Today’s guest post is from Molly Kile, an environmental epidemiologist and assistant professor at Oregon State University.
Parents with children at home should use ventilation when cooking with a gas stove. We recently published results from our study that showed an association between gas kitchen stove ventilation and asthma, asthma symptoms and chronic bronchitis.
In homes where a gas stove was used without venting, the prevalence of asthma and wheezing is higher than in homes where a gas stove was used with ventilation. Parents of all children should use ventilation while using a gas stove.
We can’t say that gas stove use without ventilation causes respiratory issues, but our study shows an association between having asthma and use of ventilation. More study is needed to understand that relationship, including whether emissions from gas stoves could cause or exacerbate asthma in children.
Asthma is a common chronic childhood disease and an estimated 48 percent of American homes have a gas stove that is used. Gas stoves are known to affect indoor air pollution levels and researchers wanted to better understand the links between air pollution from gas stoves, parents’ behavior when operating gas stoves and respiratory issues.
We found that children who lived in homes where ventilation such as an exhaust fan was used when cooking with gas stoves were 32 percent less likely to have asthma than children who lived in homes where ventilation was not used. Children in homes where ventilation was used while cooking with a gas stove were 38 percent less likely to have bronchitis and 39 percent less likely to have wheezing. Our study also showed that lung function, an important biological marker of asthma, was significantly better among girls from homes that used ventilation when operating their gas stove.
Many people in the study also reported using their gas stoves for heating. That was also related to poorer respiratory health in children, particularly when ventilation was not used. In homes where the gas kitchen stove was used for heating, children were 44 percent less likely to have asthma and 43 percent less likely to have bronchitis if ventilation was used. The results did not change even when asthma risk factors such as pets or cigarette smoking inside the home were taken into account.
Asthma is one of the most common diseases in children living in the United States. Reducing exposure to environmental factors that can exacerbate asthma can help improve the quality of life for people with this condition.
We used data from the Third National Health and Nutrition Examination Survey, or NHANES, conducted by the National Center for Health Statistics from 1988-1994. Data collected for NHANES is a nationally representative sample of the U.S. population. The third edition of the survey is the only one in which questions about use of gas stoves were asked.
Participants were interviewed in their homes and also underwent physical exams and lab tests. We examined data from about 7,300 children ages 2-16 who has asthma, wheezing or bronchitis and whose parents reported using a gas stove in the home. Of those who reported using no ventilation, 90 percent indicated they did not have an exhaust system or other ventilation in their homes.
Lots of older homes lack exhaust or other ventilation. We know this is still a problem. More research is definitely needed but we know using an effective ventilation system will reduce air pollution levels in a home, so we can definitely recommend that.
Today’s guest post is from John Brehm, MD, MPH from the Children’s Hospital of Pittsburgh of University of Pittsburgh Medical Center. He writes…
Vitamin D has become a hot topic of research over the past several years in diseases such as multiple sclerosis, cancer, and heart disease. The association between vitamin D deficiency and asthma is perhaps one of the most compelling, however, with early trial results suggesting that vitamin D supplementation may reduce the risk of asthma exacerbations in children. A large trial is necessary to answer this questions, but designing and conducting a clinical trial of vitamin D supplementation to treat asthma (or any disease) requires overcoming unique regulatory and scientific challenges.
The first challenge when designing a trial of a dietary supplement (which vitamin D is considered) is that the Federal Drug Administration (FDA) has the right to regulate studies of supplements that are intended to cure, treat, diagnose, or mitigate a disease. Dietary supplements are regulated through a different mechanism than drugs, and do not require FDA approval. In order to be used in a study that treats a disease, the dietary supplement must go through a stricter level of scrutiny to ensure that the study drug is free of contaminants, and that the stated dose of the supplement is accurate. That last point is particularly relevant to vitamin D, since a recent study found that commercially available vitamin D3 preparations had wide ranges of variability. Only one manufacturer produced a product with low variability in the stated potency.
