boucquillon & Donia Maaoui

Architects: Michel BoucquillonDonia Maaoui
Location: Tuscany, Italy
Year: 2010
Photo courtesy: Pietro Savorelli
Description:

The house on the slopes close Lucca, in the Tuscan field. The new home-studio of Michel, a planner and creator working for pioneers in this division, and Donia, engineer, artist and painter, is a home that exists in progression with nature. Olives trees, stone, white marble are the trademark components of the scene of the slope on which the house stands, a spot for work and regular life, a long way from the uproarious city. Be that as it may, this “back to nature” doesn’t include the rediscovery of vernacular structural engineering and rustic tastes, dodging contemporary reality and the weight of being present day.

The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-01

Rather, it works in the present, both regarding ecological issues, including enhancement of vitality source( absolute independence, including accumulation of downpour water, the utilization of a warmth pump, sun powered pump, sun based boards), and in finding a fragile answer for development in a characteristic setting. The reasonable, just about automatic methodology maintains a strategic distance from simple impersonation, yet mixes into the scene. The task met with the hobby and backing of the city of Lucca and the neighborhood powers. The state of the slope, the layering of rises and divides of white marble together with the green of olive trees and the local brush, proposed flanking the current, truly harmed structure with an augmentation of living space added to the house appropriate, place between vast porches confronted by the work space.

The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-02

The patios reinterpret, changing their figure and estimate, the farming porches of the past, making the insertion of the new development more congruous. This methodology as of now moves the undertaking to the vital scene scale, where the building design is not seen as “from the earlier ” to embed, but rather as a commitment to the upgrade of a part of the slope. In these terms the decision of a solitary material like white marble, utilized for the outside facings of the whole development, turns into a variable of coherence with the stone, the extremely material on which the house stands, turning into a kind of building expansion that changes the materic geology of the spot. Without cover or mask, the house utilizes its compositional procedure to declare its open, genuine innovation. The new private volume takes after the extents of its forerunner, with a pitched rooftop, denoting the declining exterior with a couple of openings sorted out in an unpredictable way that capacities for insides, and along these lines ensuring view of the primary veneer as a figure in stone, connected to the same treatment of the dike dividers of horizontal porches and of the lower bended volume of the studio.

The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-03

On the two parallel facades(the back is set up against the slope), the house opens with substantial sliding glazings, blending outside space with the vast living zone and plainly designing the complexities of full and exhaust zones, the cadence between the marble of downhill veneer, the straightforwardness of the inside spaces, the stone of the slope. The recent turns into the hero of the spaces, brought inside as a characteristic setting behind the kitchen open to the eating and living territories, and in two rooms and a shower on the upper level. The association with the stone is immediate and underscored by the straight outline of spaces, by the outfitting used, by the geometric treatment of the inward surfaces, in a relationship of deliberate stand out from the materic character of the slope. On the ground floor two compositional components describe the space: the mass of the chimney( with double, dynamic aloof warmth recuperation) contains the TV screen and a sidelong window in its corner to corner opening, just about a “canvas” the edges the field, changing shading with the evolving seasons;

The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-04

The volume of the winding staircase regarded as a sculptural component, punctured by round openings and loaded down with conceptual qualities, both because of its separated vicinity in brought together space of the parlor, and for the poppy shade of its inside, another reverberation of the found outside at specific times of year. The staircase ascends through two levels in a free, open space that underscores its size and part as a focal component. The heart of the house in non-literal terms. On the upper level the main room possesses the end zone with its own particular shower and wardrobe, while three different rooms region masterminded along a focal hallway that finishes up with a typical restroom. In the whole evening region, the house can be opened for a perspective of stars: the rooftop rises, similar to the wings of a butterfly, depended on the focal crest, to let the air give normal cooling, changing a natural advancement component into a “wonderful gadget” on a household scale.

The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-05The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-06The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-07The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-08The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-09The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-10The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-11The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-12The-Boucquillon-house-in-the-rock-by-Michel-Boucquillon-&-Donia-Maaoui-13

Thank you for reading this article!

 

Not ALL Hips Need Opening: 3 Moves for Hip Stability


http://www.yogajournal.com/slideshow/3-moves-stability-hypermobile-hips/

Not ALL Hips Need Opening: 3 Moves for Hip Stability

alice louise blunden splits

When yogis talk hips, it’s generally about opening them. But your hips CAN be too open. If you fall into the hypermobile camp, learn how to balance strength and flexibility to protect your hips.

Dedicating time during our physical yoga practice to opening the hips can be nourishing, therapeutic—and downright addictive for many of us. (How about that feel-good release in Pigeon Pose?) Let’s consider, though, whether we always need to push for more flexibility in this region of the body or if it may be more helpful for some people to build strength.

Do Your Hips Really Need Opening?

Hip strength is necessary in day-to-day life. Whether we are walking in the park, running for the bus, or cycling to work, the hip joint takes the brunt of the body’s weight and enables all of these fundamental actions. In short: Stable hips are a good thing—they carry our bodies throughout the day.

Of course if you are an athlete, runner, or someone simply born with especially tight hips, hip-opening poses are helpful in maintaining a healthy range of motion and balance between strength and flexibility. If you’re on the other end of the spectrum, though, and are naturally quite open in the hips or after years of practicing hip-opening poses now have very open hips, consider whether it’s still helpful to continue increasing the range of motion in this region of your body.

Being ‘blessed’ myself with naturally open hips, when I first started yoga, I never shied away from postures that required increased range of motion in this region of the body. (I’m the person who could actually fall asleep with my legs wrapped behind my head in Yoginandrasana.) But was it therapeutic? I certainly looked like an advanced yogi in these postures, but unfortunately my lack of knowledge and understanding of the hip joint meant that I could have been doing more damage to my body than good.

hip joint anatomy

Understanding the Hip Joint

The hip joint is a ball and socket joint composed of two bones. The femur sits in the acetabulum, which is part of the pelvis. Covering the bones of the hip is the articular cartilage. The articular cartilage is important for providing a cushion and a smooth surface when the bones move on one another. Surrounding the acetabulum is additional cartilage called the labrum, which forms a lip around the cup-shaped bone to provide additional stability in the joint.

While it is helpful to understand the anatomy of the hip, what may be more even important (if a bit frightening) is knowing that one of the deepest layers of the joint, the cartilage, does not have any nerve endings. This means you may not be aware of any damage to the cartilage until it is too late. Although cartilage doesn’t have nerve endings, the surrounding muscles, tendons, and ligaments do, which is why yoga can be helpful for tuning into the body to find a balance between strength and flexibility for health of the muscles and the integrity of the joints. By listening to our bodies with this sense of mindfulness we can begin to notice our strengths and weaknesses, which enables us to develop a nourishing practice that our bodies truly need.

See also 5 Common Myths About Athletes’ Tight Hips

3 Moves for Hip Stability

If you already enjoy the benefits of more open hips, modifying your daily yoga practice by including certain exercises to strengthen hips can be helpful for maintaining the integrity of the joint. Here are three yoga-inspired exercises that you can add into your daily practice to increase hip stability.

  • Bridge Pose, variation

    Bridge Pose, variation

    Lie on your back with your knees bent, feet hip-width apart and knees directly above your ankles. Place your arms on either side of your body with your palms facing down. Lengthen your tailbone toward the front of your mat. Lift one leg perpendicular to the floor (optional: bend knee). On your inhalation, keep your leg raised and lift your hips off the floor into a Bridge position. On your exhalation, with your leg still raised, lower your hips again. Repeat the exercise for 5 rounds of breath on each side.

    See also Anatomy 101: Understand Your Hips to Build Stability

  • Chair Pose, variation

    Chair Pose, variation

    For this exercise, hold Chair Pose with your feet hip-width apart. As you inhale, straighten one leg to the side and as your exhale bring it back to its original position. Repeat the exercise on each side 10 times or until the hip-stabilizing muscles start to fatigue.

    See also Glute Anatomy to Improve Your Yoga Practice

  • Leg Raises

    Leg Raises

    For this final exercise, lie on your side and rest your head on your arm. Bend your bottom leg to approximately 90 degrees so you have a steady base. Raise your top leg about a foot above the ground. Extend your lifted leg in a straight line from your spine and flex the foot. Hold for 10 breaths and relax the leg for 5 breaths. Repeat the exercise for 3 rounds on each side.

    See also 7 Poses to Firm + Tone Glutes for a Stronger Practice

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Psst: Yoga Medicine founder Tiffany Cruikshank will teach at Yoga Journal LIVE San Francisco, Jan. 13-16. Get your ticket today.

Alice Louise BlundenAbout Our Writer
Alice Louise Blunden is a Yoga Medicine senior teacher and assistant to Tiffany Cruikshank. She is currently completing her 500 hours and working toward her 1000-hour advanced Yoga Medicine teacher training. As well as teaching yoga in studios across London, she is the founder of The Yoga Project UK, a company that connects yoga teachers with schools across the UK. Learn more at alicelouiseyoga.com.

 

The world produces enough food to feed everyone. So why do people go hungry?


Best of 2016: Is this how to end hunger?

https://www.weforum.org/agenda/2016/07/the-world-produces-enough-food-to-feed-everyone-so-why-do-people-go-hungry?utm_content=buffer34978&utm_medium=social&utm_source=facebook.com&utm_campaign=buffer

The world produces enough food to feed everyone. So why do people go hungry?

This article is published in collaboration with Project Syndicate.
A retail trader scoops kidney beans at his shop in Jammu May 30, 2008. Surprisingly strong Indian growth and a jump in inflation above 8 percent put an interest rate rise back on the agenda on Friday, although many analysts thought the Reserve Bank of India would remain focused on cash management.

Ending hunger requires social protection and pro-poor investment, argue the authors.
Image: REUTERS/Amit Gupta
Written by
Jomo Kwame SundaramAssistant Director-General and Coordinator for Economic and Social Development, Food and Agriculture Organization, United Nations
Published
Monday 11 July 2016
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Last September, world leaders made a commitment to end hunger by 2030, as part of the United Nations Sustainable Development Goals (SDGs). It sounds like a massive undertaking. In fact, the world already produces enough food to feed everyone. So why does the problem persist?

Poverty and hunger are intimately connected, which is why the SDGs target elimination of both. For someone living at the World Bank’s poverty line of $1.90 per day, food would account for some 50-70% of income. The Bank estimatesthat almost four-fifths of the world’s poor live in rural areas, though those areas account for less than half of the world’s population. The obvious conclusion is that raising rural incomes sustainably is required to eradicate hunger.

Achievement of the millennium development goal hunger target

Image: FAO

That will not be easy. Most developing countries nowadays are burdened by high rates of unemployment and underemployment. And with current economic prospects bleak, especially given low commodity prices, and insistence on fiscal austerity continuing in most places, downward pressure on rural incomes is likely to worsen.

But even if countries do manage to achieve inclusive growth, it will not be enough to eliminate hunger by 2030. The only way to do that will be to implement well-designed social protection and scale up pro-poor investments.

According to the World Bank, one billion people in 146 low- and middle-income countries currently receive some form of social protection. Yet 870 million of those living in extreme poverty, mainly in rural areas, lack coverage.

Unsurprisingly, the greatest shortfalls are in low-income countries, where social protection covers less than one-tenth of the population, 47% of which lives in extreme poverty. In the lower-middle-income countries, social protection reaches about a quarter of those living in extreme poverty, leaving about a half-billion people without coverage. In the upper middle-income countries, about 45% of those living in extreme poverty receive social-welfare benefits.

This is clearly not good enough. Improved social protection can help to ensure adequate food consumption and enable recipients to invest in their own nutrition, health, and other productive capacities. As such investments sustainably raise incomes, they enable further increases in productive personal investments, thereby breaking the vicious cycle of poverty and hunger.

Governments, too, have investments to make, in order to ensure that those who are currently mired in poverty reach the point where they can invest in themselves. An early big investment push would generate additional incomes sooner, reducing longer-term financing costs. Moreover, it would boost aggregate demand in a world economy that badly needs it.

The world can afford the needed investment. According to estimates by the Food and Agricultural Organization (FAO), the International Fund for Agricultural Development (IFAD), and the World Food Programme (WFP), it would cost the equivalent of 0.3% of the world’s 2014 income. All that is needed is for wealthier countries to provide budgetary support and technical assistance to the low-income countries that need it. (Most middle-income countries can afford the needed financing themselves.)

It should not be difficult to generate the political will to provide the needed support, at least in theory. After all, it has been more than a half-century since the adoption of the Universal Declaration of Human Rights and its Covenant on Economic, Social, and Cultural Rights, which treats the material needs of all persons as a fundamental human right. A few years earlier, US President Franklin D. Roosevelt called “freedom from want” – which, presumably, includes freedom from hunger – one of four essential freedoms of which people “everywhere in the world” should be assured.

Now, with the adoption of the SDGs, governments everywhere are obliged to take responsibility for ending poverty and hunger, as well as for creating the conditions for ensuring that both are permanently overcome. The upcoming High-Level Political Forum on Sustainable Development presents an important opportunity to forge the path ahead, setting near- and medium-term priorities.

Ending hunger and poverty in a sustainable way is morally right, politically beneficial, and economically feasible. For world leaders, inaction is no longer an option.

Written by

Hilal Elver,

Jomo Kwame Sundaram, Assistant Director-General and Coordinator for Economic and Social Development, Food and Agriculture Organization, United Nations

This article is published in collaboration with Project Syndicate.

The views expressed in this article are those of the author alone and not the World Economic Forum.

 

in the conversation as well as in the dance,,,,,


" in the conversation as well as in the dance, everyone is the mirror of the other."

-Alain

20161229-d-008

5 DISEASES YOUR LACK OF SLEEP COULD BE CAUSING


http://www.themagicoflife.info/health/5-diseases-your-lack-of-sleep-could-be-causing/

5 DISEASES YOUR LACK OF SLEEP COULD BE CAUSING

Sleep is of extreme importance for the overall health of the individual, both, mentally and physically. It is a way to recharge after the long and stressful day.

While sleeping, millions of processes continue to happen in the body, helping the brain to store the important data in the memory, and the cells work to repair the damaged tissue and regenerate. On the other hand, when we lack sleep, all these functions fail to be done on time, and we wake up cranky and have difficulties to concentrate the entire day, but what’s more important, we experience numerous side effects which can significantly endanger our health.

5 diseases which are caused by the lack of sleep:

-Cardiovascular Disease

The link between heart problems and the lack of sleep has been suggested numerous times before, but the best evidence for the h3 correlation has been found by a recent study and presented at EuroHeartCare, the annual meeting of the European Society of Cardiology.

For 14 years, the team of researchers followed 657 Russian men between the ages of 25 and 64 and found that two-thirds of the individuals who experienced a heart attack had a sleep disorder as well.

Moreover, the men who complained to have sleep disorders also had a 1/5 to 4 times greater stroke risk, and 2.6 times higher risk of myocardial infarction.

-Ulcerative Colitis

According to a 2014 study, sleep deprivation, and excess sleep may lead to ulcerative colitis, which is an inflammatory bowel disease manifested by ulcers within the lining of the digestive tract, as well as Crohn’s Disease.

The findings of experts from Massachusetts General Hospital show that the adequate amount of sleep is of vital importance in order to curb inflammation responses within the digestive system which often causes these diseases.

Researchers studied women enrolled in the Nurses’ Health Study (NHS) I since 1976 and NHS II since 1989, and discovered that the risks of ulcerative colitis were raised as sleep per night was reduced to 6 hours or less.

Also, they found that 9 hours of sleep also raised the risks, meaning that the proper amount of sleep is a must in the prevention of these diseases.

Even though the results were found in adult women only, the increased risk of developing ulcerative colitis in the case of sleep deprivation existed despite other factors as well, including weight, age, and habits such as drinking or smoking.

-Obesity and Diabetes

Numerous studies and scientists have pointed out the relation between poor sleep and diabetes, but a team of researchers at the University of Chicago conducted a study which showed the way poor sleep potentially leads to obesity, and ultimately, causes diabetes.

