John Snow – The First Epidemiologist

By Atif Kukaswadia
Posted: March 11, 2013

There have been many breakthroughs made off the blood and sweat of Epidemiologists. They have been at the forefront of eradicating polio, smallpox, reducing deaths from cholera and even detecting thalidomide as a teratogen. But if you’re going to talk about the history of epidemiology, you have to start with John Snow.

John Snow was one of the first Epidemiologists, and he showed that cholera was water-borne, and debunked the (then-popular) Miasma theory. This Friday, organizations around the world will be marking his 200th birthday. I’ve listed a few events I’m aware of, but if your organization is hosting an event, comment with a link and I’ll add it below. Bonus points for those livestreaming or recording their events!

But lets talk about John Snow.

John Snow

John Snow, The Father of Modern Epidemiology | Picture Courtesy Wikimedia Commons

John Snow was a British physician, born on the 15th of March, 1813. Born in one of the poorest regions of York in the United Kingdom. John Snow apprenticed as a surgeon, before becoming a physician in 1850 and moving to London.

Now, before we get into the Broad Street Pump story, we have to consider the context of the time. Pre-1900′s, the predominant theory behind disease transmission was the “Miasma theory.” In short, this theory suggested that diseases were spread through “bad air.” (Wikipedia link). It was an elegant, but incorrect theory that suggested that particles from decomposed matter would become part of the air, and this “bad air” spread disease. This was before they discovered that cholera was spread through Vibrio cholerae in water, thus debunking the Miasma theory (although it remains as a spell in Final Fantasy).

Cholera Bacteria

The Bacterium Vibrio cholerae | Picture courtesy the Dartmouth Electron Microscope Facility

Back to our hero. As the summer of 1854 wound down, a major cholera outbreak struck Soho, a neighbourhood in London, England. From August 31st to September 3rd, 127 people died of Cholera. Within a week, 500 people had died and around one in seven people who developed cholera eventually died from it. This all occurred within 250 yards of the Cambridge Street and Broad Street intersection.

John Snow came in and started his investigation.

He examined the neighbourhood, and talked to everyone he could. He was looking for an underlying theme that linked these people together. He suspected some contamination of the water, but couldn’t find any organic matter in it, which you would expect under the Miasma theory. However, the more he looked, the more it seemed like the pump was responsible. Almost all the cases of cholera occurred close to the Broad Street Pump. There were only 10 cases that were closer to another pump. Of these, 5 preferred the water from the Broad Street Pump (and got their water from the Broad Street Pump) and 3 were children who went to school near the Broad Street Pump. The last two were unrelated, and likely just background levels of cholera in the population. This was pretty convincing, but Snow mapped it out to make sure that he was on the right track. You might recognize the map – it’s what we use for our blog banner here on Public Health Perspectives.

The map of all Cholera cases recorded by John Snow. Click to go to an interactive Google Map of the outbreak. | Photo courtesy Wikimedia Commons

Snow provided more evidence for his theory that the pump was responsible for the cholera outbreak. For example, there was a brewery on Poland Street where 535 people worked, that had a pump on the premises. However, while cholera raged outside, only 5 of these people developed it. He explained this by pointing out that those who worked at the brewery were allowed to drink some of the malt liquor they made – and the foreman suspected that they didn’t drink any water at all. And even if they did, they used the pump on site.

The evidence Snow presented in favour of his findings were too compelling for the local council to ignore, and while there was resistance to this finding, Snow had said enough for the local council to remove the pump handle, halting the spread of the disease. But, as Snow later pointed out, he couldn’t be sure that this stopped the disease, and the incidence of the disease might have been declining. But the end result was the same – cholera cases went down.

That is not to say that everyone believed him. The council may have taken the pump down, but it wasn’t until 1885, when Robert Koch identified V. cholerae as the bacillus causing the disease that he had proof of his theory. He was right, but wasn’t around to see this discovery himself.

John Snow died on the 16th of June 1858, at the age of 45. His legacy still lives on, over a 150 years later. Epidemiology-related conferences still feature the Broad Street Pump in their logos and designs (http://www.epicongress2011.org/, http://csebottawa.ca/), and his story is one of the first budding epidemiologists hear. He has also been immortalized by the John Snow Pub at the corner of Broadwick and Lexington Streets in London, England (Google Maps link). Membership in the John Snow Society (http://www.johnsnowsociety.org/) requires you to visit the Pub – another reason to add that to your British vacation plans!

The John Snow Pub

The John Snow Pub in London, England

While our techniques have advanced considerably since then, the basic principles established by Snow still exist in current Epidemiologic thinking.  While some may argue that there were other pioneers of Epidemiology, including John Gaunt, Hippocrates and others, John Snow, if not the first Epidemiologist, is definitely one of the fathers of the field.

Note: A version of this post appeared originally on my blog at MrEpidemiology.com.

Category: History of Public Health | Tagged , , , , | 4 Comments

Drug Resistance in MRSA is Finely-tuned

By Viet Le
Posted: March 5, 2013

Scanning electron micrograph of methicillin-resistant Staphylococcus aureus (MRSA, yellow) surrounded by cellular debris. Credit: NIAID

In hindsight, shoving my hand into a narrow drinking glass wasn’t such a good idea.  I learned this the hard way a few years ago while vigorously scrubbing the inside of a glass with a sponge. When the glass shattered in my hands, one of the shards cut the base of my index finger–right by the the knuckle–and required a trip to the local urgent care center. After being stitched up, I was sent home with some antibiotic ointment, extra gauze, and instructions to keep the wound clean. And that’s when things got worse.

Several days later, my finger became red, inflamed, and tender to the touch. There was also stomach-turning pus oozing out of the wound. Fearing that it was infected, I went back to the the urgent care center where the doctor took one look at my wound and then stated the obvious, “That looks infected.” A swab sample was taken from my wound to start a bacterial culture, which would be used to identify the nature of the infection. Since it would take a few days for the results to come back from the lab, she preemptively started me on a course of antibiotics. At the end of the week, there was a message left on my voicemail. The culture was positive for methicillin-resistant Staphylococcus aureus (MRSA).