Although FDA involvement can be circumvented by studying a “structure and function” related outcome (for example, lung function as measured by spirometry), there are several reasons why this is not preferable, the first of which is to ensure that the drug being used in the study is of the highest quality. Another important reason is that clinical trials should be designed to answer clinical questions that are supported by the previous literature. For asthma, the data strongly suggests that vitamin D insufficiency is associated with higher rates of asthma exacerbations, but the data on lung function is far less compelling. When designing a study that involves hundreds of patients, will take several years to complete, and cost several hundred thousand dollars, the outcome measured should measure an outcome that is both relevant to patients and supported by the literature. Risk of asthma exacerbation is an outcome that meets both of these criteria.
Another unique challenge in the design of studies using vitamin D (in contrast to other supplements) is that individuals produce vitamin D through skin exposure to sunlight. Since children would be randomized to receive vitamin D or placebo, this should not introduce bias, because no treatment arm should be affected more than another. However, one potential concern is that children who are assigned to placebo may be more likely to take extra vitamin D supplements when they get sick. This could occur even in a blinded study, in which children are not aware of whether they are receiving vitamin D or placebo, especially if the children assigned to placebo are sicker. It is important that investigators explain to study subjects that they should not take additional supplements other than what they usually use.
By properly considering and addressing these challenges during study design, we can ensure that a clinical trial of vitamin D supplementation is as free of bias as possible, and more likely to give us an accurate result.
Today’s guest post is from Peter Bingham, Professor of Neurology & Pediatrics at the University of Vermont. He has an interest in pediatric asthma and whether the neurosensory capacity for detecting changes in work of breathing can be developed to improve self management. He writes…
“Did you take your inhaler?” “No.” “You need to take your inhaler.” Even though I’m a pediatric neurologist, I’ve gotten interested in how these conversations between kids with asthma and their family members come about. There are a lot of reasons why a young person with asthma might seem to be ‘the last to know’ that they are having an asthma attack—Denial, Distraction, Dis-liking their medicine, … and what about a fourth “D”: a perceptual Disability for bronchospasm? We don’t usually consider perceptual problems in terms of how we experience our own bodies, but think of this: just as some of us have a fantastic ability to perceive where our bodies are in space—proprioception—we also vary widely in our perception of internal bodily events—interoception. For example, many people with asthma can’t answer the question, am I having to work harder to breathe right now?” because they simply can’t tell, even when it’s obvious to someone else, that they’re working harder to breathe! And it seems that people with the most severe asthma, the ones who are in the emergency room most often, are the ones who have the most difficulty perceiving their asthma symptoms.
One way that researchers have measured this perceptual disability, which ironically is more common in people with asthma, is by asking them if they can detect differences in the amount of work it takes to breathe when breathing through straws of slightly different caliber. Most of us could tell that it’s harder to breathe through a straw of ¼” diameter than through a one inch straw, but what if the straws differ by just a tenth of an inch? This skill is called respiratory interoception, and it’s a great skill for a person with asthma to have, because it could help them to know as early as possible if their “straws” (i.e., their airways) are getting narrower—if their lungs are brewing an asthma attack.
What if a person with asthma could learn to improve their respiratory interoception? Our experience with digital breath-games at the University of Vermont suggests that the answer is yes. We developed a computer game that is controlled by the player’s own breath, as they breathe through a device called a spirometer that measures airflow. We’ve done some preliminary testing in the clinic—enough to show that kids with asthma like playing the games, and that they can learn the “eye-breath coordination” game strategy (that’s where respiratory interoception comes in) pretty quickly. Our next steps will be to see how kids do with the game during an asthma attack (ER-based study), and then to send kids with severe asthma home with the breath-game and see if it helps them tune in to their breathing so they can get hold of their inhalers a little earlier, head off an asthma exacerbation, and increase their symptom free days. We welcome inquiries or comments from interested individuals—contact us through this link.
Today’s guest post is fromAlexander Peyton Nesmith, a Ph.D./M.D. student at Harvard SEAS and the University of Alabama at Birmingham. He writes…
The pharmaceutical industry is currently facing a crisis. The development of a new drug is an incredibly long and expensive process, lasting more than ten years and costing more than $1 billion US. The approval process of a new drug in the United States can roughly be split into two parts: a preclinical phase (i.e. not in human patients) and a clinical phase (i.e. in humans). Unfortunately, just ten percent of the drugs that enter clinical trials after successfully demonstrating that they are both safe and effective in preclinical trials end up getting approved by the FDA. This failure comes after investing roughly $500 million and 5+ years in the failed drug. This is just not a sustainable business model.