Experts examined the effects of poor sleep on the accumulation of fatty acids, as the fatty acid levels in the blood affect the speed of and the ability of insulin to regulate blood sugar.

They examined 19 different sleeping patterns of men and found that those who slept for 4 hours for three nights had increased fatty acid levels within their blood between 4 a.m. and 9 a.m. which was 15- 30 percent increase over those who slept 8.5 hours every night.

Furthermore, researchers discovered that the increased fatty acid levels led to an increased degree of insulin resistance, which indicates pre-diabetes.

-Alzheimer’s

Scientists at Johns Hopkins University conducted a study in 2013 which found that a lack of sleep can cause Alzheimer’s disease and also affect the speed of its progression.

The study was based on previous research that found that sleep is of higher importance for the brain to eliminate the “cerebral waste,” or the buildup which can accumulate and lead to dementia.

The study involves 70 adults between the ages of 53 and 91, and the lack of sleep every night led to a higher amount of beta-amyloid deposition in their brains on PET scans.

This compound has been shown to be a definitive marker of Alzheimer’s, indicating that lack of sleep prevents the brain from removing this form of “cerebral waste.”

-Prostate Cancer

The journal Cancer Epidemiology, Biomarkers and Prevention, published a 2013 study which showed that patients with sleep issues had an increased incidence and severity of prostate cancer.

Researchers followed 2,425 Icelandic men between the ages of 67 and 96 for 3-7 years and found that the risk of developing prostate cancer increased in 60 percent of men with trouble falling asleep.

The number doubled in the case of men who experienced difficulty staying asleep. Moreover, people with sleep problems were also more likely to have later stages of prostate cancer.

This link has been attributed to melanin, a sleep-regulating hormone, by researchers.

Higher melatonin levels were found to suppress tumor growth, while melatonin levels in people exposed to too much artificial light (which is a common cause of sleep deprivation) were found to have more aggressive tumor growth.

Source: http://www.biutidiy.com/

 

Back on Track: 5 Daily Poses to Ease Back Pain


http://www.yogajournal.com/article/practice-section/back-on-track/

Back on Track: 5 Daily Poses to Ease Back Pain

Free yourself from ordinary back pain by doing these 5 simple poses each day.

So oftentimes it happens that we live our lives in chains, and we never even know we have the key. —The Eagles

Yes, I’m dating myself here—quoting a ’70s rock band to illustrate a point about yoga. But these lyrics perfectly describe one of the great benefits of a regular yoga practice. Steady practice helps us to identify when our suffering is optional, and it empowers us with the tools to transform that suffering.

One of the most common forms of suffering that arises from living in a modern culture is back pain. But somehow the message that a regular yoga practice can unlock a tight, aching back and resolve chronic pain doesn’t seem to have been broadcast to the population at large. A quick Internet search on the words “back pain” turns up zero yoga-related results unless you go digging for them. On pages where users ask each other the best way to resolve their back problems, they are advised by other users to see a massage therapist, a chiropractor, or a doctor, or to take Motrin. Of course, massage, manipulation, and medicine can each help to free up tense back muscles in its own way, but these options don’t give people the tools to cast off their own shackles. And even though a few insightful respondents do recommend elementary stretches, no one has uttered so much as a tweet about the elephant in the chat room: yoga.

Maybe someone needs to write a hit song about it.

Simple Solution

The message should definitely be more widely circulated, because freeing your entire back from ordinary muscle tension, and the pain it brings, can usually be done by practicing just four simple poses— one forward bend, one pose that combines a sidebend with a forward bend, one sidebend, and one twist—plus a passive backbend, each day. These poses systematically stretch every muscle in your back, with the exception of a few arm and shoulder muscles. As you practice the sequence of poses on these pages, you’ll see that when yoga unlocks the chains that bind the back, it does so with a combination, not a key.

It’s best not to introduce these poses too abruptly. Start by spending a few days loosening your muscles partway with gentle, supported poses that involve similar movements, such as Supta Padangusthasana and Supported Child’s Pose.

Use your intuition and an honest assessment of the sensations in your back muscles to gauge when a stronger stretch would feel more like a relief than a threat to them. Then gradually introduce the back-stretch sequence. You can stave off tension-induced back pain indefinitely by practicing these poses on a regular basis, either on their own or after gentler preparatory poses. When you reach this stage, you should add a fifth pose, the passive backbend shown on page 75, to balance out your practice.

Muscles and Fitness

To fine-tune your practice and get the most out of each pose, it helps to have a general idea of how your muscles work. In addition to the well-known large muscles of the back, such as the trapezius, latissimus, and rhomboids, you have well over 200 intrinsic back muscles, and their primary function is to move or stabilize your spine and trunk. Trying to stretch all of them deeply with just four poses seems like a tall order, but that’s exactly what this sequence will do.

You can stretch all of your intrinsic back muscles, at least to some extent, by curling your head, neck, trunk, and pelvis forward toward the fetal position. This is what you’ll do in (Garland Pose), variation 1. To see why this variation of Malasana with a chair works, and to improve your practice technique, visualize your back muscles with the help of the illustrations.

Think of these muscles as a series of elastic bands—some long, some short—that connect the back of your skull, spinal vertebrae, rib cage, sacrum, and hipbones to one another. When you round forward, the anchor points where the muscles attach to the bones move apart from one another, and this is what stretches the muscles. If you connect the dots between these points, they form a wide arc that defines the curve of the back. Each muscle stretches over a segment of that arc.

To get the most stretch from this variation of Malasana, systematically lengthen each segment, without skipping any, by bending your back bit by bit, tucking your hips under, and working your way up the spine, one vertebra at a time, all the way to your neck and head. Deep, natural breathing will increase the effect, because your inhalation widens the arc of your back, and your exhalation tightens the curl.

Best Stretch

The first variation of Malasana with a chair is the best for stretching three long muscle groups that run vertically, or nearly vertically, along the vertebral column. They are the spinalis muscles, which connect to the central spines of the vertebrae; the longissimus muscles, which run from the head to the sacrum, connecting to the sides of the vertebrae along the way; and the semispinalis muscles, which start at the base of your head and continue along the vertebral column, connecting the central spine of one vertebra to the side of another one many segments below. (Adding a slight twist of the head and upper back while sidebending them in the opposite direction will increase the stretch on the semispinalis muscles.)

When you practice any trunk-flexing movement such as Malasana, be careful not to overdo it, because forced flexion can injure the disks and other soft tissue that hold your spine together. Even though you can stretch many of your intrinsic back muscles by rounding forward, you can increase the stretch on some of them by adding a sidebend to the forward bend. This movement, which you create in variation 2 of Malasana, intensifies the stretch by creating a larger gap between the vertebrae on one side of the spine than either a forward bend or a sidebend does alone.

This variation of Malasana is best for stretching a group of short muscles near the center of your lower back, the interspinales muscles in your lumbar spine. It’s important for you to limit flexion in this pose by resting your chest and belly on your thigh, because excessive spinal flexion in combination with a sidebend can be even more dangerous for the disks and other soft tissue around your spine than excessive flexion on its own.

Several muscles in two distinct groups get their strongest stretch when you simultaneously twist your trunk in one direction and sidebend the opposite way without bending forward. The variation of Upavistha Konasana (Wide-Angle Seated Forward Bend) used in this sequence maximizes the lateral arc of your body, and this creates more stretch than any other movement on certain muscles that run vertically up the sides of the vertebrae or the back of the rib cage. These include the iliocostalis, the intertransversarii, and the quadratus lumborum. To maximize the stretch on these muscles, systematically separate each rib from its neighbor, individually sidebend each vertebral segment, sidebend your waist and neck, and breathe naturally but deeply. The second group of muscles that gets maximal stretch from this variation of Upavistha Konasana responds as much to the twist as to the sidebend. It includes midlength muscles that run diagonally from the center of one vertebra to the side of another, namely, the rotatores longi and multifidus. To stretch them fully in this pose, create a very strong twist, without skipping any level, before bending to the side, and reinforce this twist as you sidebend to your maximum.

There is one set of very small muscles very deep in the spine—the rotatores breves—that you can stretch effectively only by twisting; in fact, they’re barely affected at all by forward bends or sidebends. That’s why, to complete the back-stretching sequence, it’s crucial to include a potent twist like the supported Bharadvajasana (Bharadvaja’s Twist) variation included here. You’ll benefit from practicing this pose toward the end of the sequence, because the previous poses will soften the larger back muscles that would otherwise prevent each vertebra from twisting to its full potential. As you work your way up your spine in this supported twist, consciously release and rotate every vertebra as much as you can in relation to the one below it. Since each vertebra of the upper back is attached to a pair of ribs, it’s easier to rotate these vertebrae if you allow the ribs to turn relative to one another. Finally, whenever you twist, exhale softly to release the grip of the diaphragm muscle and intercostal muscles on the rib cage.

Sweet Relief

The passive backbend that concludes this back-stretch sequence lengthens your abdominal muscles. Since the first four poses increase flexibility in the back muscles, it’s important to keep your abs flexible, too. If your back becomes looser than your belly, the relative tightness of the abdomen will bend your spine forward, and your back muscles will tense up by reflex to oppose this.

This back-stretch sequence includes a passive backbend because an active backbend makes you tighten your back muscles. Since even a passive backbend places the back muscles in a shortened position, it’s usually best not to introduce this pose into your back-stretch practice when you first learn this sequence, while your back muscles are still tight. Tight muscles are in a state of contraction, and if you shorten them, they may automatically contract even further. Instead, practice the forward bending, sidebending, and twisting poses for as many days as it takes for your back tension to subside before adding the backbend.

So go forth and practice to liberate your back from the chains that bind it! Having a tight, painful back is so familiar to many of us, and so common among the people we know, that it’s easy to assume there’s nothing we can do about it. But for ordinary back tension and the pain that comes with it, yoga offers clear relief and reliable prevention. And best of all, the most likely side effects are a peaceful mind, increased energy, and the joyful feeling of freedom restored.

Set Your Back Free: 5 Daily Poses to Ease Back Pain

Here are four poses that will systematically stretch all the intrinsic muscles of your back, plus a passive backbend to help bring your front and back body into balance. Practice on an empty stomach, and go only as far into each pose as you feel comfortable.

You’re most likely to keep your back loose and pain free by practicing these poses regularly before your muscles become tense. You can also practice this sequence to ease moderate back tightness and discomfort before it becomes chronic pain or an acute injury.

If your back muscles are already tight and painful, start with gentler, supported poses, introduced one at a time over several days, preferably under the guidance of a teacher. When you sense that a stronger stretch would feel more like a relief than a threat to your back, gradually introduce the poses in this back-stretch sequence.

NOTE: This practice is meant to relieve simple muscular tightness in your back, and it may be inappropriate for muscle spasms, disk injuries, sacroiliac-joint dysfunction, spondylolisthesis, or other back problems. If you have back pain, or suspect a disease or injury, check with your health care provider before trying it.

1. Malasana (Garland Pose), variation 1

Sit tall in a chair with your legs about a foot apart. Push your hands down on the arms or seat of the chair to take some of the weight off your pelvis. Without flexing your back or neck at first, tilt your pelvis, spine, and head forward as a unit (as you do when you’re initiating a forward bend), until you can’t tilt the pelvis any further. Now let your back round over, starting at the bottom of the spine and working your way up to the top.

Bring your torso toward or between your thighs, and rest the backs of your hands on blocks or on the floor under the chair if they go that far. Let your head hang down. If you are still comfortable and want to increase the stretch, gently tilt your tailbone down toward the chair seat and curl your back further, one vertebra at a time, from the base of your spine all the way up to your neck and head. As you progress, draw your belly up toward your lower back, your breastbone toward your upper back, and your head toward the front of your tailbone to round the spine more. Use 8 long breaths to stretch the spaces between your back ribs and to release tight spots.

2. Malasana (Garland Pose), variation 2

From variation 1, lift your chest to thigh level and place your left palm on your outer left thigh near the knee, with the thumb on top of the thigh. Place your right hand on your outer left ankle, then use both hands to sidebend your trunk gradually to the left until you can rest your chest and belly well across your left thigh. Lengthen your right waist and bend your neck gently to the left and down. Hold for 8 breaths, then repeat the sidebend on the other side.

To exit the pose, bring your trunk back to the center and push your hands down on your knees to help you sit up.

3. Upavistha Konasana (Wide-Angle Seated Forward Bend), variation

Sit on the floor with your legs wide apart and your pelvis elevated on enough folded blankets to allow you to easily keep it fully upright (not slumped back). Press your right hand down into the floor behind you and your left hand down into the floor in front of you, sit tall, and use your arm strength to twist your entire trunk to the right as far as you can.

Continuing to twist to the right, lean to the left directly over your left thigh, walking your left hand forward away from your thigh on the floor in front of you while still pressing it down. Move your right hand to your right hip. Now, without losing the twist, let your right sitting bone feel heavy and move it toward the floor. Systematically bend your spine and rib cage to the left from bottom to top, ending by turning your head to face forward, sidebending your neck and allowing your head to hang down.

Finally, reach your right arm over your right ear toward your left foot and press your left hand into the floor to rotate your breastbone toward the sky. Work deeper into the pose for 8 breaths, then repeat it on the other side.

4. Bharadvajasana (Bharadvaja’s Twist), variation

The fourth pose is an active, prone variation of Bharadvajasana. Fold two blankets long and narrow, and stack them to create a rectangle approximately 27 inches long, 9 inches wide, and 5 inches high. Sit on the floor 6 inches from one end of the blankets, with your right hip joint exactly in line with the long centerline of the blankets and your right thigh perpendicular to it.

Bend your knees and place your left ankle on top of the arch of your right foot. Sit tall, twist your whole trunk toward the blankets, and lie down, reaching your breastbone as far away from your pelvis as it can reach. If you can look to your right without straining your neck, rest your left ear on the blankets. Otherwise, look to the left and rest your head on your right ear. Push your right palm down firmly into the floor to systematically increase the twist, one vertebra and one rib at a time, from the base of the spine to the top of the neck. Work deeper into the pose for 8 breaths, and then repeat it on the other side.

5. Passive Backbend

Include this passive backbend as your final pose to stretch your abdominal muscles while allowing your back muscles to remain relaxed.

Sit on one end of the two folded blankets you used for the twist, facing away from the other end. Keeping your knees bent, lie down and rest your shoulder blades on the far end of the blankets, with the very top of your shoulder bones hanging 1 inch off the end and the rest of the bone supported by the blankets.

Rest your head on the floor. Lift your pelvis, tilt your tailbone away from your head, and set it back down. Straighten your legs forward, keeping your toes pointing upward. Reach your arms overhead and rest them on the floor, or, if your shoulders are tight, support your arms on a stack of blankets. Stay for 2 to 3 minutes and then roll to your side to release.

ABOUT OUR EXPERT
Roger Cole, Ph.D., is a certified Iyengar Yoga teacher and a research scientist specializing in the physiology of relaxation, sleep, and biological rhythms. He teaches workshops worldwide. For more information, visit rogercoleyoga.com.


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The 10 Yoga Sequences That Won 2016


http://www.yogajournal.com/slideshow/yoga-journal-top-10-yoga-sequences-2016/

The 10 Yoga Sequences That Won 2016

With as much yoga as we publish (and practice) a year, you know if a sequence makes our end-of-the-year top 10 list, it’s one worth saving. Tuck these 10 practices away where you’ll be able to find them when you’re in need of a tried-and-true flow.

See also Save These for a Stressful Day: YJ’s Top 10 Meditations of 2016

1 of 10
1 of 2

 

Cilantro can Remove 80% of Heavy Metals from the Body within 42 Days. Here is What You Need to Do…


http://runhealthylifestyle.com/2016/12/28/cilantro-can-remove-80-heavy-metals-body-within-42-days-need/

Cilantro can Remove 80% of Heavy Metals from the Body within 42 Days. Here is What You Need to Do…

If you want to detoxify your body from heavy metals and other toxic contaminants, you should consume cilantro, as this herb is one of the most efficient ones for this purpose. Cilantro is also great when it comes to extracting mercury from the body organs. The presence of heavy metals in the body has been associated with serious health problems, including cancer, brain deterioration, heart disease, kidney disease, lung disease, weak bones, and emotional issues.

