May 16, 2005 

Resources

Results of a Home-Based Environmental Intervention among Urban Children with Asthma (PDF)
The New England Journal of Medicine, Vol. 351, 9 Sept 2004
George O'Connor, M.D., Boston University, School of Medicine,  and  one of the Principal Investigators of the Inner City Asthma Study.

Call Notes

Speakers:
 * Jon Samet, Johns Hopkins University
 * George O’Connor, Boston University

Presentation (PDF) by Jonathan Samet, M.D., Chairman of the Department of Epidemiology at Johns Hopkins University, Bloomberg School of Public Health 

Jeanette Swafford, Director of Health Initiatives, Collaborative on Health and the Environment, Co-Coordinator of the Asthma and the Environment Discussion Group:

We expect about seventy  people to be on the call today. Presentations for the call are posted online at www.healthandenvironment.org. Please find Jonathan Samet’s  presentation and the New England Journal of Medicine article that  George O’Connor will use as a guide for his presentation.  We are also putting together a list of references on asthma and  air quality more generally that we will be posting soon.

 On the first call, we discussed outdoor air quality with a presentation by Rob McConnell from USC’s Keck School of Medicine and today we’re pleased to have two speakers who will focus on indoor air quality. We’ll begin with a presentation by Dr. Jon Samet  who is Chair of the Department of Epidemiology at Johns Hopkins  University in the Bloomberg School of Public Health. He’ll  present the current science on indoor exposures and asthma including  onset and exacerbation. He’ll only be able to join us for  the first twenty minutes, so we’ll take a very short Q & A  and let him go. Then we’ll shift gears and hear from Dr.  George O’Connor of Boston University School of Medicine,  one of the Principle Investigators of the Inner City Asthma Study.  He’ll be talking about environmental interventions. A lengthier  question and answer will follow from Dr. O’Connor’s  talk. If you don’t have a chance to ask your question up  front with Jon, please hold it and we’ll address it at the  end of the call.

I’d like to ask Polly Hoppin of University of Massachusetts,  Lowell to frame the conversation today and talk about how this  discussion fits in with our future calls as well.

Polly Hoppin, Program Director, Univeristy  of Massachusetts, Lowell, Co-Coordinator of the Discussion Group  on Asthma and the Environment:

Yes, thank you, and I’m going to be very brief because of Jonathan Samet’s time constraint. We’re thrilled  to have this many people joining our second call and have two such  prominent researchers in the area of indoor environmental interventions.  As Jeanette said, we heard from Rob McConnell about his research  looking at the relationship between outdoor exposures and asthma  onset and exacerbation. This second call focuses on indoor air  exposures. We anticipate our third call in July to focus on what  do we do programmatically to address both indoor and outdoor exposures,  interventions, and policies to address asthma onset and exacerbation  from the environmental side. That call will follow from these first  two calls. In terms of the importance of today’s call, there  has been a real explosion of science on the associations between  indoor air contaminants and asthma, both onset and exacerbation.  There has also been an enormous amount of recent research looking  at the effectiveness of indoor environmental interventions. Both  of these aspects of research have implications for policy and programs  among the range of the kinds of organizations that are participating  in this call, so we look forward to having some rich, detailed  background from both of our presenters and then a discussion about  what the implications of some of this may be for the kinds of programs  and policies that all of us are working on. So, Jon Samet, please  carry on, thank you.

Jonathan Samet, Chair, Department of  Epidemiology, Bloomberg School of Public Health, Johns Hopkins  University:

 I want to say hello to everybody and to the many names that I  recognize who are on the call. I will say that for some of you,  I’ll probably say things that you already know about, or  you’ll perhaps be able to add onto the things that I say.  In the materials I provided I did include some information about  outdoor contaminants, and specifically the USC work. We may want  to come back to it because much of the pollution in the indoor  environment comes from the outdoors. We really have to think of  exposure in an integrated context, recognizing that outdoor air  is an important contributor of some pollutants, especially fine  particles in many indoor environments.