MRSA-infected finger

This was cause for concern because MRSA is a bacterial pathogen that, once it enters the bloodstream, can cause severe to life-threatening infections. MRSA is also notoriously difficult to treat because it is resistant to β-lactams, a class of antibiotics generally prescribed as the first line of defense against normal staph infections. β-lactams, which include drugs like penicillin, oxacillin, and methicillin, kill bacteria by preventing the synthesis of bacterial cell walls–without which bacteria cannot survive. These drugs accomplish this by glomming onto and inactivating penicillin-binding protein (PBP), an enzyme that makes an essential component of bacterial cell walls. MRSA strains, however, are resistant to β-lactam drugs because they carry a gene called mecA. The mecA gene encodes a different form of penicillin-binding protein, PBP2a, which β-lactam drugs cannot inactivate, thus allowing normal cell wall synthesis to occur even in the presence of these drugs.

Methicillin-resistant Staphylococcus aureus (MRSA) Bacteria

Scanning electron micrograph of methicillin-resistant Staphylococcus aureus bacteria (yellow, round items) killing and escaping from a human white cell. Credit: NIAID

MRSA infections have long been associated with health care settings such as hospitals and nursing homes. These settings, characterized by a sick general population coupled with high antibiotic usage which selects for drug-resistance, are a perfect environment for MRSA strains to gain a foothold. Given that I had my stitches done at an urgent care center I just assumed that’s where I came into contact with MRSA.

In recent years, however, community-acquired MRSA (CA-MRSA) infections have been on the rise. These are infections contracted from settings like schools, childcare centers, gyms, and prisons. Infections caused by CA-MRSA strains are a particular concern because they are more virulent, spread more rapidly, and can cause more severe infections than its healthcare-acquired MRSA (HA-MRSA) counterparts. What’s worse is the line between the two are blurring as HA-MRSA strains move out into the community and CA-MRSA moves into the hospitals. Because of the increased virulence of CA-MRSA strains there are fears that these strains will eventually replace HA-MRSA strains in healthcare settings–although a recent model published in PLOS Pathogens suggests otherwise[1].

How MRSA developed β-lactam resistance is still unclear. While there are quite a few different strains of MRSA (some of which have also developed resistance to other classes of drugs) they all carry the mecA gene. The mecA gene, in turn, is part of a larger piece of foreign DNA known as the SCCmec element, which is not normally found in S. aureus. Since bacteria are quite adept at exchanging DNA with each other, scientists speculate that the SCCmec element found its way into a normal staph strain from an as-of-yet identified trading partner. This process of swapping and transferring DNA is known as horizontal gene transfer.

Interestingly, MRSA has a finely-tuned, “on-demand system” that turns mecA expression on in the presence of β-lactam drugs, while keeping expression turned off in the absence of these drugs. This regulation is carried out by proteins whose genes are also found on the SCCmec element. In the absence of β-lactams–when the bacteria doesn’t need the drug-resistant PBP2a protein around– the expression of mecA is kept in check by the protein MecI. MecI binds to the DNA promoter region of mecAand prevents gene transcription. However, in the presence of β-lactam drugs the bacteria needs PBP2a around in order to survive. In this case, expression of mecA is turned on through the action of the cell surface protein MecR1 whose job is to keep an eye out for β-lactams. When MecR1 detects the presence of β-lactams, it instructs the bacterial cell to break down the MecI inhibitor. This allows expression of the mecA gene that is essential for the bacteria’s survival to occur.

Figure 10. Model for the mecA induction by MecR1-MecI-MecR2.In the presence of a β-lactam antibiotic, MecR1 is activated and rapidly induces the expression of mecA and mecR1-mecI-mecR2. The anti-repressor activity of MecR2 is essential to sustain the mecA induction since it promotes the inactivation of MecI by proteolytic cleavage. In the absence of β-lactams, MecR1 is not activated and a steady state is established with stable MecI-dimers bound to the mecA promoter and residual copies of MecR1 at the cell membrane [2].

Recently, researchers from Portugal have identified and characterized another gene on the SCC element called mecR2 [2]. As it turns out the MecR2 protein is another component of the finely-tuned, “on-demand system”that regulates mecA expression.  When MRSA bacteria encounter β-lactam drugs it starts ramping up the production of MecR2 protein. MecR2, in turn, knocks the MecI inhibitor protein off of the mecA gene promoter, thereby increasing mecA expression. The researchers speculate that the dislodged MecI protein becomes unstable and is then degraded inside the bacterial cell.

Importantly, the researchers demonstrated that in order to get the optimal expression of mecA that would confer resistance to β-lactam drugs, the bacteria needed MecR2 protein around. When they removed the mecR2 gene, the bacteria once again became sensitive to the β-lactam drug oxacillin, which coincided with a decrease in mecA expression. This research not only helps further our understanding of drug resistance in MRSA but also highlights new targets for therapeutics. For instance, drugs could be designed that either short circuit the ability of MecR1 to alert the bacterial cell to the presence of β-lactam drugs or prevent MecR2 from dislodging the MecI inhibitor from the mecA promoter, thereby keeping mecAexpression in check.

As for my finger and me, we made it out of the MRSA scare relatively unscathed–other than a barely noticeable scar at the base of my index finger. Once the lab results came back positive for MRSA, the doctor switched my prescription to Bactrim. Luckily for me, I wasn’t dealing with one of the multi-drug resistant varieties of the bug so the infection cleared in a few days.

References:

1. Kouyos R, Klein E, Grenfell B (2013) Hospital-Community Interactions Foster Coexistence between Methicillin-Resistant Strains of Staphylococcus aureus. PLoS Pathog 9(2): e1003134. doi:10.1371/journal.ppat.1003134

2. Arêde P, Milheiriço C, de Lencastre H, Oliveira DC (2012) The Anti-Repressor MecR2 Promotes the Proteolysis of the mecA Repressor and Enables Optimal Expression of β-lactam Resistance in MRSA. PLoS Pathog 8(7): e1002816. doi:10.1371/journal.ppat.1002816

 

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The Problem with “Fighting” Cancer

By Atif Kukaswadia
Posted: February 26, 2013
B0007784 Lung cancer cells

Lung Cancer Cell by wellcome images | CC BY-NC-ND 2.0

Last time I spoke to you about wording and public health, and the unintentional impact that can have on people. I want to continue on that theme today, and talk about what is perhaps one of the most pervasive, and more controversial language choices that we as as a society have made: the military language we use around cancer. Often, the media (and by extension, society) describe someone with cancer as a “warrior” who “battles” cancer. This language isn’t rare, and has been around since the mid-70s when Susan Sontag wrote her book “Illness as a Metaphor.” Research by Seale (2001) states:

News stories commonly feature sports celebrities with cancer, as well as sporting activities by ordinary people with cancer, designed to generate a sense of (usually successful) personal struggle.