  • Health Benefits of Cilantro

Cilantro has no cholesterol and it is very low in calories. Moreover, the leaves of cilantro are packed with dietary fiber, folic acid, riboflavin, niacin, vitamin-A, beta carotene, vitamin-C, essential oils, and antioxidants. Hence, they have a countless number of health benefits, such as:

– Reducing LDL cholesterol levels

– Regulating heart rate and blood pressure levels

– Stimulating the production of red blood cells

– Maintaining healthy mucosa and skin

– Improving vision

– Protecting from lung cancer and oral cavity cancers

– Treating Alzheimer’s disease by limiting neuronal damage in the brain

 Cilantro can Remove 80% of Heavy Metals from the Body within 42 Days. Here is What You Need to Do...

  • How to Use Cilantro

Here’s one inexpensive, effective method you can do on a daily basis.

Blend a handful of fresh, organic cilantro into your daily smoothie is one option. Add chopped cilantro to your dishes.

  • Cilantro Inflammation-Busting Recipe

Ingredients:

– ½ a cup of packed chopped fresh organic cilantro

– 1 teaspoon wheatgrass powder (or any other green powder)

– ½ a cup of organic apple juice

– ½ a cup of water

Preparation:

Put all ingredients in a blender and blend until you get a smooth mixture.

  • Cilantro Essential Oil

The cilantro essential oil improves and accelerates the flushing out of heavy metals from the body through the urine. You can use this oil on a regular basis by adding it to the water you drink.

 

全台6千家合法中違章工廠評比,台中、彰化最多,6成是污染源事業


https://farmland.e-info.org.tw/?p=270

全台6千家合法中違章工廠評比,台中、彰化最多,6成是污染源事業

全台違章工廠或未登記工廠數量近6萬4千家,這些工廠多佔用農地,又不受環保法規約束,對我國糧食生產與食安造成相當大的威脅。2010年起低污染性違章工廠可申請臨時工廠登記繼續經營,至今已近6年,各縣市實際執行情形如何?政府到底容許的哪些工廠在農地上經營?而現在的政策是否有利農地與食安的維護?

為守護農地環境及維護國人食安健康,台灣環境資訊協會利用政府公開資料,篩出全台取得臨時工廠登記的5,821家違章工廠。在目前經濟部的輔導規劃中,想要繼續經營的違章工廠業者,第一步必須申請臨時工廠登記,後續才有資格變更農地為工業使用,在原地或就近成為合法工廠。

全國近1成違章工廠取得臨時登記,集中在台中、彰化

本會根據政府公開的登記工廠名錄資料集http://data.gov.tw/node/6569),資料收錄期間是從2001/3/14到2016/7/8為止,找出目前生產中的工廠中,依照《工廠管理輔導法》第33及34條核准的臨時工廠登記業者,共計有5,821家。取得臨時工廠登記業者,可暫不受建築及土地法規管制,直到2020年6月2日輔導期結束。

目前取得臨登工廠的數量,佔經濟部估計違章工廠總數6萬4千家的10%。數量最多的前6縣市是:台中、彰化、高雄、新北、台南、桃園。台中和彰化地區合法化速度最快,合計佔臨登工廠總數的45%。東部和離島地區數量最少。

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資料來源 / 政府資料開放平台,資料收錄 / 2001.3.14 – 2016.7.8

圖表製作 / 台灣環境資訊協會

4成違章工廠製造金屬製品,6成以上涉及環保污染事業

臨登工廠所營事業非常多元,有生產紙器、電腦、成衣、水泥加工、金屬品、各式機械,甚至汽車車體等不一而足。數量最多的是金屬製品製造、機械設備製造、食品製造、塑膠製品製造、紡織業、非金屬礦物製品製造業6種,共有4,453家,佔所有臨登工廠的76.5%(多業別工廠單一計算)。

%e8%9e%a2%e5%b9%95%e5%bf%ab%e7%85%a7-2016-12-23-%e4%b8%8b%e5%8d%8810-52-25

臨登工廠6大行業 (製作 / 台灣環境資訊協會)(圖片來源:https://goo.gl/qZDNJBhttps://goo.gl/JvNSWThttps://goo.gl/xwnNFQ

這6大行業當中,除了機械設備製造以外,其他5大行業都是受到一至多種環保法規管制的污染源事業,包括了《空氣污染防制法》、《水污染防治法》、《廢棄物清理法》、《土壤及地下水污染整治法》。機械設備製造業別在環保法規中雖未明列,但因為涉及金屬熱處理、表面處理製程、焊接等製程,仍受《空氣污染防制法》和《土壤及地下水污染整治法》管制,由於資料上並無製程欄位,此處暫不予計算。而受到環保法規管制的5大行業工廠共有3,654家,佔所有臨登工廠的6成左右(62.8%)。

以數量第一的金屬製品製造業為例,被歸類在此業別的有2,332家工廠,幾佔臨登工廠總數的4成(40.1%)。底下又可分為15個細類業別,包含從事金屬製的手工具、模具、結構及建築組件、容器、含有金屬加工處理程序,以及上述以外的其他金屬製品(如螺絲)製造的行業。

金屬製品製造常見製程有熔解、加工、研磨、剪裁、沖床、鍛造、清洗等,易產生金屬冶煉爐渣、廢鐵、廢潤滑油及廢水。螺絲、螺帽、鉚釘等製品製造更會因為酸洗和水洗程序產生大量廢污水。

4個環保法規當中,屬《水污染防治法》最為嚴格,只要從事金屬製品製造業15個細項的任一業別,並且設計或實際最大廢水產生量每日在5十立方公尺(公噸/日) 以上者,事業在設立或變更前,都必須先檢具水污染防治措施計畫之事業種類、範圍及規模,送主管機關審查核准。《廢棄物清理法》也針對其中13個業別,要求在一定登記資本額或廢棄物產量範圍以外應檢具事業廢棄物清理計畫書,送請審查核准以後才得營運。土污法特別管制編號2544的金屬表面處理業和2543金屬熱處理業,也包括涉及相同製造程序的其他事業。空污法則是除以上兩種行業和製程,同時增列2542粉末冶金業。

這15種金屬製造業細項業別裡面,經濟部只管制了2種:2544金屬表面處理業和2543金屬熱處理業,並且不包括其他可能涉及電鍍等表面加工處理的事業。剩下的13種金屬製造業細項業別,經濟部則容許申請臨時工廠登記,在農地上繼續製造螺絲、鐵線、鍛造品、鋼管等器具。

6大臨登工廠行業所受到管制的環保法規,及經濟部所管制的項目對應比較請見下表。

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環保管制與經濟部管制比較 (製作 / 台灣環境資訊協會)

從表中可知,臨登工廠6大行業當中,5大行業整體上也都受到多種環保法規管制,機械設備製造因為涉及焊接、金屬表面處理、金屬熱處理等污染程序,依然受《空污法》及《土污法》管制。相比之下,經濟部的管理強度弱了許多,有鑒於許多違章工廠地段是在農地上,弱化的違章工廠管理制度,等同容許污染事業繼續危害我們的農地,影響國人的食安!

只要有利企業投資,中高污事業也可以是「低污染」

目前經濟部這套管理機制主要依據《未登記工廠補辦臨時工廠登記辦法》第4條附件的36種非屬低污染事業。只要榜上有名的事業別,就沒有申請補辦臨時工廠登記的資格,無法在原地繼續營業,必須轉型或遷廠至他處合法使用地。

2011年,經濟部曾就非屬低污事業範圍邀集縣市和中央環保、農政主管機關進行討論,是否要從原來的50項刪減為36項,儘管農委會表示反對,擔心放寬後會造成農田水路的污染,廢水排放管理也會成問題,並指出經濟部刪減缺乏一致的標準,也有縣市如台北市和花蓮縣表示,中央刪減後將與地方管制污染事業產生衝突(見會議記錄非屬低污事業刪減對照表)。

環保署的與會人員則提到違章工廠對環境污染及公安的可能危害,希望經濟部可以全面納管違章工廠,因此對經濟部刪減非屬低污事業表示支持,認為有助讓更多工廠進入政府管理系統。

最後,經濟部做成決議,將原50項中高污染行業刪減為現行的36項,後面加上一條地方彈性條款,「各縣市政府得視地方產業發展政策與特性,因地制宜增列非屬低污染項目」。決議公布後,刪去的14個事業別均可申請臨登,在農地上經營到至少2020年6月2日輔導期結束,位在特定地區上的工廠甚至可以取得合法資格。

為了產業發展,經濟部從「中高污染」改成「低污染」的事業包括:

  1. 2101輪胎製造業 (刪減)
  2. 2311010平板玻璃 (刪減)
  3. 2311020強化玻璃 (刪減)
  4. 2313玻璃纖維製造業 (刪減)
  5. 2322黏土建築材料製造業 (刪減)
  6. 2332預拌混凝土製造業 (刪減)
  7. 2333水泥製品製造業 (刪減)
  8. 2399未分類其他非金屬礦物製品製造業 (具砂石碎解、洗選非金屬礦物製品製造業) (刪減)
  9. 2399940瀝青混凝土 (刪減)
  10. 2412鋼鐵鑄造業 (刪減)
  11. 2422鋁鑄造業 (刪減)
  12. 2432銅鑄造業 (刪減)
  13. 2491其他基本金屬鑄造業 (刪減)
  14. 2692電子管製造業 (刪減)

工廠管理不能再走30年前的回頭路

現行的違章工廠管理規範漏洞百出。過去台灣因為環保及土地利用法規不夠周延,造成工農混雜現象及工業聚落下游的農地污染問題。今天如果繼續縱容更多不利環安的零星工業在農地上落地生根,形同走上30年前的回頭路。

我們要求經濟部、環保署及農委會,還有各地方政府,針對此問題回應,依法儘速公佈完整的違章工廠現況,並重新檢視輔導政策和方向,拒絕污染事業走進農地,為民眾守護安全的農業生態,維護食安和國人健康。我們已將合法化違章工廠繪製成地圖,原始資料也全數上網,提供社會大眾查詢使用。

相關資料

登記工廠名錄 http://data.gov.tw/node/6569
臨登工廠資料 https://goo.gl/0OMmNz
臨登工廠地圖 https://goo.gl/0B2inM

 

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4 thoughts on “全台6千家合法中違章工廠評比,台中、彰化最多,6成是污染源事業”

 

【守護農地】首份違章工廠資料出爐,竟有6成是污染源事業


 

本月農地小組利用政府公開資料,篩出了全台「合法中」的近6千家違章工廠資料。這是目前第一份有關違章工廠比較完整的原始資料,有助大眾了解政府如何管理農地工廠,也能提供相關專家學者進一步評估管理方向的成效與衝擊。

農地小組利用政府開放資料平台上的登記工廠名錄資料集,找出了目前生產中的臨時工廠登記業者,共有5,821家。這個「臨時工廠登記」制度是經濟部提供給全台6萬多家違章工廠,在2020年之前進行土地和建物合法化的途徑。

部分工廠可以藉由這個途徑,取得臨時登記後,進行農地變更為工業用地的程序,最後就地合法。其他取得臨時登記的工廠,至少可在原地繼續經營,不受《區域計畫法》、《都市計畫法》、《建築法》有關違反土地及建築物使用的處罰。

截至今年7月為止,取得臨時登記的工廠有5,821家,佔違章工廠總數的10%。數量最多的前6縣市是:台中、彰化、高雄、新北、台南、桃園。台中和彰化地區合法化速度最快,合計佔臨登工廠總數的45%。東部和離島地區數量最少。

另外,我們也看到,臨登工廠有6成以上經營的是金屬製造、機械設備製造、食品製造、塑膠製造、紡織業、預拌混凝土等,這些都是受到多種環保法規管制的污染源事業。

以數量最多的金屬製品製造業為例。目前有2,332家臨登工廠經營金屬製品的製造,佔所有臨登工廠總數的4成。這些廠商可能製造金屬製的手工具、模具、結構及建築組件、容器等或是進行金屬加工處理。常見製程容易產生金屬冶煉爐渣、廢鐵、廢潤滑油及廢水。螺絲、螺帽、鉚釘等製造更會因為酸洗和水洗程序而產生大量廢污水。

《空氣污染防制法》、《水污染防治法》、《廢棄物清理法》、《土壤及地下水污染整治法》分別列管了這個業別底下的15個細項,但是經濟部只管制2個細項,其他的13 種業別,都可以申請臨時工廠登記,在農地上繼續營業,甚至取得法律上的「合法資格」。

現行的違章工廠管理形同縱容不利農安和食安的零星工業在農地上落地生根。下一步我們將要求經濟部、環保署及農委會、各地方政府針對此一問題回應,呼籲政府重新檢視輔導政策和方向,拒絕污染走進農地!

我們已將近6千家臨登工廠資料繪製成圖,原始資料也全數上網,提供社會大眾查詢使用。後續我們要設法取得全國6萬多家的違章工廠,讓違章工廠問題更加透明,改變才可能發生!

張淑貞
台灣環境資訊協會 研究員

2016/12/28

想知道更多

逛地圖
玩資料
全台6千家合法中違章工廠評比,台中、彰化最多,6成是污染源事業

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Species-specific control of external superoxide levels by the coral holobiont during a natural bleaching event


http://www.nature.com/articles/ncomms13801

Species-specific control of external superoxide levels by the coral holobiont during a natural bleaching event

Received:
24 May 2016
Accepted:
02 November 2016
Published online:
07 December 2016

Abstract

The reactive oxygen species superoxide (O2·−) is both beneficial and detrimental to life. Within corals, superoxide may contribute to pathogen resistance but also bleaching, the loss of essential algal symbionts. Yet, the role of superoxide in coral health and physiology is not completely understood owing to a lack of direct in situ observations. By conducting field measurements of superoxide produced by corals during a bleaching event, we show substantial species-specific variation in external superoxide levels, which reflect the balance of production and degradation processes. Extracellular superoxide concentrations are independent of light, algal symbiont abundance and bleaching status, but depend on coral species and bacterial community composition. Furthermore, coral-derived superoxide concentrations ranged from levels below bulk seawater up to 120 nM, some of the highest superoxide concentrations observed in marine systems. Overall, these results unveil the ability of corals and/or their microbiomes to regulate superoxide in their immediate surroundings, which suggests species-specific roles of superoxide in coral health and physiology.

Introduction

Coral reefs are among the most biologically rich and economically valuable ecosystems on the planet1,2. However, more than 30% of the world’s coral reefs have vanished over the past 35 years largely due to coral bleaching and diseases3,4 that are triggered by increasing ocean temperatures5. Given the present course of climate change and forecasted temperature increases6, there is growing concern that coral reef ecosystems will continue to decline rapidly. Indeed, record-breaking ocean warming associated with El Niño from 2014 to 2016 has devastated coral reefs across the world, resulting in the longest mass coral bleaching event ever recorded7.

Coral bleaching involves the loss of Symbiodinium—essential algal endosymbionts that provide colour, organic carbon and nutrients to the coral host8. These algae are critical members of a highly diverse assemblage of microbes (bacteria, archaea, fungi and other protists) comprising the coral holobiont. Some corals may fully recover, or even resist bleaching completely4,9, which is primarily attributed to the ability of certain groups of Symbiodinium to tolerate elevated temperatures10,11. However, much less is known about the role of coral hosts and their microbiome in bleaching susceptibility, resistance and recovery. To predict and mitigate future threats to coral reefs across the globe, a more holistic understanding of the processes responsible for maintaining coral health is necessary.