But the question is: why are some drugs safe and effective in animals but then go on to be dangerous or ineffective when given to you or me? The answer is probably really complex. But maybe, it is also really simple. When you see a drug get pulled from the market for being dangerous and causing side effects, those effects are usually in just a small percentage of the population. In other words, a drug that works for me may actually harm or kill you. So if there is such a drastically different response to the same drug among humans, it seems obvious to expect an even larger difference to occur between animals of different species! Well, if animals are not predictive of what will be an effective drug in a human, then what is?
At Harvard’s Wyss Institute and School of Engineering and Applied Sciences, our best bet is that the answer is a “micro-human”. That is, building on advances in fields like nanotechnology, stem cells, material science, and tissue engineering, we believe that we can build the simplest structural and functional units of organs like the heart, the lung, the liver, and the airway (and more) from human-derived cells and tissues. Individually, we call these Organs on Chips. But for Organs on Chips to be useful for pharmaceutical companies, they also need to have the ability to model disease.
With this in mind, in this study, we sought to build a device that could simulate both healthy and asthmatic airway function. We chose to focus specifically on airway muscle, as its job is to open and close the airway. As we began this work, we used the human airway as a design template. Replicating the structure of the airway muscle is extremely important for developing healthy and diseased models as there are many examples in medicine where if the normal structure of an organ is disrupted disease results. So we looked at the structure and organization of the muscle within healthy and asthmatic human airways and then used a technique called microcontact printing which enabled us to have precise control over the organization of the muscle. Once we were able to replicate the normal structure of human airway muscle, we wanted to demonstrate normal function. So we employed microfabrication techniques to build a device that would enable culture of this muscle in 2-dimensions but then perform experiments in 3-dimensions. Using a well-established mechanics theory and knowing the material properties of the polymers we used, we were able to calculate the contraction strength of the airway muscle be measuring the bending of thin polymer film.
To confirm appropriate function of our airway muscle, we designed an experiment based of one of the main lung function tests performed clinically: spirometry. In these diagnostic studies, clinicians measure the patient’s ability to blow air out of their lungs. Then, they use a drug called methacholine to cause the muscle to contract and the airway to narrow, then measure again the amount of air a patient can blow out. Here, we used a similar drug to cause our muscle to contract and we measured the contractile strength.
Then, as a proof of principle, we used a chemical released by immune cells commonly found in the airway of asthmatics, called IL-13, which causes changes within the muscle that causes hypercontraction, to induce an asthma condition. We then evaluated our ability to use known as well new drugs to either prevent or restore proper contraction strength.
Moving forward, we hope to partner with pharmaceutical companies to test new drugs.
I’m guilty. I’ve called individuals with asthma “asthmatic.”
To fund my research, I write grants. These grants usually have word limits and when I am over the page limit (which is always), I have a few trusted strategies. One of these strategies has been changing “individuals with asthma,” a phrase that I use hundreds of time into “asthmatic.”
That saves me 15 characters. Hundreds of times in a grant. It never felt right to use the word “asthmatic” but I got the point across while meeting page limits.
I once agreed to shortening the title of a paper to using the word “asthmatic” because the journal asked me to in order to decrease the word count.
I justified this behavior for a couple of reasons.
1. Is “asthmatic” a real word? I looked in the dictionary, and sure enough, asthmatic means an individual who suffers from asthma.
2. I started to ask patients if it was offensive to be called an asthmatic. Everybody I asked thought it was fine.
3. And we do use the words diabetic and arthritic. (Though I think we should stop that too.)
But we aren’t our disease. And we shouldn’t be. It’s not like the slogan, “You are what you eat.” Do we call people with high cholesterol “high cholesterolemics” or people with hypertension “hypertensionatics” or individuals suffering from cancer “cancerers?”
I’m not arguing that the word “asthmatic” should never be used. One might have an asthmatic cough or wheeze, I suppose.
But the 300 million individuals with asthma happen to have one of the most common chronic diseases in the world. They aren’t their disease.
They aren’t asthmatics.