The usually successful component is what results in problems. When we take the metaphor further, we describe it as “conquering cancer” when cancer goes into remission, or describe someone as a “survivor” of cancer. This is then further complicated by how medical professionals and researchers use the term “survivor” as they will have a very specific definition in mind. Some research studies use a five-year survival window following diagnoses, (see the Coleman study referenced below), while the CDC says:

The term cancer survivor refers to a person who has been diagnosed with cancer, from the time of diagnosis throughout his or her life.

This makes all the difference. “Survivorship” for research is a very precise, very defined term. It may not be the same as what an individual defines as being a survivor, and some definitions (such as the one above) may not include anything about quality of life following diagnosis. But even when cancer goes into remission, there’s still a worry that it might come back, and so the term “survivor” may be a misnomer.

On the surface, I get why we use this language. The language is meant to be positive – it’s meant to evoke support. It’s a tough and trying time, and family/friends/colleagues want to provide help in an way they can. So we follow the template set for us by the media and charities to try and help, as words fail us. I should point out though that this language (i.e. “surviving” “battling” “conquering”) isn’t used exclusively for military metaphors; it can also be used in a religious sense, or used in conjunction with sport metaphors, and there are distinct gender differences in how cancer is reported between men and women in the language and imagery we use.

But what’s the other side of that conversation? Someone who “loses” their “fight” against cancer? Someone who has “fallen”? And to take it to the extreme, would they have “made it” if they “fought harder”? Kristen Garrison writes:

How can a woman with metastatic bone lesions read Lance Armstrong’s story of conquering the disease and feel anything but failure? His story may be true, but does not represent the average person, and such narratives, which get so much press attention and bookshelf space, undercut the comparably determined but unsuccessful efforts of people fighting cancer.

There’s a negative side to that language that is coming out, as those diagnosed with cancer speak up. Blogs and social media give people a platform from which to voice their displeasure and connect with others who feel the same way. Heather Cleland (herself diagnosed with cancer) writes:

The language around cancer—of “battles” fought, won, lost, and succumbed to—fails to consider the sheer chance of it all. Sure there are cancers that we bring upon ourselves, but most are a result of the tiniest bits of bodies going rogue for reasons we’ve yet to understand. To speak of lost battles as though the warrior didn’t want victory badly enough projects our proclivity to control outcomes onto something that cannot be controlled.

In the same vein, I recommend these two pieces written after Canadian politician Jack Layton passed away by Carly Weeks and Edward Keenan. Both discuss the outpouring of support for Jack Layton that described him as “losing his fight against cancer” and the issues around those word choices. Similarly, other people have spoken up; some notable pieces include Beyond Breast Cancer, an open letter by Aria Jones and finally, an excellent piece by the late Julie Mason. There are a number of people who are against the current language choices we made, and I think they raise some very valid and very compelling points.

While some people may not like the metaphor, some might find strength and solace in it. For those, this language helps them, and if they want to consider themselves a warrior, all the power to them. That’s their decision and their prerogative. The Canadian Cancer Society sums it up well:

You may feel like a “survivor” or have heard the term used in conversation. But what does it mean? It means different things to different people. You may not like the way the word is used, or you might feel that it doesn’t apply to you. But the word “survivor” helps many people. It can be powerful, and for some, it’s a positive way of looking at themselves. Using it helps them to cope with their life after cancer.

 

References

Seale, C. (2001). Sporting cancer: struggle language in news reports of people with cancer. Available at: http://onlinelibrary.wiley.com/doi/10.1111/1467-9566.00254/abstract

Seale, C. (2002). Cancer Heroics: A Study of News Reports with Particular Reference to Gender. Available at: http://soc.sagepub.com/content/36/1/107.abstract

Coleman et al. (2008) Cancer survival in five continents: a worldwide population-based study (CONCORD). Available at: http://www.ncbi.nlm.nih.gov/pubmed/18639491

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What determines health?

By Lindsay Kobayashi
Posted: February 19, 2013

Health inequity is a global and a local problem.
Image source: Caro’s Lines CC BY 2.0, 2008

Epidemiologists are concerned with uncovering the factors in populations that determine who gets sick, who stays healthy, who lives, and who dies. Human life is inherently social, and looking toward our societies and geography can help explain who is healthy or sick, and why. “Location, location, location” is a mantra that rings true with respect to life expectancy. In Canada and the United States, men can expect to live to 79 or 76 years, respectively, while women can expect to live to over 80 years. The story is similar for most wealthy and developed countries. By contrast, take Afghanistan or any of several sub-Saharan African countries, where a baby born today could expect to live until his or her mid-40s or 50s.

Temporarily setting aside biologic limitations on health (a loaded issue for another blog post), human-made health limitations clearly exist in our world. A person’s life chances greatly depend on where he or she is born and some people do not reach the same level of health achievable by others. Inequities in life expectancy exist within countries as well: Canada-wide, women residing in the poorest neighbourhoods live two years less on average than women residing in the richest neighbourhoods, and this difference is four years for men. This striking inequity brings us back to the original question: What determines health?

Assuming that human biology is roughly equal between rich and poor places, whether they are neighbourhood or country, we must turn to social factors to answer this question. How human society affects health is the focus of social epidemiologists, who grapple with this exceedingly complex issue every day. Two of these scholars, Dennis Raphael and Juha Mikkonen, have compiled a Canadian-specific list of the determinants of health that have social origins (the “social determinants of health”): Aboriginal status, gender, race, disability, housing, early life, education, income and income distribution, employment and working conditions, unemployment and job security, food insecurity, health services, social safety nets, and social exclusion. A comprehensive and straight-forward review of these factors in Canada can be found in their publication, “The Social Determinants of Health: The Canadian Facts“.

Source: “The Social Determinants of Health: The Canadian Facts”

And the fact is that income inequality in Canada is rising. Canada is one of the two OECD countries that saw increases in income inequality over the past two decades. The Canadian middle class is “hollowing-out”, with more people being on the richest and poorest ends of the scale. Knock down the “Occupy” movement all you like, their point still remains a valid concern for health and social well-being that we have not even begun to solve. Raphael and Mikkonen’s social determinants of health are all influenced at the structural level by governmental policy and society. Our solutions to health problems, however, are mostly relegated to the health sector, which can only attempt to bandage the wound. Any real solution to inequities in health and life expectancy must come from sectors outside of health that can address the structural “root causes” of health inequities.