Reactive oxygen species (ROS) play a critical yet enigmatic role in coral bleaching and health. ROS include intermediates in the reduction of molecular oxygen to water, such as the superoxide radical anion (O2·−). During bleaching, light and heat stress damage the photosynthetic machinery of Symbiodinium cells and impair mitochondrial electron transport in the coral host, which is thought to result in the over production of intracellular ROS, the onset of oxidative stress and an antioxidant response throughout the coral holobiont5,12,13. Excessive levels of ROS degrade vital cell components14, and superoxide can initiate apoptosis signalling pathways15 involved in bleaching and host mortality16. However, other potential sources and pathways of ROS production within the coral holobiont have recently been identified. For instance, a wide diversity of heterotrophic bacteria enzymatically produce extracellular superoxide in the dark, including representative isolates of Roseobacter, Vibrio and other genera commonly found in coral microbiomes17. Furthermore, two Symbiodinium isolates representing clades A and C produce extracellular superoxide even in the absence of heat and light stress, potentially via transmembrane oxidoreductases, such as NADPH oxidase18. In fact, NADPH oxidases were recently implicated as a source of superoxide at the surface of the coral Stylophora pistillata in aquaria incubations under non-stressful conditions18.

Although the buildup of internal ROS can lead to oxidative stress, external production of superoxide may have positive impacts on coral health. For instance, coral-derived NAD(P)H oxidoreductases putatively involved in the production of extracellular superoxide are associated with increased thermotolerance of the coral Acropora millepora19 and resistance to pathogenic white band disease in Acropora cervicornis20. In addition, extracellular superoxide dismutase (SOD) is a necessary virulence factor of the pathogen Vibrio shiloi, which causes bleaching in the coral Oculina patagonica21, thus pointing to coral-derived superoxide as a potential means of resisting pathogens. Given the known role of superoxide in cell signalling, differentiation and proliferation22,23,24, growth promotion25,26, defence27,28,29 and acquisition of the micronutrient iron30,31 in many macro- and microorganisms, extracellular production of superoxide may have other benefits to coral health as well. Overall, previous research suggests that the potential origins of superoxide in the coral holobiont are diverse, and biologically controlled levels of superoxide production by corals may be an integral component of coral physiology and immune defence, as seen in higher eukaryotes27.

Both intracellular and extracellular superoxide production are clearly important to maintaining the redox homoeostasis and health of corals. Despite the vast array of possible superoxide sources identified in corals, however, the actual origins, distributions and ecological underpinnings of superoxide production in natural coral communities remain largely unknown due to a lack of direct superoxide measurements. Indirect evidence of oxidative stress in bleaching corals is based on observations of antioxidant activity, gene expression and proteomic profiles, yet the methodologies available for directly measuring intracellular ROS are invasive and artifact prone32,33,34, making in vivo measurements of ROS difficult. To advance our understanding of superoxide dynamics in the coral holobiont, we capitalized on recent advances in non-invasive chemiluminescent techniques to make the first in situ measurements of external superoxide production by several species of thermally stressed and bleaching corals in a natural reef environment.

The goal of this study was to determine whether and to what degree various coral species produce external superoxide on a natural reef and to assess the potential role of coral symbionts in this superoxide production. Results revealed significant species-level control of external superoxide concentrations by the corals Fungia scutaria, Montipora capitata, Pocillopora damicornis, Porites compressa and Porites lobata. Superoxide concentrations at coral surfaces could not be explained by abiotic photo-driven mechanisms of ROS production, photosynthesis, bleaching status or Symbiodinium abundances. Extracellular superoxide production by bacterial symbionts and asymbiotic coral larvae was confirmed in laboratory experiments, supporting the conclusion that superoxide production at the coral surface may originate from the activity of epibionts or the coral host itself.

Results

Superoxide production by corals is species-specific

During a bleaching event in the Hawaiian Islands in October 2014, a broad range of superoxide concentrations were measured at the surfaces of five coral species in Kaneohe Bay (Supplementary Fig. 1). Background superoxide levels within the reef seawater located at the same depth as the corals but >10 cm from their surface ranged from 4 to 11 nM—values consistent with previously reported superoxide levels in productive marine waters but up to several orders of magnitude higher than in typical open ocean sites35,36,37,38,39. Average superoxide concentrations measured only millimetres above coral surfaces ranged from levels below bulk seawater (M. capitata) to steady-state concentrations that were 120 nM higher than bulk seawater (P. lobata) (Fig. 1, Supplementary Table 1). These superoxide concentrations are among the highest reported in marine systems yet are consistent with the ability of organisms to substantially increase superoxide concentrations in seawater. For example, in previous aquaria studies, the corals Stylophora pistillata and Porites astreoides increased seawater superoxide concentrations from 2 to 20–35 nM (ref. 18) and from 1 to 35 nM (ref. 40), respectively. Furthermore, up to 33 nM superoxide was detected in the deep chlorophyll maximum at the subtropical front east of New Zealand35. In addition, the most prolific microbial producer of extracellular superoxide, the toxic bloom-forming alga Chatonella marina, can produce steady-state concentrations of superoxide reaching 140 nM at bloom-level cell densities in vitro41.

Figure 1: Superoxide produced by bleached and pigmented colonies of field-based corals.
Figure 1

(a) Representative FeLume trace showing superoxide concentrations millimetres above the surface of a Porites lobata colony that had both bleached and pigmented sections. Superoxide data were collected over time by positioning the sample tubing at a static location over the bleached section of the coral for several minutes, and then moving the tubing to a single location over the pigmented section for a similar amount of time. Chemiluminescence signals were converted to superoxide concentrations by first subtracting out signals of an aged filtered seawater baseline (not shown), and then corrected signals were converted to concentrations using the daily calibration curve. The specific coral-derived signal (dashed arrow) was then determined by subtracting the signal obtained at the coral surface from the seawater signal obtained 5–15 cm away from the coral. The average superoxide concentrations between bleached and pigmented sections are not significantly different, as revealed by a two-sample t-test (P>0.05). Once the tubing was removed from the coral surface, superoxide concentrations rapidly declined back to background seawater (SW) levels (solid arrow). Finally, the addition of SOD, which selectively degrades superoxide, confirmed that chemiluminescence signals were attributable to superoxide. Superoxide concentrations are reported as average±s.d. of the temporal signal. (b) Superoxide levels measured for bleached and pigmented colonies of each coral species corrected for background SW concentrations. Circles indicate peak superoxide levels measured for each specimen. For M. capitata, superoxide concentrations at the surface of the colony were lower than the background SW, resulting in a negative SW-normalized superoxide concentration. Average species-specific superoxide levels not connected by the same letter (indicated on the x-axis below the bars) are significantly different (P<0.05). Error bars indicate s.d., n=2 (F. scutaria bleached), n=2 (F. scutaria pigmented), n=10 (M. capitata bleached), n=8 (M. capitata pigmented), n=13 (P. compressa bleached), n=9 (P. compressa pigmented), n=9 (P. damicornis bleached), n=9 (P. damicornis pigmented), n=13 (P. lobata bleached) and n=16 (P. lobata pigmented).

Full factorial ANOVA was conducted to compare the effects of coral species and health state (bleached versus pigmented) on superoxide concentrations. This analysis revealed that average coral-derived superoxide levels were significantly different as a function of coral species (F4,81=34.8, P<0.01; Fig. 1b). However, health state had no effect on average superoxide levels overall (F1,81=1.27, P=0.26) or when health was separately compared for each species (F4,81=1.15, P=0.34; Fig. 1b). Average superoxide levels were also significantly different in seven out of ten interspecies comparisons using Tukey’s honest significant difference test (P<0.05; Fig. 1b). Only the species with the lowest superoxide levels were statistically similar, specifically F. scutaria and M. capitata (P=1.0), F. scutaria and P. damicornis (P=0.83) and M. capitata and P. damicornis (P=0.24; Fig. 1b).

A number of lines of evidence confirm that the observed superoxide is derived from the coral holobiont. First, superoxide concentrations at coral surfaces rapidly declined to background seawater levels over short distances away from the corals (for example, a centimetre or less), suggesting that corals are a point source, consistent with the short lifetime of superoxide in these waters (maximum half-life in bulk reef water=30 s) (Fig. 1a). Second, the presence of statistically similar superoxide levels at the surface of P. compressa colonies over a wide range of photosynthetically active radiation levels (PAR=0–1,109 μmol s−1m−2; ANOVA F4,2=1.13, P=0.52; Fig. 2 and Supplementary Table 2) rules out abiotic photo-oxidation mechanisms as a major mode of superoxide generation. Similarly, a recent aquaria-based study also found dark production of extracellular superoxide by another Porites species, P. astreoides40. Lastly, the fact that superoxide levels are species-specific (Fig. 1b), even across adjoining colonies of two species (Fig. 3), further indicates that the superoxide detected was derived from the coral holobiont.

Figure 2: Diel variability in superoxide concentrations produced by Porites compressa.
Figure 2

To normalize coral-derived superoxide concentrations, superoxide levels in background seawater (SW) at 5–15 cm from the coral surface were subtracted. PAR values are indicated as grey circles. Periods of daylight (white) and darkness (black) are indicated in the horizontal scale at the top of the chart. Error bars indicate s.d. of the temporal signal collected at a rate of 0.5 points per second (n=21–124 points).

Figure 3: Superoxide concentrations across adjoining M. capitataand P. compressa.
Figure 3

(a) Close-up photo of adjoining M. capitata (left) and P. compressa (right). (b) Continuous superoxide measurements were made by moving the sample tubing across the coral surfaces, pausing for 20–60 s at the following positions: along the M. capitata surface at distances of (a) 10 cm, (b) 5 cm, (c) 1 cm and (d) <1 cm (shaded area) from the species interface; and along the P. compressa surface at distances of (e) <1 cm, (f) 1 cm, (g) 5 cm and (h) 10 cm away from the species interface. Chemiluminescence signals were converted to superoxide concentrations by first subtracting out signals of an aged filtered seawater baseline (not shown), and then corrected signals were converted to concentration using the daily calibration curve. The superoxide concentrations shown for the corals include both the coral-derived signal and the seawater (SW) signal (not SW corrected on the trace). Superoxide concentrations for M. capitata (averaged from a to c) and P. compressa (averaged from e to h) were significantly different (P=0.014) based on a two-sample t-test and are indicated below the superoxide trace, along with average superoxide levels in the background SW adjacent to each coral. On the basis of a two-sample t-test, superoxide levels at the M. capitata surface (a–c) were statistically similar (P>0.1) to the levels in the background SW, except right at the edge of the species interface (d, shaded area). Superoxide concentrations are reported as average±s.d. of the temporal signal.

The potential direct and indirect pathways of external superoxide formation by corals are currently unresolved. In addition to superoxide, corals also release dissolved organic carbon42,43 and hydrogen peroxide44 to seawater, both of which could in theory contribute to the indirect formation of superoxide. Yet, the observation that coral-derived superoxide is detectable only several millimetres beyond the coral surface reflects the rapid decay kinetics of superoxide, which is inconsistent with the higher residence times and transport distances for dissolved organic carbon and hydrogen peroxide in relation to the coral surface44,45. Further, organic carbon fluxes from corals and within coral reefs have a pronounced diel nature46,47, which is not observed here for superoxide production, suggesting that dissolved organic carbon-derived superoxide is not a dominant contributor to the superoxide concentrations reported herein. Further, given the previously reported ability of corals to generate external superoxide through putative NADPH oxidoreductases18, most of the observed superoxide likely originates through direct enzymatic pathways.

The species-level trends observed in average superoxide levels are in line with previous measurements of the ROS hydrogen peroxide, which also demonstrated a broad range of species-specific levels at coral surfaces44. Specifically, as we observed for superoxide (Fig. 1), steady-state hydrogen peroxide levels measured in a previous study were high for Porites sp. (500 nM), intermediate for Pocillopora sp. (250 nM) and near zero for Fungia sp.44. Species-specific variability in ROS levels may reflect differences in ROS production, degradation or both. Indeed, heterotrophic bacteria17 and corals44 have previously been shown to simultaneously produce and degrade extracellular ROS. In fact, corals have been shown to release antioxidants into their surroundings18,40,44,48, which also varies widely as a function of coral species44. This differential antioxidant release may explain why superoxide concentrations in the direct vicinity of M. capitata were lower than the surrounding seawater. Moreover, the presence of stable, non-zero levels of superoxide and hydrogen peroxide at the surfaces of coral species that have the ability to degrade external ROS indicates that these external ROS concentrations are not detrimental. While superoxide levels as low as 1 nM can inactivate certain enzymes49, this toxicity threshold may vary depending on the site and mechanism of superoxide production, as well as the biological species.

ROS production by coral endosymbionts can contribute to external fluxes of hydrogen peroxide because hydrogen peroxide readily diffuses through cells48. On the other hand, superoxide is a charged and much shorter-lived molecule at physiological pH. On the basis of its low diffusivity, it cannot readily pass across biological membranes50 unless they are severely compromised12. Even if superoxide could diffuse across biological membranes, its intracellular lifetime (μs) and diffusive distance (100s of nm)14 are too short to explain external superoxide concentrations. Thus, endosymbionts are unlikely to contribute to external superoxide levels simply due to their location within the coral. In particular, Symbiodinium cells inhabit the symbiosome inside the host’s gastrodermal tissue beneath the coral’s outermost (epithelial) cell layer. Despite recent evidence that the symbiosome has a pH of 4 (ref. 51), which could allow for diffusion of the protonated form of superoxide into the host, the superoxide anion would again dominate in the coral gastrodermal cells where the pH is 7 (refs 51, 52). Superoxide produced by Symbiodinium would therefore have to pass several biological membranes, multiple cellular compartments and the external mucus layer to contribute to external superoxide levels at the coral surface.

Consistent with the unlikelihood of endosymbionts as a source of external superoxide, several lines of evidence suggest that external superoxide production is decoupled from Symbiodinium, even in thermally stressed and bleaching corals. First, Symbiodinium were less abundant in bleached versus pigmented coral colonies of the same species (Fig. 4 and Supplementary Table 3), but bleached and pigmented colonies of each species were associated with similar superoxide levels (Fig. 1). In fact, Symbiodinium abundances did not correlate significantly with coral-derived superoxide concentrations (Supplementary Fig. 2). Furthermore, superoxide production by P. compressa was not significantly different over a diel cycle of PAR levels, even when bleached and pigmented colonies were considered together (ANOVA, F4,2=1.13, P=0.52) or separately (ANOVA, F4,2=0.23, P=0.90) (Fig. 2 and Supplementary Table 2), which precludes photosynthetic mechanisms of superoxide production as a major source. On the basis of these results and the low diffusivity of superoxide, the most likely sources of external superoxide are coral epithelial cells and/or microbial epibionts residing on the coral’s surface mucus layer, rather than Symbiodinium. Similarly, previous studies also showed superoxide production at the surface of aquaria-hosted pigmented colonies of P. astreoides and both bleached and pigmented colonies of S. pistillata in the absence of light, pointing to non-algal superoxide sources18,40. Yet in the presence of light, superoxide production by S. pistillata was moderately elevated for pigmented colonies but not bleached corals in this previous study18. This result was interpreted to indicate a potential indirect role for algae in stimulating coral-derived extracellular superoxide in the presence of light (for example, stimulation of coral NAD(P)H oxidase activity via light-enhanced algal NAD(P)H production)18. However, we did not observe this effect for corals on a natural reef.

Figure 4: Symbiodinium cell abundances and microbial community composition in corals.
Figure 4

Representative pigmented (a,c,e,g,i) and bleached (b,d,f,h,j) colonies of F. scutaria (a,b), M. capitata (c,d), P. damicornis (e,f), P. compressa (g,h) and P. lobata (i,j). (k) Abundance of coral-hosted Symbiodinium within pigmented and bleached specimens of each species (except F. scutaria because it was not permitted for collection) are reported as average±s.d. P values associated with the two-sample t-test of average Symbiodinium counts for bleached versus pigmented colonies of each species are provided in the upper right corner of each plot. Sample size is indicated next to each bar. (l) The bacterial and archaeal communities associated with the corals were found to be similar by coral species rather than by bleaching (BL) or pigmented (P) health state, as indicated by a cluster dendogram of bacterial and archaeal V4 SSU rRNA gene sequences from tissue and mucus samples of coral colonies, compared using Bray–Curtis similarity.