Today’s guest post is from Ruchi Gupta, MD MPH, an associate professor of pediatrics at Northwestern and a physician at Ann & Robert H. Lurie Children’s Hospital of Chicago. She writes about a study she just published in Pediatrics that was conducted in partnership with Chicago Public Schools. The study found that children with asthma and food allergies are left without vital safety net for many hours in school.
Given the amount of time kids spend in school, it’s critical for school staff, clinicians, and parents to make sure there’s a health management plan in place for students with health conditions. Not having a health management plan leaves students without a vital safety net during the school day. With kids now returning to school, this is the time to get it done.
In order for schools to be well prepared to handle these medical conditions, including daily control of their health and emergencies, school personnel need to have a health management plan from the child’s clinician on file. Chronic medical conditions affect up to 25 percent of children in the US, with asthma and food allergies being among the most common.
A health management plan specifies special requirements for the child during school if medications are needed, and what to do in case of an emergency.
Through a partnership between Northwestern’s Center for Community Health and the Chicago Public School Office of Student Health and Wellness, the study focused on understanding the district’s chronic disease reporting and management process in order to better serve the health care needs of students with conditions such as asthma and food allergies.
We looked at the database of Chicago Public Schools, the third largest U.S. school district, to identify students with asthma and food allergies.
The study found only one in four students with asthma and half of students with food allergy had a school health management plan. Students were less likely to have a plan in place if they were a racial/ethnic minority and if they were low income, measured by whether they qualified for a free or reduced-price lunch. This critical study brings to light the underutilization of school health management plans district wide and underscores the fact that the most underserved students are left particularly vulnerable.
Many students also had more than one chronic condition. Of asthmatic students, 9.3 percent had a food allergy; of food allergic students, 40.1 percent had asthma. Students with both conditions were more likely to have a management plan on file.
This is definitely a national problem in schools around the country. We think the situation in Chicago schools is representative of schools everywhere. It’s critical for all students with any chronic condition to have a health management plan in place at school.
This study was funded by Mylan Specialty, LP and Northwestern’s Alliance for Research in Chicagoland Communities.
Today’s blog post is about a recently published study in the Journal of Clinical Immunology. The authors studied lignans and isoflavones, two plant-derived chemicals that are inversely associated with asthma and wheezing. So, the higher the levels of lignans and isoflavones, the lower likelihood of wheezing and asthma.
What are lignans and isoflavones?
- Lignans are found in flaxseeds, wine, coffee, tea, sesame, wheat, and rye.
- Isoflavones are found in soybeans, clover, and mung beans.
Why lignans and isoflavones?
- These two appear to have potent anti-inflammatory and antioxidant effects.
The authors used data from NHANES, a US based survey that included questions on dietary history and urinary levels of lignan and isoflavone metabolites. The study included 9,633 subjects ages 6 to 85 years of age.
- The odds of having current asthma was 0.69 times less if the individual had high levels of enterolactone (was in the highest tertile of enterolactone).
- The odds for nonasthmatic wheeze was half as likely if the individual had high levels of urinary enterolactone.
- And, individuals were 0.64 times likely to have nonasthmatic wheeze if they were in the highest tertile of urinary O-DMA. Nonasthmatic wheeze was defined as having wheezed or had a whistling in the chest in the past 12 months but not having a diagnosis of asthma.
Both urinary enterolactone and O-DMA (metabolite of isoflavones) were inversely associated with nonasthmatic wheezing within the past year. These results were similar among adults and children. Results were also similar among smokers and nonsmokers, having high levels of dietary fiber intake or not.
The authors concluded that interventions to increase levels of enterolactone and O-DMA may help prevent and treat asthma.
Is it time to eat foods to increase levels of enterolactone and O-DMA? I don’t know, but eating whole wheat multigrain bread with flaxseeds, sesame, wheat, and rye for breakfast with tea or coffee might not be so tough.
Yesterday’s post was about the relationship between infection and asthma. Coincidentally, a 10 year old child with asthma drew this picture for me. She said, “When I have an asthma attack, it feels like clogging in the chest. My chest gets real tight. It feels like germs are going in there.”
So, I told her about yesterday’s post — that infections can trigger asthma flares, but persons with asthma are also more likely to have infections.
Here’s her picture….