What role do epidemiologists have to play? Understanding the social determinants of health will allow us to frame our work within the societal landscapes of the places in which we conduct our research. This understanding will allow us to indirectly address health inequities by ensuring that our research, from recruitment and data collection to knowledge translation, is undertaken with inequity in mind, and to answer big research questions such as, “how do our ever-changing social landscapes and governmental policies affect health and health inequities in society?”. A role does exist for scientist-as-advocate, because the overall objective of all epidemiologists (and health scientists for that matter) is to improve health and reduce disease in populations. A critical understanding of our society’s role in the unequal distribution of health and disease is only our first step.

This blog post was originally published as a guest post on Atif‘s blog, Mr. Epidemiology, on March 14, 2012.

Correction Feb. 22, 2013 – Juha Mikkonen’s name was incorrectly spelled as “Jukka” in the original posting of this article. Apologies, Juha.

Category: Uncategorized | 1 Comment

The Public Health Problem of Anti-LGBT Bullying

By Jason Silverstein
Posted: February 12, 2013

Bullying of LGBT teens is a serious public health problem. To address it, we must start with legislation to overhaul school environments. Only fourteen states specifically protect LGBT students from bullying. And there is no federal law. But two bills could change this – if Congress acts.

Bullying poses serious mental and physical health risks – and the risks are greatest for LGBT teens. They suffer from an increased risk of depression, anxiety, and suicide attempts. School doesn’t only feel unsafe – though that’s the experience of 71% of rural and 62% of suburban kids. School is unsafe for nearly one of five, who have been physically assaulted. When school feels and is unsafe, it’s the last place these kids want to be – and, when there, some of the smartest can’t excel.

Our schools do not protect them. But this could change in the 113th Congress. Two bills are expected to be reintroduced. Both bills amend existing law. First, the Safe Schools Improvement Act (SSIA) would amend the Safe and Drug-Free Schools and Communities Act. It would require federally-funded schools to prohibit bullying on the basis of sexual orientation and gender identity. It would also require states to report cases of bullying to the Department of Education. The second bill is the Student Non-Discrimination Act (SDNA). It is modeled on Title IX, which prohibits discrimination on the basis of sex. Likewise, the SDNA would prohibit discrimination on the basis of perceived sexual orientation and gender identity. But both bills have failed before.

“Loneliness.” Ktoine. CC BY 2.0, 2011.

There’s reason to believe legislation could help fix the public health problem. Not only do most states not protect LGBT students, but some states have statutes or policies that staff must “remain neutral on matters regarding sexual orientation.” But these neutrality policies are often only neutral in name. Recently, Tennessee’s ‘neutrality’ policy resurfaced. Commonly known as the “Don’t Say Gay” bill, the proposed bill would ban any discussion of homosexuality – except, in its latest incarnation, for teachers who must report suspected homosexuality to a student’s parents. Even though the bill’s official title is the “Classroom Protection Act,” it’s obvious that the bill would subject LGBT teens to increased stigma, social isolation, and eliminate safe pathways to report harassment.

Even when students have pathways to report, some remain silent out of fear. But it is not always a fear of retaliation by another student. It may be the fear of teachers, administrators, and officials who help create an anti-LGBT environment. In a law review article on finding a legislative solution for ‘bullycide’, Jason A. Wallace explains the reason students failed to report harassment was because a staggering “two-thirds of students hear[d] teachers and school staff make homophobic comments.” We know bullying is often the product of social isolation. But bullying is also the product of social immersion, which makes physical and emotional violence into a routine, often guaranteed by those who are trusted to ensure safety.

Can legislation really help? We already have some evidence that a positive social environment – and anti-bullying policies – reduces the health risk of anti-LGBT bullying. Mark L. Hatzenbuehler’s 2011 study in Pediatrics shows that a supportive social environment reduces suicide attempts by LGB teens. Hatzenbuehler created a novel index of social environment that included five measures: “(1) proportion of same-sex couples living in the counties; (2) proportion of Democrats living in the counties; (3) proportion of schools with gay-straight alliances; (4) proportion of schools with antibullying policies specifically protecting LGB students; and (5) proportion of schools with antidiscrimination policies that included sexual orientation.” Having surveyed 31,852 eleventh-grade students, Hatzenbuehler found that:

Lesbian, gay, and bisexual youth were significantly more likely to attempt suicide in the previous 12 months, compared with heterosexuals (21.5% vs 4.2%). Among lesbian, gay, and bisexual youth, the risk of attempting suicide was 20% greater in unsupportive environments compared to supportive environments. A more supportive social environment was significantly associated with fewer suicide attempts, controlling for sociodemographic variables and multiple risk factors for suicide attempts, including depressive symptoms, binge drinking, peer victimization, and physical abuse by an adult (odds ratio: 0.97 [95% confidence interval: 0.96–0.99]).

While this study doesn’t allow him to identify the precise mechanism, Hatzenbuehler emphasizes one connection. “One potential pathway is through increased exposure to status-based stressors,” Hatzenbuehler writes. Where are these stressors most highly reported? In states that deny LGB adults legal protections.

In response to the suicides of bullied teens, including Billy Lucas, Raymond Chase, Tyler Clementi, Ryan Halligan, Asher Brown, and Seth Walsh, Dan Savage and his husband Terry Miller launched the “It Gets Better” project in 2010. It is a breathtaking project – educational, inspirational, and an important public health intervention. But students shouldn’t have to bear the bad. Their lives should not be sacrificed in someone else’s rite of passage. And what others have heroically overcome does not need to become a part of growing up. The good news is that we can start to repair this public health problem by addressing the social environment of LGBT students. The bad news is that we must depend on Congress to act.

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Meeting your hospital roommates, one q-tip at a time

By Beth Skwarecki
Posted: February 5, 2013

I dropped something on the floor at the hospital.

My parents were visiting me and my one-day-old son, and I dropped something behind the bassinet, something disposable. A diaper, perhaps. My dad, who had spent all his adult life working in hospitals, stopped me from picking it up.

“I know they clean,” he said, “but I never touch anything that’s been on a hospital floor.”

I was, after all, in what comedian Jim Gaffigan calls “the germ-infested building where people go to die.”