Despite their lack of contribution to external superoxide production by corals, Symbiodinium cells are still undoubtedly a source of internal superoxide to their coral hosts (see ref. 12 and references therein). Indeed, the ability of cultured Symbiodinium isolates to generate extracellular superoxide18,40 demonstrates that Symbiodinium-derived superoxide may have the potential to directly interact with host gastrodermal cells. In contrast to superoxide, external hydrogen peroxide may ultimately derive from Symbiodinium. For instance, pigmented colonies of S. pistillata were previously found to produce external hydrogen peroxide, yet bleached colonies did not—thereby implicating symbiotic algae as the source48. In this case, the transport of internal hydrogen peroxide into seawater may help to maintain redox homoeostasis48. Yet non-Symbiodinium sources of superoxide at the coral surface are also likely to contribute indirectly to external hydrogen peroxide concentrations, since the dismutation of superoxide produces hydrogen peroxide. Regardless of the ability of Symbiodinium to generate ROS within coral tissues, however, recent evidence has demonstrated a lack of correspondence between coral host and Symbiodinium redox metabolism during bleaching conditions, suggesting that Symbiodinium-derived ROS may not be the ultimate trigger of coral bleaching53,54.

Coral microbiome community composition

Many prokaryotic groups associate with diverse species of corals and are thought to benefit their host by recycling nutrients and producing antibiotic compounds55. To investigate potential microbial population-level control over external superoxide concentrations, we examined the bacterial and archaeal community composition of corals in Kaneohe Bay, with the exception of Fungia scutaria, which was not sampled due to permit restrictions. Sequencing of small subunit ribosomal RNA gene amplicons revealed the presence of common coral bacterial genera, including Endozoicomonas, which was particularly abundant in P. compressa (on average 56% and 34% of sequences within bleached and healthy P. compressa colonies, respectively), and minimal archaeal sequences. In addition, members of Verrucomicrobia and Planctomycetes were prominently associated with M. capitata and P. damicornis (Supplementary Table 4). Moreover, like superoxide production, microbial community composition varied significantly as a function of coral species (ANOSIM, R=0.79, P=0.01) but not health state (pigmented versus bleached) (ANOSIM, R=−0.035, P=0.62) (Fig. 4l). Pairwise comparisons of the microbial community composition assessed using Bray–Curtis similarity revealed that each species was significantly different from the others (ANOSIM, R=0.52–0.99; P<0.05), except for P. damicornis and M. capitata (ANOSIM, R=0.56, P=0.07), which exhibited the most similar external superoxide levels among the species examined for microbial community composition (Fig. 1b). This community analysis takes into account bacteria associated with the coral mucus and tissue, but probably only the mucus-associated microbes contribute directly to external superoxide levels (see above). Nevertheless, these results are in line with other studies demonstrating that coral microbial communities are species-specific56,57. Thus, the coral microbiome may contribute to coral species-specific external superoxide production.

Superoxide from bacteria and asymbiotic coral larvae

To evaluate the coral host and epibiotic bacteria as potential sources of superoxide on the coral surface, we measured extracellular superoxide production by symbiont-free (asymbiotic) coral larvae and coral-derived bacterial symbionts in vitro. The majority of coral species examined in Kaneohe Bay vertically inherit Symbiodinium from maternal colonies, precluding the ability to collect and interrogate symbiont-free larvae. Therefore, to assess the coral host’s ability to produce extracellular superoxide in the absence of Symbiodinium or bacterial symbionts, gametes were obtained from broadcast spawning corals on a reef in Curaçao. Following fertilization and rearing in sterile seawater (at least 24 h of development), asymbiotic larvae of the corals Orbicella faveolata, Diploria labyrinthiformis and Colpophyllia natans produced extracellular superoxide at considerably high rates (260–821 fmol larva−1h−1) (Supplementary Table 5). Disrupted electron transport in mitochondrial membranes has been suggested as the primary pathway of superoxide production in stressed symbiotic cnidarians58,59. However, our results indicate a pathway of superoxide production by healthy coral larvae that is independent of intracellular sources because our method only detects extracellular superoxide17 and the superoxide anion does not readily cross healthy biological membranes50. Although larval responses do not necessarily reflect superoxide dynamics in adult corals, these results nonetheless demonstrate the potential of several coral species to produce extracellular superoxide independently of their microbial symbionts.

In addition to asymbiotic coral larvae, we also examined coral-associated bacteria for their ability to make extracellular superoxide in vitro. A wide phylogenetic and ecological diversity of heterotrophic bacteria, including genera commonly found in corals, were recently shown to produce extracellular superoxide17. However, bacteria specifically isolated from corals were not examined as part of that study. As such, we confirmed that representative coral bacteria have the ability to produce extracellular superoxide, including an example of the widespread and numerically abundant coral symbiont Endozoicomonas60 (E. montiporae, LMG 24815), which was a prevalent organism in the Porites spp. microbiomes studied in Kaneohe Bay. We tested other common coral bacteria, cultured from corals in Micronesia, which also produced substantial extracellular superoxide, including Ruegeria sp. (isolate WHOIMSCC16 from S. pistillata) and Vibrio sp. (isolate WHOIMSCC50, from P. lobata). Extracellular superoxide production by these coral-derived bacteria ranged from 0.13±0.06 to 2.2±1.2 amol cell−1 h−1 (Supplementary Table 5), which is similar to extracellular superoxide production by other heterotrophic bacteria17.

Discussion

Overall, our findings demonstrate that corals and/or their microbial epibionts regulate external superoxide levels in a species-specific manner, which suggests an important role for external superoxide in the physiology and health of the coral holobiont. Most current theoretical models of coral bleaching are based on internal biochemical dynamics, especially the build-up of ROS within coral tissues. Alternatively, external ROS fluxes may be involved in bleaching, as well. For example, addition of the ROS scavengers ascorbate and catalase decreased bleaching in Agaricia tenuifolia in a previous study61. Although ascorbate is a small molecule that can be transported across cell membranes, catalase is a large enzyme that cannot readily penetrate the cell surface, unless it is actively engulfed via endocytosis. Thus, at least some benefit of these exogenous antioxidants may be explained by a decrease in external rather than internal ROS levels. Indeed, exogenous catalase61 or active release of hydrogen peroxide by the coral itself48 may alleviate internal redox stress and thereby protect the coral from ROS-induced bleaching.

Elevated ROS levels are commonly assumed to play an antagonistic role in corals (that is, oxidative stress), but ROS may also be beneficial to coral physiology. In fact, healthy corals, Symbiodinium cells, and bacteria produce extracellular superoxide and hydrogen peroxide under non-stressful conditions, confirming that ROS production is not always correlated to oxidative stress17,18,40,48. Similarly, a previous study documented basal levels of singlet oxygen in the symbiotic anemone Aiptasia, which did not increase during heat-induced bleaching under low illumination62. In a wide range of macro- and microorganisms, extracellular superoxide production is a beneficial trait commonly mediated by transmembrane or outer membrane oxidoreductases (for example, NAD(P)H oxidases, peroxidases), as seen in model bacteria, non-symbiotic phytoplankton and the symbiotic anemone Nematostella vectensis63,64,65,66. For example, oxidoreductase-mediated production of extracellular superoxide promotes cell division and differentiation in a variety of organisms, including fungi24, microbial eukaryotes24 and bacteria22,23. Enzymatic production of extracellular superoxide is also involved in wound repair by plants66, defence against epiphytic parasites in macroalgae28 and the immune response of mammalian leucocytes27. Interestingly, in a previous study, the oxidoreducatase inhibitor diphenylene iodinium impeded extracellular superoxide production by a Symbiodinium clade C representative (CCMP 2466) as well as bleached and pigmented colonies of S. pistillata18. These results suggest that oxidoreductases are involved in extracellular superoxide production by corals and their symbionts and, moreover, these findings underscore the potentially beneficial roles of extracellular superoxide in coral physiology and health24,63.

The potential beneficial roles of extracellular ROS in coral function and health are likely diverse and vary in the presence and absence of external stressors. For example, according to a recent study, corals may release external hydrogen peroxide to facilitate feeding on zooplankton or as a mode of defence against pathogens regulated by physical and chemical stimuli67. Consistent with the ability of superoxide to act as a cell density-dependent growth promoter, and with previous observations from phytoplankton and heterotrophic bacteria68, we found that extracellular superoxide production by actively developing coral larvae was inversely related to larval density (Supplementary Fig. 3). Furthermore, several previous studies suggest a possible role of NAD(P)H oxidoreductases19,20 and extracellular superoxide production21in the coral immune defence system. Recent evidence even indicates that bacteria associated with the model organism Caenorhabditis elegans protect their host from parasites by generating superoxide29, suggesting that a similar mutualism may be present in corals. Although our results show that external superoxide production is decoupled from bleaching and symbiont abundance within a single coral species, extracellular superoxide production may be inversely related to bleaching susceptibility across coral species. For example, Porites spp., which produced the highest external superoxide concentrations, are among the most resilient species to thermal bleaching, while Montipora spp., which had the lowest superoxide levels, are more susceptible69. While purely speculative at this point, this potentially beneficial role of external superoxide contradicts previous observations that exogenous antioxidants protect against bleaching61, highlighting the need to further investigate the possible beneficial versus detrimental roles of external superoxide in coral immune defence, development and overall health.

Given the light-independent and species-specific control of superoxide levels revealed here, coupled with similar findings for aquaria-hosted corals grown under non-stressful conditions (refs 18, 40), it is clear that external superoxide plays a role in coral physiology that may also be species-specific. Although the role of external superoxide in coral biology and health remains unclear, it may be involved in a range of positive and negative functions, from pathogen defence to bleaching. On the basis of the possible species-specific health effects of external superoxide, whether beneficial or detrimental, we speculate that the capacity of corals to regulate superoxide levels in their immediate vicinity may potentially underlie the ecological distribution of species and/or species-level bleaching patterns on reefs. Indeed, preliminary comparison of the species-specific superoxide levels that we observed to broad trends in interspecific bleaching patterns69 suggests that external superoxide may be inversely related to bleaching susceptibility. Clearly, targeted investigations of this correlation, as well as other links between superoxide and coral health and function, should follow. Although superoxide is an important target for future study (for example, it is directly linked to the apoptosis pathway15 involved in coral bleaching16 and yet facilitates essential physiological functions), the internal and external roles of other ROS such as hydrogen peroxide and hydroxyl radical should also be more fully examined and incorporated into coral physiological models. Additional direct measurements of ROS production and degradation by the coral holobiont and diverse individual members of this community will advance a more holistic view of ROS cycling within corals. In turn, these advancements will improve our current understanding of coral ecosystem health and development, and ultimately, the future of coral reefs under sustained climate change.

Methods

Reef sites, corals and sampling

In situ superoxide measurements were conducted between 10:00 and 15:00 hours on pigmented and bleached colonies of Porites compressa, Porites lobata, Montipora capitata, Pocillopora damicornis and Fungia scutaria, at six different reef sites in Kaneohe Bay, Hawaii including sites A (21.4599° N, 157.8228° W), B (21.45502° N, 157.8226° W), C (21.46073° N, 157.8225° W), D (21.45443° N, 157.8034° W), E (21.46135° N, 157.793° W) and F (21.45702° N, 157.8002° W) (Supplementary Fig. 1). Small tissue and skeletal pieces were removed from all colonies except F. scutaria (due to lack of a permit) under the State of Hawaii Department of Land and Natural Resources Special Activity Permit #2015-49 using a hammer and chisel, placed on ice for no more than 3 h, and frozen to −80 °C. Additionally, diel superoxide measurements were conducted on adjacent colonies of Porites compressa located off the Point of Coconut Island (Site P), (21.43286° N, 157.7863° W). We were not permitted to remove tissue from colonies at this site. For diel measurements, photosynthetically active radiation (PAR) was measured using an underwater sensor (LI-COR, data collected by a LI-1500 light sensor logger).

In situ superoxide measurements

Superoxide concentrations were measured with a flow-through FeLume Mini system (Waterville Analytical, Waterville ME) via the specific reaction between superoxide and the chemiluminescent probe methyl Cypridina luciferin analogue (MCLA, Santa Cruz Biotechnology). The FeLume system is composed of two separate fluid lines, one of which is dedicated to the analyte solution and the other to the MCLA reagent. The reagent and, as indicated, the analyte solutions, are amended with 50 μM diethylene-triaminepentaacetic acid (DTPA) to sequester trace metal contaminants that would otherwise significantly reduce the lifetime of superoxide. To measure superoxide, both the analyte solution and the MCLA reagent are independently flushed through the FeLume system at an identical flow rate using a peristaltic pump. The MCLA reagent consisted of 4.0 μM MCLA (similar to concentrations used previously and by other investigators38,39,70,71) in 0.10 M MES with 50 μM DTPA adjusted to pH 6.0. The solutions converge in a spiral flow cell immediately adjacent to a photomultiplier tube, which continuously acquires data that is displayed in real time using a PC interface. Similar systems have been used to generate high sensitivity measurements of natural superoxide concentrations and decay rates36,70, as well as extracellular superoxide production by bacteria17 and phytoplankton isolates37,72.

For in situ superoxide measurements, the FeLume was hosted onboard a small boat. To eliminate abiotic photochemical processes that may produce superoxide during in situ measurements, opaque tubing was used, and the entire analytical system was shielded from light. The MCLA reagent was kept on ice during all field analyses, which greatly improved the stability of measurements. Seawater was directly pumped into the FeLume by placing the analyte tubing at discrete positions millimetres above the coral surface at specific points of interest, as indicated in the main text and figure legends, or in the surrounding seawater with the help of a snorkeller. To minimize the length of tubing (travel time) required to transport the water from the coral surface to the instrument, the boat was positioned adjacent to the coral being measured (but without shading the coral). Flow rates were consistent within FeLume runs and varied from 6 to 8 ml min−1 between runs.

For in situ superoxide measurements on the reef, we first ran a reagent blank on the boat to account for superoxide generated from the autooxidation of MCLA36. The reagent blank consisted of aged filtered reef water (AFRW), which was collected the previous day from the same depth as the corals (<0.5 m), filtered gently (0.2 μm Sterivex, Millipore), aged in the dark overnight (>12 h) and supplemented with DTPA (50 μM), and then aged for an additional >12 h. The AFRW+DTPA solution was kept at in situ temperature by suspending it in a bottle in the water alongside of the boat. By doing this, slight increases in the baseline signal with increasing in situ temperature as observed previously36were eliminated. Signal from the reagent blank was acquired for 2 min to generate stable chemiluminescent baseline signals (<4% coefficient of variation). The tubing was then passed to a snorkeller, who held the tubing at the seawater surface, 5–15 cm from the coral surface, at the coral surface (millimetre scale, without touching the coral), and then back to seawater background positions. The tubing was slowly moved along the coral surface to minimize entrainment of background seawater. Signals were collected until a relatively stable, steady-state reading was achieved and maintained for at least 2 min. Finally, SOD was added (0.8 U ml−1, final) to an aliquot of water taken from the coral surface to confirm that superoxide was responsible for the signal observed. SOD routinely lowers seawater baseline signals, reflecting the non-zero concentration of superoxide in the seawater (seawater blank), as well as the reagent blank. The coral-derived signal was obtained by subtracting the seawater signal obtained at 5–15 cm away from the coral surface from the coral surface signal, which removes both the seawater blank and reagent blank. Coral-derived superoxide concentrations were not corrected for superoxide decay during sampling and thus represent conservative estimates. The surface and coral-depth background seawater signals were corrected by subtracting the AFRW+DTPA baseline (that is, subtraction of the reagent blank only).