Some very scary microbes live in hospitals. They’re the place to be if you’re a nasty germ – convince your host to bring you to a hospital, and you may get a chance to hop a ride on a piece of equipment, or somebody’s unwashed hands, and then – bonus! – have access to a ton of people with compromised immune systems. Hospitals are also a sort of professional conference for the aspiring superbug, exposing germs to antimicrobials and introducing them to buddies who may be willing to share a resistance gene or two.

Aseptic technique and hand washing are standard practice, but drug-resistant superbugs are still a crisis in health care. If we knew more about how microbes live and travel in hospitals, could we prevent infections?

Trillions of roommates

You know by now that your body carries more bacteria than it does human cells. If you are a parent, you know (because all the ads tell you) that everything your child touches is covered in germs. Everyone from high school biology students to Lysol-funded research institutes can swab the surfaces all around you – your toothbrush, your keyboard, the bathroom at the hotel you stayed in – and tell you how many gazillions of microbes there are. Microbes live in antarctica, in nuclear reactors, at the bottom of the ocean and (thanks to us) in space.

Within a year, my son was crawling on the floor of our home, among traces of dust and dog fur and the accumulated microbial communities that sixty years of foot traffic had brought into the house. Some of the germs came from us; we shed more than a billion of our own cells each day, and bacterial cells come with them. Some were from previous occupants. Some were from the factories in distant lands where our things were made.

A microbial community has to come from somewhere, and unless you could autoclave a whole building, there’s no such thing as a blank slate. Your house or apartment begins to take on your personal microbial fingerprint after a few days. What about your hospital room?

The hospital as a body, and a world
Later this month the doors will open on a new hospital in Chicago. It will be already colonized with microbes from its building materials, from the contractors that worked there and the people who toured it during construction; from the dirt and airborne particles that make their way in to all buildings; and other sources besides (like the tap water that flows in every day).

What’s unique about this hospital is that some of those microbes have already been collected and analyzed, and for the next year, an enthusiastic team with a lot of Q-tips is going to swab surfaces in the hospital with an eye to how the bacterial communities change from place to place, and patient to patient. It’s called the Hospital Microbiome Project.

The PI on this endeavor, Jack Gilbert, also works on the Home Microbiome Project and the Earth Microbiome Project. He started out studying microbial communities in moving water; despite strong currents, the same types of microbes could always be sampled from the same spot. Now he’s turned his interest to a different type of current: the motion of people into and out of a place.

A building is a bit like a body – complex, with lots of parts that interact. We have respiratory systems, buildings have ventilation systems. We have digestive tracts, they have plumbing. At the same time, a building (or body) is a world where populations live and interact. It has a climate and seasons; when you turn up the thermostat, it’s a sort of global warming for the microbes in your house.

Could we manipulate the conditions in a hospital to encourage the good microbes to flourish? Are there good microbes in a hospital, or are they only neutral? Opening windows may be a start, says Gilbert, who told the Guardian that surgeons are “constantly sterilising the bejeebers out of their operating room[s]” and that may be a mistake: as in the human body, microbes in a building can be part of its defenses.

After all, we can never totally get away from germs, but maybe we can try to spend our time in the company of good ones.

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Ethnicity and the Genetics of Glaucoma

By Viet Le
Posted: January 29, 2013

By the time you realize that you’re a victim of the “silent thief of sight,” it may be too late. Vision loss due to glaucoma is permanent. Glaucoma, the second leading cause of blindness in the world, is a disease generally characterized by fluid buildup in the eye that increases intraocular pressure (IOP). Over time, the increased pressure damages the optic nerve (image) and leads to the loss of retinal ganglion cells, which transmit visual information from the eye to the brain. This causes progressive loss of peripheral vision and eventual blindness if left untreated (click for glaucoma simulator). Because vision loss is slow, it’s easy for patients not to realize that they are losing their sight until they are bumping into tables and tripping over misplaced shoes.

Eye disease simulation, normal vision

Normal range of vision

Eye disease simulation, glaucoma

A scene as it might be viewed by a person with glaucoma.

Glaucoma isn’t exactly an equal opportunity thief, either. While it is estimated that over 4 million Americans have glaucoma, the prevalence of glaucoma in African Americans and Latino (particularly Mexican) Americans is significantly greater than in Caucasian Americans. African Americans are also more likely to develop glaucoma at a younger age and suffer blindness from the disease. While roughly 90% of all glaucoma cases in the US are what is known as primary open angle glaucoma (POAG), Asian Americans are at the greatest risk of all ethnicities to develop a different form of glaucoma called primary angle closure glaucoma (PACG)(1). The genetic causes underlying glaucoma remain unclear, but these ethnic disparities in the risk of developing glaucoma suggest a genetic basis that is ethnicity-specific.

Recently, scientists have undertaken large scale genetic studies to identify mutations in genes that might contribute to the causes of glaucoma. Identifying these mutations may help in the diagnosis, prevention, and perhaps treatment of glaucoma. These studies, known as genome-wide association studies (GWAS), exploit the fact that DNA sequences between human genomes vary. These sequence variations, called single nucleotide polymorphisms (SNP), occur throughout the genome, including within genes. In many ways SNPs can be thought of as different “spellings” of a gene.

In a GWAS, scientists compare the DNA sequences of two groups of people: one group with a particular trait or condition (in this case glaucoma) and another group without that trait or condition. When a particular SNP keeps popping up within the group that has the condition, then scientists flag that SNP (and the associated gene) as being associated with the condition. This would be similar to comparing books from the UK and the US and noting that the particular spelling of “behaviour” correlates with books from the UK. In some cases, these correlations can give us insight into the causes of a condition.

GWASs have been conducted in the past to identify SNPs that correlate with glaucoma. However, these studies, like two GWASs recently published in PLOS Genetics, have tended to focus mainly on PACG in Caucasian populations (2 & 3). Last year, the results from an exhaustive GWAS were published in Nature Genetics–significant, because rather than POAG, it focused on PACG in Asian populations (4). They report 3 SNPs that correlate with PACG. The first is found in the PLEKHA7 gene, which encodes the protein “pleckstrin homology domain–containing protein 7.” This protein has been implicated in maintaining structures, known as adherens junctions, that help connect cells to each other. In the eye, adherens junctions may help keep cells “sealed” together to prevent fluid leakage. This SNP may affect PLEKHA7’s ability to form a tight seal allowing the fluid buildup in the eye that raises IOP in glaucoma.

The second SNP was found in the gene COL11A1, which encodes one of the α chains of type XI collagen. Mutations in this gene have been associated with diseases that are characterized by hyperopia (farsightedness). Instead of hyperopia, however, the authors speculate that this particular variant might predispose an individual to myopia (nearsightedness), which is a known risk factor for glaucoma. The last SNP that correlated with PACG was located in DNA between two genes, PCMTD1 and ST18. It is unclear how this SNP might affect either genes (e.g. gene expression) and to date no potential connections with glaucoma have been determined for either gene.

It is important to note again that these studies reveal only correlation. The gene variants that these studies turn up may or may not contribute to the onset of glaucoma. For one, either through evolutionary selection or chance, a gene variant and a trait can become correlated in a population without the gene being the cause for that trait. For instance, consider the correlation between red hair and fair complexion. The gene variant for red, which is found most often in northern or western European ancestry, isn’t responsible for their fair complexion. Secondly, not all of these gene variants represent mutations that affect the function of the gene. This is because genes can tolerate some degree of sequence variation without major consequences. Again, thinking about genes as words and SNPs as spelling, we know that “behaviour” and “behavior” mean the same thing despite different spellings. “Two” and “too,” however, are entirely different words and replacing one with the other would dramatically alter the meaning of a sentence. One of the challenges that scientists face upon identifying a SNP by GWAS is determining if that SNP is simply an alternative spelling or a “typo” that carries with it consequences that impact health.

Currently, there is no cure for glaucoma. While a study from last year reported that human stem cells were able to partially restore vision in rats with damaged retinal ganglion cells, stem cell treatment for glaucoma in humans is still a long ways off. Therefore, prevention remains the best strategy against glaucoma. Even though IOP or ocular hypertension is one of the most dependable risk indicators for glaucoma, measuring eye pressure alone is often not enough. The NIH recommends dilated eye exams where “drops are placed in the eyes to dilate, or widen, the pupils. This allows an eye care professional to examine the optic nerve for signs of damage and other possible problems.”

Unfortunately, the ethnic disparities do not end with the risk of developing glaucoma. A recent report indicates that Hispanic Americans are least likely of any ethnic group to “get routine follow-up testing to make sure their vision wasn’t getting worse.” While I am unaware of any large scale GWASs conducted on populations of African or Latino descent, the rates of glaucoma are expected to increase dramatically for African and Latino/Hispanic Americans. Coupled with a fast growing Asian American population improving screening and diagnosis of glaucoma in minority groups will be critical in safeguarding their vision from being stolen.

*January is Glaucoma Awareness Month.*

References:

1. Stein JD, Kim DS, Niziol LM, Talwar N, Nan B, Musch DC, Richards JE. Differences in rates of glaucoma among Asian Americans and other racial groups, and among various Asian ethnic groups. Ophthalmology. 2011 Jun;118(6):1031-7. doi:10.1016/j.ophtha.2010.10.024.

2. van Koolwijk LME, Ramdas WD, Ikram MK, Jansonius NM, Pasutto F, et al. (2012) Common Genetic Determinants of Intraocular Pressure and Primary Open-Angle Glaucoma. PLoS Genet 8(5): e1002611. doi:10.1371/journal.pgen.1002611

3. Wiggs JL, Yaspan BL, Hauser MA, Kang JH, Allingham RR, et al. (2012) Common Variants at 9p21 and 8q22 Are Associated with Increased Susceptibility to Optic Nerve Degeneration in Glaucoma. PLoS Genet 8(4): e1002654. doi:10.1371/journal.pgen.1002654

4. Vithana EN, Khor CC, Qiao C, Nongpiur ME, George R, Chen LJ, Do T, Abu-Amero K, Huang CK, Low S, Tajudin LS, Perera SA, Cheng CY, Xu L, Jia H, Ho CL, Sim KS, Wu RY, Tham CC, Chew PT, Su DH, Oen FT, Sarangapani S, Soumittra N, Osman EA, Wong HT, Tang G, Fan S, Meng H, Huong DT, Wang H, Feng B, Baskaran M, Shantha B, Ramprasad VL, Kumaramanickavel G, Iyengar SK, How AC, Lee KY, Sivakumaran TA, Yong VH, Ting SM, Li Y, Wang YX, Tay WT, Sim X, Lavanya R, Cornes BK, Zheng YF, Wong TT, Loon SC, Yong VK, Waseem N, Yaakub A, Chia KS, Allingham RR, Hauser MA, Lam DS, Hibberd ML, Bhattacharya SS, Zhang M, Teo YY, Tan DT, Jonas JB, Tai ES, Saw SM, Hon do N, Al-Obeidan SA, Liu J, Chau TN, Simmons CP, Bei JX, Zeng YX, Foster PJ, Vijaya L, Wong TY, Pang CP, Wang N, Aung T. Genome-wide association analyses identify three new susceptibility loci for primary angle closure glaucoma. Nat Genet. 2012 Oct;44(10):1142-6. doi:10.1038/ng.2390

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Beyond Crime and Punishment

By Jason Silverstein
Posted: January 22, 2013

 

We have a problem, you know, and it’s only getting worse. It doesn’t strike us equally – it’s a problem that mostly affects young men, minorities, and people without high school diplomas. It’s worse in the US than anywhere else in the world – and five times as bad in the state of Louisiana than it is in Iran. Its survivors usually don’t make good advocates – not while they fight for employment, hold onto their families, and, in some states, lose the right to vote. The problem of mass incarceration is a problem some don’t want to address, because the felon class represents those who must have known they would trade for their crimes a piece of their lives. But the health risk of prison doesn’t end when their sentences do. In some cases, it has only just begun – and not just for them.

It is one of the great ironies of American society: prisoners are constitutionally guaranteed healthcare, but former prisoners are not. The prison health paradox is one dramatic way to think about the health disparities of impoverished minorities in the United States. In 2010, Evelyn Patterson found that “prison appears to be a healthier place than the typical environment of the nonincarcerated black male population.” Indeed, during incarceration, black-white mortality differences vanish. But once released, we see something else entirely. The mortality rate skyrockets. The deadliest time is the first two weeks after release, when former inmates have a 12.7 times higher risk of death than the general population and a 129 times higher risk of drug overdose.

One explanation is that prisoners are often returned to their old neighborhoods – and returned to their old risk factors for homicide and drug overdose. This cycling to and from prison has been called “coercive mobility,” as it concentrates people with fewer and fewer resources into smaller and smaller areas. But another explanation is poor transitional planning. For example, poor transitional planning for prisoners with mental illness translates into an excess risk of suicide within the first weeks that follow release. But this is not only a short term problem. Because there is a long term health problem that former prisoners face that is not infectious, mental, or violent: the problem of being former prisoners.