Corrected signals were converted to superoxide concentrations via calibration with multi-point standard curves using the superoxide source potassium dioxide (KO2). The calibrations were conducted in the lab using the same tubing, flow rate and temperature as the in situ measurements. Considering the short lifetime of superoxide, standards were prepared immediately before analysis. Primary stock solutions were made by dissolving a small quantity of KO2 in a basic matrix (0.03 N NaOH, 50 μM DTPA, pH=12.5). Superoxide concentrations in primary standards were quantified by measuring the difference in absorbance at 240 nm before and after the addition of SOD (8 U ml−1, final) and then converting to molar units based on the molar absorptivity of superoxide (2,183 l mol−1 cm−1 at 240 nm, pH=12.5, and corrected for the absorption of hydrogen peroxide formed during decay)73. Primary stocks had to be substantially diluted to generate representative concentrations for analysis on the FeLume. To generate secondary stocks, the primary stock solution was diluted with AFRW+DTPA. Final superoxide concentrations in secondary stocks were 3–38 nM.

For each calibration point, a separate FeLume run was conducted as follows: first, a blank AFRW+DTPA solution was allowed to react with the MCLA reagent until a stable baseline (<4% coefficient of variation) was achieved for 1 min. Then the secondary standards were pumped directly into the FeLume, and the decay of superoxide was monitored for at least 1 min. Finally, SOD was added to the secondary standard (0.8 U ml−1, final) to confirm that the signal was attributable to superoxide. In all cases, the chemiluminescence signal decreased rapidly to or slightly below AFRW+DTPA baseline levels after the addition of SOD. Chemiluminescence signals collected during the decay of superoxide were extrapolated backwards in time (0.28–63 s) to the point when the primary standard was quantified. Extrapolations assumed first-order decay kinetics because decay data were log-linear.

Calibration curves were constructed on the basis of the linear regression of multiple standard points (extrapolated luminescence versus superoxide concentration). Calibrations yielded linear curves (for example, R>0.93), with a sensitivity that ranged from 0.1 to 0.4 luminescence units per pM superoxide. The half-life of superoxide in the calibration matrices ranged from 0.41 to 0.56 min. These half-lives represent maximum estimates of the lifetime of superoxide on the reef because they were derived from AFRW amended with DTPA, which sequesters trace metals that would otherwise significantly reduce the lifetime of superoxide. The detection limit of this method, calculated as three times the s.d. of a series of blank measurements, was 0.24 nM. Given the sensitivity of superoxide to trace metal contamination, all vials and glassware were pre-cleaned with 10% HCl and washed with ultrapure (18 MΩ) water before use. All reagents were trace metal grade.

Symbiodinium cell counts from coral tissue

Frozen coral tissues were defrosted on ice and tissue was removed from the skeleton using an airbrush with 0.2 μm filtered seawater, blended for 30 s and centrifuged at 5,000 r.p.m. for 5 min. The supernatant was discarded, and the algal pellet was resuspended in filtered seawater and repeatedly vortexed and pelleted until the symbiont cells were free of host material. The algal pellet was finally preserved in 4% paraformaldehyde with filtered seawater and stored at 4 °C. For quantification, cells were concentrated onto 5 μm membrane filters (Millipore), mounted onto slides and imaged using Cy5 and TL DIC channels simultaneously with × 20 objective and × 1.6 optovar with a Zeiss Axio Observer.Z1 microscope and AxioCam MRm Rev.3w camera (Carl Zeiss Inc). Each image contained 1,388 × 1,040 pixels, with each pixel sized 0.32 × 0.32 μm, relevant to a 447.63 × 335.40 μm area. For each sample, 12 images from 12 fields of view under the same imaging conditions were captured with Zen 2011 software (Carl Zeiss, Inc.), and cell counts were then automated using a custom Matlab script and normalized to skeletal surface area, which was obtained from either a cork borer diameter (for Porites) or using aluminium foil (other colonies)74. Replicate Symbiodinium counts on the same specimen typically agreed within ±5% (s.d.).

Coral microbiome community analysis

Samples of coral tissue were collected after the superoxide measurements using a hammer and chisel and were placed into whirl-pack bags underwater. Samples were kept on ice until arriving back at the laboratory, where they were wrapped in aluminium foil and frozen to −80 °C until processing. Coral mucus and tissue were airbrushed from the coral tissue as previously described75, and DNA was extracted using the UltraClean Tissue and Cells DNA isolation Kit (Mo Bio Laboratories) with the addition of Proteinase K digestion (15 μl; 20 mg ml−1 at 60 °C for 30 min). DNA was quantified with the Qubit HS dsDNA fluorescent assay (Invitrogen), and samples were shipped to the University of Illinois for amplification and sequencing. A mastermix for each sample was prepared using the Roche High Fidelity Fast Start Kit and 20 × Access Array loading reagent. Mastermix was aliquoted to 48 wells of a PCR plate. To each well, 1 μl DNA and 1 μl Fluidigm Illumina linkers with unique barcode were added. Primer sequences for respective variable regions76 with Fuidigm CS1 (for 515F) and CS2 5′ (for 806R) tails (non-underlined) included: V4-515F: 5′-ACACTGACGACATGGTTCTACAGTGYCAGCMGCCGCGGTAA-3′ and V4-806RB: 5′-TACGGTAGCAGAGACTTGGTCTGGACTACNVGGGTWTCTAAT-3′ primers76. A 4 μl sample aliquot was loaded in the sample inlets and 4 μl of primer loaded in primer inlets of a previously primed Fluidigm 48.48 Access Array integrated fluidic circuit (IFC). The IFC was placed in an AX controller (Fluidigm Corp.) for microfluidic loading of all primer/sample combinations. Following the loading stage, the IFC plate was loaded on the Fluidigm Biomark HD PCR machine and samples were amplified using the default Access Array cycling programme without imaging. Following amplification, 2 μl of Fluidigm Harvest Buffer was loaded in the sample inlets and loaded on the AX controller for harvesting PCR products. Collected product was then transferred to a new 96 well plate quantified on a Qubit fluorometer and stored at −20°C. All samples were run on a Fragment Analyzer (Advanced Analytics, Ames, IA) and amplicon regions quantified. Samples were then pooled in equal amounts according to product concentration. The pooled products were then size selected on a 2% agarose E-gel (Life Technologies) and extracted from the isolated gel slice with a gel extraction kit (Qiagen). Cleaned size-selected product was run on an Agilent Bioanalyzer to confirm appropriate profile and determination of average size. The final pooled Fluidigm library pool was quantitated by qPCR on a BioRad CFX Connect Real-Time System (Bio-Rad Laboratories, Inc. CA) to ensure accuracy of quantitation of the library containing properly adapted fragments. The final denatured library pool was spiked with 15% non-indexed PhiX control library provided by Illumina and loaded onto the MiSeq V2 flow cell at a concentration of 8 pM for cluster formation and sequencing (Illumina). The PhiX control library provides a balanced genome for calculation of matrix, phasing and pre-phasing, which are essential for accurate basecalling. The libraries were sequenced from both ends of the molecules to a total read length of 250 nt from each end. Sequence analyses were conducted using mothur v.3.3.3 (ref. 77) and included assembly of the paired ends, amplicon size selection and alignment to the SSU rRNA gene. Chimeras were detected using UCHIME78 and subsequently removed. Taxonomic classification of sequences was conducted with the SILVA SSU Ref database (release 123)79 using the k-nearest neighbour algorithm, and subsequently chloroplast, mitochrondia and eukaryotic sequences were removed. Sequences were grouped into operational taxonomic units using minimum entropy decomposition80for statistical analysis using Primer-E (v.7.0.9, Primer- E Ltd.).

Cultivation of bacteria

Endozoicomonas montiporae (LMG 24815) was obtained from the Belgian Coordinated Collections of Microorganisms. E. montiporae was grown in liquid marine broth at 23 °C. Ruegeria s.p. (WHOIMSCC16) was obtained from Stylophora pistillata and Vibrio s.p. (WHOIMSCC50) from Porites lobata, both isolated in the Federated States of Micronesia, and were grown using dilute nutrient media (0.8 g nutrient broth, 0.5 g casamino acids, 0.1 g yeast extract, 860 ml seawater and 140 ml sterile water). Growth of all bacteria was quantified with cell counts after staining with 2-(4-amidinophenyl)-1H-indole-6-carboxamidine (DAPI).

Collection and rearing of coral larvae

Egg and sperm from at least three colonies of Orbicella faveolata, Colpophyllia natans and Diploria labyrinthiformis were collected in the evening 6–12 days following the full moon at the Water Factory site in Curaçao (12.11298° N, 68.96103° W) using standard collection nets. The gametes were pooled and fertilized for 30 min, initially diluted into 0.45 μm filtered seawater and subsequently maintained in 0.2 μm filtered seawater with daily water changes once they developed into larvae.

Extracellular superoxide measurements of cultures and larvae

Extracellular superoxide produced by laboratory cultures and coral larvae was measured using a previously described MCLA/FeLume method17 with a few modifications (see above for general description of the FeLume system). Briefly, carrier solutions were gently pumped (2 ml min−1) across a sterile syringe filter placed in the FeLume’s analyte line for 2 min to generate stable baseline signals (<4% coefficient of variation). For larvae, the carrier solution consisted of AFRW amended with 75 μM DTPA (AFRW+DTPA). For bacteria, the carrier solution was 20 mM phosphate-buffered (pH=7.6) artificial seawater (NaCl, 0.3 M; MgSO4, 50 mM; CaCl2, 10 mM; KCl, 10 mM) amended with 75 μM DTPA (PBASW+DTPA). Next, the pump was stopped, the syringe filter was removed and using a syringe, specimens were gently deposited on the filter (larvae=10 μm, bacteria=0.2 μm). Then the specimen-loaded filter was placed back inline, and the pump was restarted (2 ml min−1). In principle, superoxide produced extracellularly is entrained by the carrier solution and detected upon mixing with MCLA in the flow cell downstream of the specimens. Biological signals were collected until a stable, steady-state reading was achieved (<4% coefficient of variation) and maintained for at least 1 min. Finally, SOD was added to the carrier solution (0.8 U ml−1, final) to confirm that superoxide was responsible for the signal observed.

Stable biological signals were averaged and corrected for background luminescence by subtracting the average initial baseline (that is, obtained with the clean syringe filter inline, immediately before the addition of organisms and without the addition of SOD). Corrected biological signals were converted to superoxide concentrations via calibration with multi-point KO2 standard curves under identical conditions as biological experiments, similarly to the protocol described elsewhere17 and outlined above for in situ superoxide measurements. Under the conditions used for these experiments (for example, flow rate, flushing volume, specimen load and so on), steady-state superoxide concentrations ranged from 0.22 to 12 nM. The typical detection limit (defined as three times the average s.d. of replicate baseline signals) was 0.24±0.11 nM (avg±s.d.). As determined from calibration experiments, superoxide half-lives varied inversely with superoxide concentration and ranged from 0.7 to 3.3 min (AFRW+DTPA in Curaçao) and 4.9 to 24.8 min (PBASW+DTPA). Some half-lives in PBASW+DTPA are relatively high compared with most natural waters, but similar to superoxide decay rates measured in water samples from the Costa Rica Dome that were also filtered and amended with DTPA37. Moreover, the relatively long half-lives we measured in PBASW+DTPA are not surprising because, unlike natural waters, PBASW lacks any organics that could contribute to the decay of superoxide. Thus, these half-lives do not and are not meant to accurately represent the lifetime of superoxide in the presence of corals, their symbionts or natural seawater.

Extrapolation times were typically 64.6±10.6 s (avg±s.d.) under our experimental conditions. Biogenic superoxide concentrations were not corrected for superoxide decay and thus represent conservative estimates. As above, calibrations yielded highly linear curves (for example, R>0.97 for Curaçao AFRW+DTPA; R>0.98 for PBASW+DTPA), with a sensitivity that averaged 2.2±0.6 pM per luminescence count. Net superoxide production rates were calculated as the product of the steady-state superoxide concentration and flow rate (final units of amol per hour). The production rate of superoxide by each replicate was normalized to the total number of cells or larvae loaded on the filter (final units of amol per organism per hour).

Statistical analysis

Superoxide data and Symbiodinium counts were analysed using JMP Pro 12.1.0 statistical analysis software. The effects of coral species and health state on average seawater-normalized superoxide levels (Fig. 1b) were examined via full factorial ANOVA and post-hoc analysis via Tukey’s honest significant difference test. Mixed-factor repeated measures ANOVA was used to evaluate the effects of PAR and health state on time-series superoxide measurements from Porites compressa (Fig. 2). Species-specific Symbiodinium counts for bleached versus pigmented colonies (Fig. 4k) were performed using two-sample t-tests assuming unequal variance. Other two-sample comparisons (for example, bleached versus pigmented superoxide levels for a single species (Fig. 1b), superoxide levels between species (Fig. 3b) and superoxide levels between corals and bulk seawater (Fig. 3b) were also assessed with Student’s t-test. Statistical analysis of microbiome sequence data was conducted using Primer (v.7, Primer-E Ltd, Ivybridge, UK).

Data availability

Full-length SSU rRNA gene sequences of the coral bacterial cultures are available in GenBank under accession numbers KT957318 and KT957319. Amplicon sequence data are available in as NCBI bioproject PRJNA324813. Additional data may be available from the authors upon request.

Additional information

How to cite this article: Diaz, J. M. et al. Species-specific control of external superoxide levels by the coral holobiont during a natural bleaching event. Nat. Commun. 7, 13801 doi: 10.1038/ncomms13801 (2016).

Publisher’s note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Acknowledgements

This work was supported by a Postdoctoral Fellowship from the Ford Foundation (J.M.D.), the National Science Foundation under grants OCE 1225801 (J.M.D.) and OCE 1233612 (A.A.), the Ocean and Climate Change Institute of the Woods Hole Oceanographic Institution (C.M.H.), the Sidney Stern Memorial Trust (C.M.H. and A.A.) and an anonymous donor. We thank Ruth Gates and the staff of the University of Hawaii’s Hawaii Institute of Marine Biology (UH-HIMB) for supporting our time-sensitive field work in Kaneohe Bay. We extend special thanks to Anne Rosinski of the State of Hawaii Department of Land and Natural Resources (DLNR) and Raphael Ritson-Williams of UH-HIMB for sharing reef site information. In Curaçao, we are grateful to Mark Vermeij, Kristen Marhaver and the CARMABI Research Institute for logistical support as well as the 2014 spawning team of Valérie Chamberland, Ashlee Lillis, Rémon Malawauw, Callum Reid and Lisa Röpke. We also thank Alyson Santoro and Matthew Neave for assistance with isolating the coral bacterial cultures. The samples analysed in this study were collected under DLNR Special Activity permit 2015-49 issued by the State of Hawaii and AN-00l issued by Curaçao.

Author information

Author notes

    • Julia M. Diaz
    •  & Colleen M. Hansel

    These authors contributed equally to this work

Affiliations

  1. Department of Marine Chemistry and Geochemistry, Woods Hole Oceanographic Institution, 266 Woods Hole Rd, Woods Hole, Massachusetts 02543, USA

    • Julia M. Diaz
    • , Colleen M. Hansel
    • , Amy Apprill
    • , Tong Zhang
    • , Laura Weber
    • , Sean McNally
    •  & Liping Xun
  2. Skidaway Institute of Oceanography, Department of Marine Sciences, University of Georgia, 10 Ocean Science Circle, Savannah, Georgia 31411, USA

    • Julia M. Diaz
  3. Department of Chemistry, Imperial College London, Imperial College Road, London SW7 2AZ, UK

    • Caterina Brighi
  4. MOE Key Laboratory of Pollution Processes and Environmental Criteria, College of Environmental Science and Engineering, Nankai University, 38 Tongyan Road, Tianjin 300350, China

    • Tong Zhang
  5. School for the Environment, University of Massachusetts Boston, 100 Morrissey Boulevard, Boston, Massachusetts 02125, USA

    • Sean McNally

Contributions

J.M.D., C.M.H. and A.A. designed research, analysed data and wrote the paper. All authors performed research and contributed to the paper.

Competing interests

The authors declare no competing financial interests.

Corresponding authors

Correspondence to Colleen M. Hansel or Amy Apprill.

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  1. 1.