“Jail.” 826 Paranormal. CC BY 2.0, 2010.

Former prisoners pay a social penalty for incarceration – and it affects their health and their community. Former prisoners are doubly disadvantaged as they struggle for employment and they are eliminated from welfare. In a recent Annual Review of Public Health article, we learn that “a prison record eliminates eligibility for public assistance such as food stamps, public housing, and student loans.” A prison record also reduces the ability of former prisoners to find employment – especially employment that provides suitable health care coverage. Medicaid may not be an option for them, or at least not an easy one, since 90% of states withdraw Medicaid coverage once an inmate’s sentence begins. Not only does incarceration disrupt employment, which we know affects health status, but also marriage, which is another indicator of physical health. Marriage and employment are “two key tenets of adult health,” Michael Massoglia writes, which disproportionately impact African Americans.

In the Du Bois Review’s special issue on “Racial Inequality and Health,” three sociologists discuss the ‘spillover effect’ of incarceration. That is, parental incarceration harms children, especially those who live in areas highly concentrated with former prisoners. In her article, “Punishment Beyond the Offender,” Megan Comfort shows how children may be collateral damage in the exercise of the state’s punishment. Beyond the offender, their children become exposed to risky behaviors that decrease their life chances and increase their risk for mental illness. These children often end up funneled into the criminal justice system themselves.

The people most likely to suffer the negative health effects of incarceration are also the people most likely to already suffer from health disparities. Because African Americans are incarcerated at a rate higher than whites, racial health disparities are ultimately worsened by the effects of incarceration. In their Du Bois Review piece, Schnittker, Massolgia, and Uggen remind us that the mass in mass incarceration “is indeed ‘mass’ in the sense that it is now large enough to affect an entire demographic group.” In Michelle Alexander’s The New Jim Crow: Mass Incarceration in the Age of Color Blindness, we learn that more African American men are imprisoned today than enslaved in 1850. Incarceration does not only threaten the long-term health of individuals, but entire communities. In a justice system plagued by racial bias, incarceration threatens the health of an entire race.

Incarceration has become a feature of American life. We are told incarceration creates a barrier between the criminal class and innocent civilians. Incarceration keeps us safe. Why should we help those who threaten us? But inflicting social, civic, and political penalties on former prisoners does not reduce criminal behavior; it only encourages it. We should focus on strengthening transitional services to facilitate reintegration – in both our prisons and jails – and release the punitive grip on healthcare, welfare, housing, voting rights, and student loans. Or else we risk cementing health disparities in the name of a questionable justice.

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The Under-Recognised Public Health Problem of Food Waste

By Lindsay Kobayashi
Posted: January 15, 2013

Image source: Getty Images

Last week, the Institution of Mechanical Engineers published a chilling report on the problem of global food waste. They estimated that 30-50% of all food produced on the planet is lost or wasted before it can be consumed. That is between 1.2 and 2 billion metric tonnes of food. This damning figure has implications for every single person living on this earth both today and in the future.

First off, the reasons for food loss and waste vary by global region. Helpfully, the authors of the report divided the globe into three broad groups based on stage of economic development where this variation occurs. In countries at early stages of development and industrialisation, such as several countries in Africa, food loss occurs at the earliest point in the supply chain: at the level of the farmer and producer (1). The report cites inefficient harvesting, inadequate transportation, and poor infrastructure as the main reasons for food loss in these regions (1). The second group is countries in late stages of development and industrialisation, such as China, and the third is fully developed and post-industrial societies, such as those in Europe and North America (1). Not surprisingly, food waste occurs closer to the level of the consumer in more developed societies, with most wastage occurring at supermarkets and in people’s homes (1). For example, consumer demand for fresh, physically attractive fruits and vegetables means that supermarkets will not purchase produce that does not meet marketing standards (1).

There are several consequences of food loss and waste. The amount of water, land space, and energy used in producing never-consumed food is staggering. As our global population grows over the next few centuries, this ancillary wastage will become an even direr problem for environmental sustainability. The IME report states that almost 4 trillion cubic metres of water are currently used by the global population per annum with about 70% of that used for food production (1). According to population growth forecasts, the amount of water estimated to be required for food production alone by 2050 is 10-13 trillion cubic metres, a 2.5-3.5 fold increase (1). Second, the report states that about half of the usable land surface area on our planet is currently used for agriculture (1). Expansion of agricultural land use is of course not ideal, as we need the unused land to support the earth’s ecosystems. However, population growth and increasing demands for meat-based diets (raising animals requires considerably more land space than growing produce (2)) mean that more land is likely to be used for food production, at cost to the environment. Finally, the fertiliser, pesticides, machinery, and transportation required for food production use energy, often in the form of fossil fuels (1). Food wastage contributes to global warming and again, as our population grows, this is likely to only increase in future.

Because food loss and waste is inextricably linked to the health of our environment and societal attitudes toward food production and consumption, it is also fundamentally tied to human health.  Major issues of under-nutrition in many developing countries and over-nutrition in developed countries are given a deep and interesting context when considered in light of the mostly infrastructure-based reasons for food loss in the former group and the consumer-based reasons for waste in the latter. In sub-Saharan Africa, food loss due to inadequate infrastructure during the production to retailing process is estimated at just over 150 kg/year per capita (3). Many countries in this region are among those with the greatest proportions of children under age 5 who are moderately or severely underweight. Clearly, improved and efficient food production technology and infrastructure is sorely needed to improve the health of populations in these countries. By contrast, the branding of food as a consumer product in developed countries such as those in North America displays societal attitudes to food in these countries as disposable, plentiful, and of low value. The correlation between these attitudes and population obesity rates in rich countries can be no accident. Rather damning for rich, privileged countries, this comparison between regions in differing stages of economic development shines a hard light on the gross inequities in food systems across the globe.

Despite this global inequity, food loss and waste are absent from mention in the United Nation’s Millennium Development Goals (4). True, food loss and waste are issues related to the objectives of environmental sustainability, poverty, and global hunger, which are included in the goals. But, the magnitude of the global food waste problem and its potential to escalate in coming generations as the world’s population cannot be ignored. If societal attitudes toward food in rich developed nations were to change to place greater value on food and the nutrition it brings, then perhaps consumer wastage would reduce and diets would shift away from a reliance on packaged and processed foods. In doing so, rates of obesity, diabetes, cancer, and cardiovascular disease would likely decrease in developed countries. In line with the Millennium Development Goals, less food loss and improved food production systems in many developing countries would reduce problems of malnutrition in these places.