    Supplementary Information

    Supplementary Figures 1-3 and Supplementary Tables 1-5

 

New Studies Take a Second Look at Coral Bleaching Culprit


https://www.whoi.edu/news-release/new-studies-take-a-second-look-at-coral-bleaching-culprit

New Studies Take a Second Look at Coral Bleaching Culprit

Superoxide has ‘Jekyll-and-Hyde’ attributes, research shows

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DECEMBER 7, 2016

When it comes to coral health, superoxide—a natural toxin all oxygen-breathing organisms produce—gets a bad rap.

Scientists have called superoxide out as the main culprit behind coral bleaching: The idea is that as this toxin build up inside coral cells, the corals fight back by ejecting the tiny energy- and color-producing algae living inside them. In doing so, they lose their vibrancy, turn a sickly white, and are left weak, damaged, and vulnerable to disease.

Now, a new study from the Woods Hole Oceanographic Institution (WHOI) is casting a more positive light on superoxide. It suggests that when these molecules are produced at coral surfaces—outside of their cells—they may actually play a beneficial role in coral health and resilience. The research that results from this finding may contribute to future strategies for preventing corals from bleaching.

“Superoxide has largely been vilified as a stress molecule and implicated as the main cause of coral bleaching,” said Colleen Hansel, a WHOI biogeochemist and lead author of the study published December 7 in the journal Nature Communications. “But when we measured superoxide concentrations at the surface of corals during a natural bleaching event, we saw a completely different dynamic. It appears this ‘toxin’ may have provided a benefit to the corals—perhaps helping some species to resist bleaching.”

Hansel said the researchers were surprised to see that, during the bleaching event, coral species that were more susceptible to bleaching weren’t producing external superoxide, while those that resisted bleaching produced high concentrations.

“While we don’t yet understand how corals produce superoxide externally, this discovery points to a fundamental misunderstanding of what this group of compounds does for coral health,” she said.

First-ever field measurements

Hansel believes the dark shadow cast on superoxide stems from a lack of direct measurements. “To date, our understanding of the role these molecules play in coral health is based on indirect lab measurements of superoxide inside coral tissue. No one had ever attempted direct measurements of superoxide produced outside corals living within reefs. This is most likely because superoxide is very difficult to measure as it is highly reactive and has a lifespan of only roughly 30 seconds in natural waters. You can’t just take the samples back to the lab for analysis.”

To overcome this, she and her research team devised a novel approach for taking real-time measurements of coral superoxide production in a natural reef environment. During a week-long field visit to Hawaii’s Kaneohe Bay in October, 2014, they lugged a laboratory instrument used for superoxide analysis onto a tiny motor boat and took samples from six different shallow reef sites.

“The measurements were very tricky to collect as we had to sample superoxide produced by the coral using a small tube held just above the coral surface,” said Hansel.  “From there, it had to be pumped up to the instrument on the boat within 30 seconds, before the superoxide was gone. While all this was happening, we had to hold the boat over the corals being measured and keep the boat steady as waves were coming in.”

WHOI microbiologist Amy Apprill was underwater holding the sampling tube in place as her colleagues “shouted out with excitement from seeing the real-time data.” Apprill said it was amazing to see wide variations in superoxide production among different coral species, some making “a ton” of superoxide, while others making very little. Their analysis showed the corals producing more superoxide had greater resilience to bleaching than the coral producing very little.

Another noteworthy discovery, according to the scientists, was that corals were producing superoxide even when there were no evident stressors, such as hotter seas, which are known to trigger superoxide production.

In a parallel study published November 24 in the journal Frontiers in Marine Science, the team found similar results with corals grown under non-stressful conditions in the lab. The corals, and their microbial partners (symbionts), produced high levels of superoxide at the surface independent of temperature and other variables such as time of day or presence of light.

“This made our eyes open a little bit wider,” Apprill added, “and reinforced the idea that, while we have a better understanding of the negative impacts associated with internally-produced superoxide, the role of superoxide produced outside cells has been overlooked and is not been well understood.”

Playing a positive role

The possibility that superoxide may help corals resist bleaching was eye opening for the scientists, but it isn’t the first time these toxins have proven beneficial to organisms. In fact, research conducted on bacteria and fungi has shown that superoxide is purposely made outside the cell to stimulate cell growth, increase nutrient uptake, and fend off invasive pathogens.

“Superoxide is not always bad,” said Hansel. “In fact, it is an essential molecule that all organisms need. Similar to other organisms, we believe that these compounds may be an integral component of the physiology and immune system of corals. It’s not as black and white as once believed.”

Next steps

Understanding the positive impacts of superoxide on corals may be a stepping stone towards improving coral health and developing bleaching mitigation strategies in the future—particularly if the molecules are in fact protecting corals from stress rather than inducing it. The information could ultimately be used to help determine how to engineer corals to be more resilient. But Hansel feels more work is needed.

“The next step is to conduct a temporal study in the field to get more information on how superoxide is being regulated over time as a function of stress and during the course of a bleaching event,” she said. “This includes when they’re completely healthy, as warmer temperatures increase and stress begins, during peak stress and bleaching, and through recovery. We’d also like to couple this with controlled lab studies where we can grow corals that range in bleaching susceptibility and introduce them to stressors including pathogens to see if they trigger superoxide production. We want to mimic a range of natural conditions in the lab to tease out the benefits superoxide is providing.”

Hansel said that while the fieldwork made it possible to explore corals in a natural environment that is more realistic to the conditions they experience, lab experiments allow them to change one variable at a time while keeping everything else constant so direct relationships can more easily be seen.

“To truly link variables like heat and stress, we need to minimize variability in other variables, like light, changes in flow patterns, and nutrient inputs,” she said.

According to Apprill, the new findings suggest that superoxide may play a variety of roles in coral health, and have led to a new realization of the complexities the toxins play in corals.

“Coral bleaching is one of the biggest problems facing the ocean today,” said Apprill. “We understand the factors that contribute to bleaching events, but the mechanisms appear to be more complicated than we had thought. Fortunately, corals are a really good system to focus on in terms of studying the health impacts of superoxide, since drastic changes in coral health are very visible and can be quickly seen—even from space.”

This research was funded by the National Science Foundation, the Sidney Stern Memorial Trust, the Ocean and Climate Change Institute of the Woods Hole Oceanographic Institution, and an anonymous donor.

The Woods Hole Oceanographic Institution is a private, non-profit organization on Cape Cod, Mass., dedicated to marine research, engineering, and higher education. Established in 1930 on a recommendation from the National Academy of Sciences, its primary mission is to understand the ocean and its interaction with the Earth as a whole, and to communicate a basic understanding of the ocean’s role in the changing global environment. For more information, please visit www.whoi.edu.

 

破珊瑚白化新進展 嫌疑犯「超氧化小體」有了新定位


http://e-info.org.tw/node/202121?utm_source=%E7%92%B0%E5%A2%83%E8%B3%87%E8%A8%8A%E9%9B%BB%E5%AD%90%E5%A0%B1&utm_campaign=7ee030b865-EMAIL_CAMPAIGN_2016_12_28&utm_medium=email&utm_term=0_f99f939cdc-7ee030b865-84956681

破珊瑚白化新進展 嫌疑犯「超氧化小體」有了新定位

 建立於 2016/12/28

作者:馮加伶

還記得今年(2016年)3月澳洲大堡礁珊瑚大白化的事件嗎?這個全世界最大最長的珊瑚礁群,因為夏季水溫居高不下,讓9成的珊瑚礁都受到白化影響。澳洲的珊瑚研究團隊還出動直升機和調查船,進行大規模的海空調查。

圖一、研究人員於2016年4月在大堡礁木礁(Wood Reef, the Great Barrier Reef)所拍攝的照片,照片中白色、淡黃色或是粉色的珊瑚,都是正在白化或已經白化的珊瑚。不只表層,連較深水域的礁體也有珊瑚白化的情形。圖片來源:郭兆揚。

這樣慘況不是只有發生在大堡礁,台灣的水下攝影師 Yorko Summer 於今年(2016年)4月拜訪塞席爾(位於非洲東部印度洋的群島國家)時,也目睹了大規模的珊瑚白化事件。

【影片】 一眼望去整片的白化珊瑚,看似夢幻,卻是珊瑚病危的警訊。

https://www.facebook.com/plugins/video.php?href=https%3A%2F%2Fwww.facebook.com%2Fhiexplocean%2Fvideos%2F1222361537829010%2F&show_text=0&width=560

影片來源:Yorko Summer,臉書粉絲專頁"好嗨 HiExplocean”

珊瑚白化是什麼?

俗話說一白遮三醜,亞洲女性都嚮往有著一身白皙透亮的肌膚,但是在珊瑚的世界裡,可完全不是這麼回事,當珊瑚變白的時候,通常都是生病或是狀況不好的時候。

要了解珊瑚白化是什麼,我們要先從珊瑚的結構開始看起,無論是高達數公尺的大珊瑚團塊或是幾公分的小珊瑚,它們都有著一樣的基本結構,都是由一隻一隻的珊瑚蟲個體所構成的。珊瑚蟲(polyp)是珊瑚的基本生存單位,珊瑚蟲的上半部為開口,開口周圍有著一圈觸手,觸手表面有刺絲胞可用來捕食海水中的浮游生物,再將食物送入口中,內部有著消化腔和生殖組織(可以產生精子、卵子或是精卵束),珊瑚蟲的底部則是珊瑚的骨骼,珊瑚生長時會分泌碳酸鈣,經年累月逐漸累積,形成珊瑚礁。

圖二、珊瑚蟲的示意圖:珊瑚蟲的上半部為開口,開口(mouth)周圍有著一圈觸手(tentacles),觸手表面有刺絲胞(nematocyst)可用來捕食海水中的浮游生物,再將食物送入口中,內部有著消化腔(gastrovascular cavity)和生殖組織(可以產生精子、卵子或是精卵束),底部則是珊瑚的骨骼(skeleton)。圖片來源:大英百科全書,1999。

雖然珊瑚可以自行捕食,但是功力有限,如果不開外掛就無法打贏這場生存戰役。為了生存,珊瑚有一群超級好夥伴──共生藻,這些單細胞藻類住在珊瑚蟲觸手的細胞裡面,利用珊瑚產生的廢物當作養分和陽光進行光合作用,再將光合作用產生的物質分給珊瑚,像是脂質、葡萄糖和胺基酸等物質,供應了珊瑚絕大部分(近八成)的營養來源。除了共生藻,珊瑚也是其他微生物的家,像是真菌、細菌、古細菌或是病毒,這些微生物也能夠提供珊瑚營養,還會產生抗菌物質,協助維持珊瑚宿主的健康。

圖三、珊瑚蟲和共生藻:(A)光學顯微鏡下的珊瑚蟲,一顆顆黃褐色的圓點都是共生藻;(B)螢光顯微鏡下的珊瑚蟲,紅色圓點都是共生藻,藍色和綠色則是珊瑚蟲自己的螢光蛋白。圖片來源:(A)Chuya Shinzato,OIST沖繩科學技術大學院大學;(B)Christine Farrar,Hawaii Institute of Marine Biology夏威夷大學海洋生物研究所。

當陽光、水溫、水質等一切的條件都正好的時候,珊瑚和好夥伴共生藻彼此合作無間,除了提供珊瑚營養,還讓珊瑚增添色彩,不同種類的共生藻加上珊瑚本身的螢光蛋白,讓珊瑚礁有著繽紛亮麗的各種面貌。

圖四、 澎湖東吉島的薰衣草森林,一整片的紫色鹿角珊瑚,讓人驚豔。
圖片來源:Marco Chang,Marco Chang Underwater Photography 臉書粉絲專頁

但是珊瑚對環境變化很敏感,海水溫度的改變(低溫或高溫)、混濁的水質和污染等環境因素,都會讓珊瑚與共生藻感到壓力,共生藻因此停止工作、慢慢死亡或是離開珊瑚蟲,珊瑚的顏色也會變得越來越淡,最後只剩下透明的珊瑚蟲與白色骨骼,這個現象稱作『珊瑚白化』。珊瑚絕大部分的營養來源都是由共生藻所供給,如果白化的時間持續過久,珊瑚就會因饑餓而導致死亡。有時候生病的珊瑚也會出現局部白化的現象,總之,珊瑚真的不是越白越漂亮,而是珊瑚健康出狀況的一個警訊。

圖五、自從西元1980年代,氣候變遷和汙染加劇之後,珊瑚疾病和白化的情況就越來越嚴重,圖片中的珊瑚局部白化為白帶病(white band syndrone),曾經讓加勒比海地區的珊瑚大量死亡。圖片來源:Neal Cantin,Wood Hole Oceangraphic institution 伍茲霍爾海洋研究所。

珊瑚礁的生物多樣性極高,是許多珊瑚礁魚類和無脊椎動物的家、也是許多大型迴游性魚類的孵育場,這些海洋生物是人類賴以為生的糧食來源; 珊瑚所分泌的天然物質是許多現代醫學的寶物,有些成分具有美白、保濕,甚至還開發成為抗癌和阿茲海默症的藥物; 珊瑚的碳酸鈣骨骼,既堅硬又兼具透氣排水的特性,被許多沿海地區的居民當作建材,像是澎湖地區著名的雙心石滬和石厝。有著美麗珊瑚礁的地區,也經常是受歡迎的觀光景點,帶來了龐大的經濟收益。除此之外,珊瑚礁的複雜結構可以削弱海浪對陸地的衝擊,是最天然的消波塊,無時無刻保衛著我們的家園。

圖六、整片的珊瑚就像盛開的花團,深深吸引著來自世界各地的潛水員。 圖片來源:Marco Chang, Marco Chang Underwater Photography 臉書粉絲專頁。

珊瑚礁所提供的服務和好處,佔據了我們食醫住行(旅行)的各個層面,但是這些好處,都有個先決條件,那就是它們必須是健康的。因此,許多科學家都特別關注珊瑚白化的成因和機制,希望能找到預防和減緩珊瑚白化的方法。

最近,科學界有個出人意表的新發現,超氧化小體(superoxide),一種存在於所有耗氧生物體內的天然毒素,以前都被視為是造成珊瑚白化的罪魁禍首,現在除了洗刷罪名,還被發現可能對珊瑚的健康有助益,可說是重獲新生。

什麼是超氧化小體?