Reassuringly, action does seem near in the future. The Institution for Mechanical Engineers made three recommendations in their report: first, that the UN Food and Agriculture Organisation work with the international engineering community to improve technology and programmes for food production; second, that governments developing countries incorporate waste minimisation in future food transport infrastructure and storage facilities; and third, that governments in developed nations create and implement policy to change consumer culture surrounding food (1). A report on food security from the Commission on Sustainable Agriculture and Climate Change from March 2012 contains a similar recommendation regarding food loss and waste (5). Most importantly, governments are beginning to take note: the European Parliament has pledged to reduce household food disposal by 50% by 2020 (6). Whether or not these recommendations and policy will be followed is the next question. In the meantime, we all could use a little bit of awareness and change of practice as individuals to help correct this global problem.

References

1) Institution of Mechanical Engineers. Global Food: Waste Not, Want Not. Westminster, London; 2013.

2) Pimentel D, Pimentel M. Sustainability of meat-based and plant-based diets and the environment. Am J Clin Nutr 2003;78(3 Suppl):660S-663S.

3) Gustavsson J, Cederberg C, Sonesson U, van Otterdijk R, Meybeck A. Global food losses and food waste: extent, causes and prevention. Food and Agricultural Organization of the United Nations, Rome; 2011.

4) United Nations. The Millennium Development Goals Report 2012. New York; 2012.

5) Beddington J, Asaduzzaman M, Clark M, Fernández A, Guillou M, Jahn M, Erda L, Mamo T, Van Bo N, Nobre CA, Scholes R, Sharma R, Wakhungu J. 2012. Achieving food security in the face of climate change: Final report from the Commission on Sustainable Agriculture and Climate Change. CGIAR Research Program on Climate Change, Agriculture and Food Security (CCAFS). Copenhagen, Denmark. Available online at: www.ccafs.cgiar.org/commission.

6) European Commission. Communication from the Commission to the European Parliament, the Council, the European Economic and Social Committee and the Committee of Regions: Roadmap to a Resource Efficient Europe. Brussels; 2011.

 

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The Power of Words

By Atif Kukaswadia
Posted: January 10, 2013
Words

Words are powerful. Photo courtesy ManchesterMonkey

In public health we’re faced with a dilemma. We want to help people – that’s our goal, that’s why we do what we do. But at the same time, we also need to be careful how we approach public health concerns – the last thing we want to do is further stigmatize the very people we’re trying to help. One of the most subtle, but most powerful ways we can either empower or belittle others is in the language we use.

One area at the forefront of this is the field of mental health research. The “traditional” language would be a “X person,” where X refers to any mental health issue. But this isn’t the best language to use. For one, it defines the person by their illness – not by who they are. They have X, first and foremost. Not their interests, their personalities, their hobbies. They’re labelled and defined.

However, there’s been a shift in the language used to be respectful and inclusive. Perhaps the most notable change is that appropriate language now is “person with X.” So for example, you would refer to someone as a person with autism, or a person who is hard of hearing. That shift, while subtle, has huge ramifications. They are no longer defined by one aspect of their personality – that is simply another facet of them, rather than a defining feature. I should point out here though that appropriate language does vary between countries, within countries, and even between individuals. I used the term “hard of hearing” above, but some people may prefer deaf. Some people may be okay with certain language while others are not – person-centric language has not been universally adopted.

The shift in language has also been accompanied with the retiring of archaic and stigmatizing language in favour of more inclusive and respectful language (a comparison of terms available here). Those who work with people with disabilities have been quite proactive about engaging stakeholders along with the individuals they serve, going as far as to set up guidelines and offering information pamphlets (see here, here and here) to help train others, as often people don’t know what the appropriate term is. Other fields are learning, and many are now using a similar approach in their research/public health area.

However, while we’re actively trying to tackle stigma as public health professionals, we’ve also got to consider the effect of the media and how the media reports the same issues that we’re concerned about. Fabiana Kubke over at Mind the Brain had a great post about this following the tragic events of Newtown, CT, highlighting how by adding the word “mental” implies that this is something different to “regular” health. It’s a subtle difference, but once you see it, you can’t unsee it. Why is mental health somehow viewed differently to physical health? Why can’t we refer to it as health? Again, we see how adding a label to something changes how we perceive it.

The Canadian Obesity Network has a gallery of pictures that “portray obese individuals in ways that are positive and non-stereotypical.” Click the image to see more examples (all images are freely available).

My research interest is in obesity, which has had a rocky relationship with the media. It’s something Travis Saunders at Obesity Panacea has discussed with respect to Georgia’s Strong 4 Life campaign, and we discussed the relationship between obesity and the media on a podcast together. The obesity research community is now making an effort, and work spearheaded by Dr Rebecca Puhl at the Rudd Center for Food Policy and Obesity has been at the forefront of bringing awareness to “casual” discriminatory language that is in use. Organizations are slowly providing tools to prevent this; for example the Canadian Obesity Network has a photo album freely available as part of their Perfect At Every Size image bank.

The flip side to the above is when people, with perfectly good intentions, make the situation worse. Perhaps the most powerful article I read around language was “We are not here for your inspiration.” It was posted in response to a picture of a little girl with prosthetic legs running next to Oscar Pistorius with the caption “The only disability in life is a bad attitude.” I highly recommend reading it, and to quote from the article:

… these modified images exceptionalise and objectify those of us they claim to represent. It’s no coincidence that these genuinely adorable disabled kids in these images are never named: it doesn’t matter what their names are, they’re just there as objects of inspiration.

But using these images as feel-good tools, as “inspiration”, is based on an assumption that the people in them have terrible lives, and that it takes some extra kind of pluck or courage to live them.

For many of us, that is just not true.

It’s a brilliant piece, and it highlights how we can (unintentionally) make things worse.

Because really, it all starts with us. If we make a conscious effort to change our language and encourage our colleagues to do the same, we can start the cycle of change. Simple things, like making sure ramps are clear, can make buildings more accessible. Encouraging colleagues and others to use appropriate language, and setting an example by using that language ourselves is the first step to making sure that we don’t hurt anyone by our words.

Special thanks to Shira T, Ally M, Kim F and Hilary B for feedback on this post.

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