超氧化小體,是生物進行有氧代謝過程中所產生的副產品,這些粒子非常微小,加上有著不穩定分子結構(未配對的自由電子),因此十分活躍,很容易就和其他化學分子互動,在細胞內進行化學反應。如果這些超氧化小體的濃度太高,很容易造成細胞的壓力和損壞。

過往,科學家認為珊瑚體內的超氧化小體,就像非常活潑到處搗蛋的小頑童,跑到細胞膜會讓細胞膜氧化,在細胞內部會讓蛋白質變性或是讓核酸受損,甚至可以引發細胞自殺的指令。這些種種破壞行徑,都會消耗珊瑚和共生藻的能量,使其失去活力、變白和容易生病。

這篇發表於今年(2016年)12月的文章,則提供了不同以往的觀點,這些來自美國伍茲霍爾海洋研究所(Woods Hole Oceanographic Institution, WHOI)的科學家發現,如果這些超氧化小體是在珊瑚表面產生的,不在珊瑚的細胞內,反而對珊瑚的健康和韌性*( resilience)有所助益。

圖七、紅色小字的O2-,就是超氧化小體。當超氧化小體在珊瑚細胞內濃度過高的時候,會讓共生藻的數量減少,而產生白化現象(上半部插圖)。但是當這些超氧化小體在珊瑚體外形成時,反而像是一道防禦圍牆,協助珊瑚對抗白化(下半部插圖)。
圖片來源:Eric Taylor,Woods Hole Oceanographic Institution 伍茲霍爾海洋研究所。

科學家在珊瑚經歷白化事件時,利用化學冷光的分析儀器實際測量珊瑚表面的超氧化小體濃度,同時利用俗稱為PAM(攜帶型葉綠素螢光光合作用分析設備)來推估珊瑚體內共生藻進行光合作用的程度。這也是研究最困難的地方之一,因為超氧化小體的測定相當困難,這些化學分子相當活躍,在自然環境中大約只有30秒的壽命,無法在野外採樣再帶回實驗室進行分析。

為了克服採集上的困難,這群科學家想出了在野外及時採樣的方法,他們將分析儀器帶到船上,還設計了一個特殊的吸頭,收集珊瑚表層的海水,測量水流的速度,盡可能加快分析的時間,減少超氧化小體濃度測量的誤差。

研究發現這些珊瑚對抗白化的能力和珊瑚表面的超氧化小體有關,某些對白化抵抗力特別差的珊瑚種類,它們表面的超氧化小體濃度都很低。相反的,韌性很高,能夠存活下來的白化珊瑚,其表層超氧化小體的濃度都很高。

圖八、研究人員(右1)利用浮潛的方式,將採集小管放置於珊瑚上方,船上的研究人員則利用船上的儀器及時的分析水樣,才能在超氧化小體與其他物質進行反應前測得數值。圖片來源:Amy Apprill,Woods Hole Oceanographic Institution伍茲霍爾海洋研究所。

除此之外,研究結果顯示,珊瑚表面超氧化小體的濃度和光線強度、珊瑚體內共生藻濃度和珊瑚白化程度等因子,沒有任何直接的關聯,反而是與珊瑚的種類和其體內細菌的組成有關。這些結果揭露了珊瑚的另一面,那就是它們與其體內的微生物,都具有調控周圍環境的能力,也讓我們知道原來超氧化小體對珊瑚健康和生理狀態的影響,可是「種類限定」的。

雖然這些珊瑚表層的超氧化小體從何而來?作用機制為何?都還是尚未解開的謎題。但是這個嶄新的發現,讓我們重新思考珊瑚白化的成因和機制,也給超氧化小體這個毒素一個新的定位。未來,或許還能成為對抗珊瑚白化的一帖良藥。

【註】生態韌性( ecological resilience):受到環境干擾後的珊瑚礁生態系的恢復能力,尤指維持或恢復與干擾前相同的結構或功能狀態。參考資料:http://e-info.org.tw/node/201419

 

Ring-tailed lemurs face extinction amid sapphire-mining rush in Madagascar


http://www.independent.co.uk/environment/lemurs-ring-tailed-extinction-madagascar-sapphire-mining-rush-planet-earth-ii-a7488181.html

Ring-tailed lemurs face extinction amid sapphire-mining rush in Madagascar

‘They are disappearing right under our noses. It’s likely that the ring-tailed lemur population will eventually collapse’

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The ring-tailed lemur of Madagascar is “disappearing right under our noses” as the iconic animal is hunted and trapped to extinction and its forest home destroyed by people hunting for sapphires.

Lemurs are the most threatened group of vertebrates on the planet but it was thought the resourceful ring-tailed species – which featured in the hit cartoon film series Madagascar and the BBC’s recent Planet Earth II documentary – would be the last to die out.

However, despite their ability to survive in some of the harshest environments on the Indian Ocean island, they have been mostly reduced to small groups, researchers warned in a paper called Going, Going Gone: Is the Iconic Ring-railed Lemur Headed for Imminent Extirpation? in the journal Primate Conservation.

Populations of more than 200 were found in just three places, with 12 other groups of 30 animals or less. At another 15 sites, they had either died out or were in danger of doing so. In total there are now believed to be less than 2,500 individuals.

One of the researchers, Professor Michelle Sauther, who has studied the animal for 30 years, said: “This is very troubling. They are disappearing right under our noses.

“It’s likely that the ring-tailed lemur population will eventually collapse.

“We are getting an early warning that if we don’t do something very quickly, the species is going to become extinct.

“And this is the one primate species in Madagascar we never thought this would happen to.”

The plight of the ring-tails suggests the other lemur species will also be struggling.

“Ring-tailed lemurs are like the canary in a coal mine,” said Professor Sauther, of the University of Colorado Boulder in the US.

“If they are going down the drain, what will happen to the other lemur species on the island that have more specific habitat and diet requirements?"

One threat to lemurs is the creation of open-cast sapphire mines that have drawn in thousands of people in search of their fortunes, on an island where 90 per cent of people live on less than $2 (about £1.60) a day.

This has led to the destruction of significant areas of the lemurs’ forest habitat and an influx of people who need to be fed, increasing hunting for bushmeat. Lemurs are also captured and sold for an illegal pet trade, boosted by the popularity of the DreamWorks’ films.

Professor Sauther said: “I think it’s important to keep in mind that what is driving habitat loss and ring-tailed lemur declines is human poverty.”

Fellow researcher Professor Lisa Gould, of the University of Victoria, said many areas that once contained important populations of ring-tailed lemurs now had none.

“It was important to try and document as many populations of ring-tailed lemurs in as many regions as possible,” she said.

“While I was discovering previously unknown lemur populations, many of them are likely to be extirpated in the near future.”

 

藍寶石熱潮不退 馬達加斯加環尾狐猴慘遭殃


http://e-info.org.tw/node/202097?utm_source=%E7%92%B0%E5%A2%83%E8%B3%87%E8%A8%8A%E9%9B%BB%E5%AD%90%E5%A0%B1&utm_campaign=7ee030b865-EMAIL_CAMPAIGN_2016_12_28&utm_medium=email&utm_term=0_f99f939cdc-7ee030b865-84956681

藍寶石熱潮不退 馬達加斯加環尾狐猴慘遭殃

 建立於 2016/12/28

本報2016年12月28日綜合外電報導,姜唯編譯;蔡麗伶審校

馬達加斯加採藍寶石正夯,當地的明星動物環尾狐猴卻被採礦者獵捕至瀕危,森林棲地也遭破壞。

狐猴是地球上最受威脅的脊椎動物之一,其中聰明的環尾狐猴——也就是卡通「馬達加斯加」裡的那一群——原本人們以為牠們的生存危機是最小的。但是近期一篇《靈長類保育》期刊的研究卻顯示,雖然環尾狐猴能適應馬達加斯加島上最艱困的環境,族群卻有越來越小的趨勢。

Mathias Appel(CC0 1.0)
馬達加斯加環尾狐猴。圖片來源:Mathias Appel(CC0 1.0)

環尾狐猴僅剩2500隻 生態指標垂危

島上只有三個地點有個體數超過200的族群,其他12個族群只剩下不到30隻個體,在另外15個狐猴棲地則是已經沒有狐猴或是所剩無幾。學者相信島上總個體數已不到2500隻。

研究作者之一的Michelle Sauther已經研究狐猴30年,他說環尾狐猴族群很有可能崩壞,再不儘快採取行動,原本以為全馬達加斯加最不可能滅絕的環尾狐猴也會滅絕。

環尾狐猴出現生存危機,其他的狐猴物種處境可能也很艱難。

「環尾狐猴是領先指標。如果牠們消失,其他對棲地和飲食要求更高的狐猴物種怎麼辦?」Sauther說。

藍寶石礦場引人潮 狐猴成狩獵目標

狐猴的生存威脅之一是吸引數千人前來淘寶的露天藍寶石礦場。在馬達加斯加,90%的人一天收入不到2美元,藍寶石是非常大的誘因。

礦場開發破壞狐猴的森林棲地;湧入的人潮需要食物,狐猴便成為狩獵目標。此外,「馬達加斯加」卡通爆紅也導致狐猴被非法捕捉,進入非法寵物供應鏈。

Sauther教授強調,「棲地破壞和環尾狐猴減少的真正原因,是人們的貧窮。」

採藍寶石的過程造成水源污染。作者:Rosey Perkins。圖片來源:影片截圖。
採藍寶石的過程也造成水源污染。作者:Rosey Perkins。圖片來源:影片截圖。

另一位研究者、維多利亞大學教授古爾德(Lisa Gould)說,許多曾經棲息重要環尾狐猴族群的地點現在已不復見。

「盡可能在最多地點記錄下最多環尾狐猴族群是很重要的研究工作。雖然曾發現一些過去不曾被發現的族群,但也很可能在不久的將來遭到消滅。」古爾德說。

nomis-simon(CC BY 2.0)
環尾狐猴很可能在不久的將來滅絕。圖片來源:nomis-simon(CC BY 2.0)

參考資料

作者

蔡麗伶(LiLing Barricman)

In my healing journey and learning to attain the breath awareness, I become aware of the reality that all the creatures of the world are breathing the same breath. Take action, here and now. From my physical being to the every corner of this out of balance’s planet.

姜唯

如果有一件事是重要的,如果能為孩子實現一個願望,那就是人類與大自然和諧共存。

 

金紙燒掉2萬台車排放量 環署推全國宮廟減燒


http://e-info.org.tw/node/202098?utm_source=%E7%92%B0%E5%A2%83%E8%B3%87%E8%A8%8A%E9%9B%BB%E5%AD%90%E5%A0%B1&utm_campaign=7ee030b865-EMAIL_CAMPAIGN_2016_12_28&utm_medium=email&utm_term=0_f99f939cdc-7ee030b865-84956681

金紙燒掉2萬台車排放量 環署推全國宮廟減燒

 建立於 2016/12/27

本報2016年12月27日新北訊,賴品瑀報導

農曆春節在即,國人為了祭拜,每年平均燒掉24萬噸的金紙與3000噸的香,也等同2萬台車的排放量。環保署長李應元與國內十多個宗教團體27日研商減燒策略,並喊出明年全台50%、後年100%的宮廟,一起加入減燒行列。

為了消災祈福,民間信仰上往往在農曆初一、十五與逢年過節、中元普渡等祭拜,但是也產生了二氧化碳、PM2.5、硫氧化物、碳氧化物、一氧化碳與多環芳香烴等有害的空氣污染物。

2016-12-27_12-51-54
環署署長李應元與宗教團體研商減燒,目標明年50%、後年100%的宮廟加入減燒。賴品瑀拍攝。

李應元表示,尤其是秋冬時的氣候與地形條件,讓中南部的空污問題較為嚴重,因此廟宇減燒也遭環署納為空污防制的重點。「也要神也要人」,李應元強調,空污減量要做好是需要天助自助。神明要疼惜、保佑人民健康,也需要信眾減燒。

李應元以放鞭炮為例,民眾為了表達誠心而準備了太多鞭炮來放,卻因為鞭炮太多太集中,只有黑煙而不見美麗的火光,同時大量燃放的鞭炮也讓場所沒有了氧氣,只有煙塵跟PM2.5,傷害的是在場信眾的健康。

除了各地宮廟將持續減少金紙與香的使用外,台北市民政局局長藍世聰更將鼓勵信眾「以功代金」、「以米代金」,例如將買紙錢的費用直接捐助慈善活動、或是改奉「平安米」,祭祀後可自行食用、捐給寺廟或弱勢團體。都是不減誠心但更環保的作法。

目前已有不少的宮廟逐漸減少金紙與香的燃燒,朝向不燒、集中燒、使用環保金爐等作法。例如行天宮去年已經不燒香、龍山寺在2000年封了金爐。藍世聰表示,目前台北市已經有九成宮廟不燒金紙。

龍山寺除了不燒金紙,原先的21支香減少2005年的7支、再減為去年的3支香。龍山寺副董黃書瑋表示,幾次的改革信眾都非常配合,他們還打算未來再撤掉一些香爐。

「一柱清香無限祝福。」李應元表示,要達到四年內PM2.5紅色警戒天數減半,每個方面都要努力,像是宮廟把香從21支減為七支,就已經是減量2/3了,環署將繼續向國內大小宮廟宣導,目標明年50%、後年100%的宮廟加入減燒。

作者

賴品瑀

新店溪下游人,曾在成大中文與南藝紀錄所練功打怪撿裝備,留下《我們迷獅子》、《我是阿布》兩部紀錄片作品。現為人類觀察員,並每日鍛鍊肌肉與腦內啡,同時為環境資訊電子報專任記者,為大家搭起友誼的橋樑。

 

環署擬調漲空污費救秋冬空品 業者反問夏季缺電怎解


http://e-info.org.tw/node/202103?utm_source=%E7%92%B0%E5%A2%83%E8%B3%87%E8%A8%8A%E9%9B%BB%E5%AD%90%E5%A0%B1&utm_campaign=7ee030b865-EMAIL_CAMPAIGN_2016_12_28&utm_medium=email&utm_term=0_f99f939cdc-7ee030b865-84956681

環署擬調漲空污費救秋冬空品 業者反問夏季缺電怎解

 建立於 2016/12/27

本報2016年12月27日台北訊,賴品瑀報導

為了解決秋冬空污問題,環署要祭出固定污染源的空污費費率調整,希望以經濟誘因讓業者在秋冬降載減產,改到春夏時段增產。此草案已報院,原本更打算最快明年一月就要實施。但27日下午的公聽會中,「第四季才是電子業的大季」、「夏天才是缺電的時候」製造業者也從國家能源、市場需求的角度,提出要落實的困難之處。

2016-12-27_05-06-45
環署擬調漲空污費救秋冬空品,空保處為此召開公聽會。賴品瑀攝影。

相同排放量的空污物,因為季別不同,對環境的影響也有差別,因此環署將提高秋冬季節費率,在秋冬(第一季、第四季)時,SOx、NOx的費率平均每公斤提高2元、VOCs提高每公斤5元,但若業者從產能減產、提高防治設備處理效率,將有適用費率與優惠係數的減免優惠。

受衝擊的業者,多為電力及燃氣供應與基本金屬、化學原材料、非金屬礦品、塑膠製品、電子零組件等製造業,合計約有3565家業者。環署空保處評估,會有30%的業者在費率調整後,進行10%的降載,因此每季可以減少2,136公噸的排放量,等同台中火力電廠停轉21天。

2016-12-27_05-13-07
空保處評估,會有30%的業者在費率調整後,進行10%的降載,因此每季可以減少2,136公噸的排放量,等同台中火力電廠停轉21天。翻拍自簡報資料。

不過,業者們除了不滿每次環署都想找製造業開刀並不公平外,更提出全球市場需求變化快速,不可能受季節限制、台灣的供電狀況是夏季吃緊等問題。更提出應該有「好學生條款」,對於已經採取最佳可行性技術,目前已無法再提升的業者,也應該拉大優惠係數等來鼓勵他們,更應該檢討目前依照產能來算空污費的計算方法,因為他們在改善技術後,並沒有隨著產能變大而增加排放。

經濟部工業局表示,會持續協助業者改良設備,「贏回空污費」,但也提醒,應該給予已經改採天然氣等清潔燃料的業者、或是已經採用最佳可行性技術者一些獎勵,不要再提高他們的空污費,才是給「更大的蘿蔔」。台電代表也表示,目前已經有電廠開始配合政府秋冬降載,但卻沒有獎勵,若是也能納入,將是鼓勵更多電廠願意配合降載。

幾千億的訂單  幾千萬空污費不成誘因

在降低產能一途上,多位業者代表提到,國際市場需求變動快速,他們並無法夏季生產囤到秋冬才賣。電子業者更指出,他們一季的訂單是幾千億,幾千萬的空污費對他們而言誘因不大,而質疑這個政策的效果。面板公會更直指,對於歐美市場來說,因為聖誕節的消費潮,第四季才正是產能最大的時段。

鋼鐵公會更指出,環署要提出這個政策也該顧及台灣的能源政策,夏季一向是國內用電高峰期,台電鼓勵業者在冬季用電,如今環署卻要提高秋冬的空污費率,兩者有矛盾。而國內的勞動力也需要考量,以電弧廠有22家為例,業者要怎麼怎麼臨時增加人手,都是落實這個政策的問題。

對於工業的排放佔全台空污3成,卻總是成為眾矢之的,業者有滿腹苦水,直問為何其他排放來源就是享有獎勵與誘導,製造業卻是面臨處罰,工業局甚至強調,工業佔了全台GDP的三成,很多人都仰賴工業生存。

也有業者反問空保處這些增加的空污費,環署收了之後又打算用在哪裡?玻璃公會更直指,目前的空污境外污染是主因,政府應該與周邊國家進行協商,而非一直對工業。

空保處副處長謝炳輝表示,會再考量這些業者的意見,不過這個既定的政策,雖然原本預定明年一月完成修正恐怕來不及,但仍爭取年後儘早上路。

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