Moving to my slides, the first one I’d like to call attention  to is this diagram called “the changing epidemiology of asthma.” What  we have all been struggling with is to try and understand why this  disease has changed so much from an epidemiological perspective.  It is very clear that prevalence has risen and that the rise of  prevalence is more than simply a tendency to re-label people who  might have had another label in the past, like “chronic bronchitis.” The  prevalence has gone up and I think that the incidence, or the number  of new cases, has gone up. Particularly in childhood, once diagnosed,  this disease persists. There are some very tricky issues related  to how many different kinds of asthma, phenotypes, of childhood asthma  there are

With regard to different symptoms, we ask questions like, how does  early childhood wheezing that is sometimes transient relate to  more sustained wheezing? What we do know is that the prevalence  of diagnosed asthma has gone up, and if we look at some real indicators  at the population level like airways reactivity, we find indication  of an increase and this means that incidence has likely gone up  and therefore there has been a change in risk factors. Part of  our problem in trying to sort this out epidemiologically is that  we do very poorly when we are confronted with a scenario of multiple  changes in disease occurrence like what I’ve shown on this  slide. When we look backwards and say “oh, these occurrences  changed,” then retrospectively we’re handicapped to  see what has changed because we don’t have the data available  that we need. So we then begin to do things prospectively.

Let’s move on to the next slide that says “Two key  questions.” If we view asthma as a disease of gene-environment  interaction, what do we mean when we talk about environmental risk  factors? One of the challenges that we have found far more difficult  than anticipated is identifying the genetic basis of asthma. I  first began research on the genetics of asthma about fourteen or  fifteen years ago when everyone thought that the “asthma  genes” would soon be found. That’s not exactly what  has happened, but if you think of a disease with shared causation,  childhood asthma is clearly familial.

What is the role of environment? Does it actually cause asthma,  in the sense of being necessary to the onset of the disease? Does  having the wrong set of environmental exposures hasten the onset  of the disease, or perhaps make it more serious or sustained? I  think these are questions that we’re only going to sort out  when we have better understanding of the genetic basis of the disease.  We can look at risk factors, some of these are labeled here on  the left: the genes still being characterized, inhaled particles and gases, outdoors and indoors, acute respiratory infection, diet,  obesity, possibly activity level. Then of course, very interesting  theories that the lung’s immunological response to the world,  the so-called “immuno-phenotype” is shaped by early  exposures to allergens and respiratory pathogens, something you  may have heard about called the “hygiene hypothesis.”

 If we look at what might have changed over the last three decades,  the usual indicators of what has been changing in developed countries,  such as particles, and ozone have been dropping. That’s not  the case in all of the mega-cities of the world. As for indoor  air pollution, we don’t have a very good, long-range trajectory  on indoor contaminants. It’s likely that second-hand smoke  is dropping, but we don’t know about the others. Patterns  of respiratory illness are changing, in part, because of day-care,  and diet and obesity have changed, but again, despite the interesting  work, we have no answers yet.

I’ve moved onto my fifth slide that discusses what has changed  in the environment. I think that the configuration of indoor air  exposures has changed. It’s very hard to point to any particular  aspect of the indoor air mix to say this might be important for  childhood asthma, either in terms of onset of new cases, or in  severity of the disease. There has been interesting work on long-present  but poorly studied agents like indo-toxins, for example. Has there  been a changing set of exposures over the last 20-30 years? It’s unclear. One of the myths to set aside is that air exchange rates  have dropped drastically in the last decades, and we are holed  up with a lot of toxins. In general, perhaps newer housing stock  has lower air exchange, but I don’t think we have data that  tightening of homes with increased concentrations of toxins is  critical.

The next slide lists some of the pollutants of concern around asthma  and childhood asthma. Indoors there are many allergens, for example  a substantial portion of homes in the U.S. have dogs or cats: 35-40%.  I have theories that exposures to our pets may be different than  before. By anecdote, when I had a dog as a child, that dog slept  outside, and not in the bed. Cats were not crawling all over, possibly  creating allergen exposures. Fortunately, the prevalence of second-hand  smoke exposure is generally declining, but the home remains a major  locus for exposure. Homes do have a soup of volatile organic compounds; depending on furnishings, products, electronics, we know that these  materials can be measured in homes, but it’s hard to point  to any one of the volatile organics as likely to be key. Nitrogen  oxides, largely from gas stoves and space heaters are still there  and the links to asthma are under investigation. You may have seen  a fairly substantial series of publications coming from the group  at Yale who are studying a large cohort.

 I’m going to point quickly to the Institute of Medicine Report,  on the seventh slide, called “Clearing the Air” that  came out several years ago. This was an evidence-based review of  asthma and indoor air exposures and was the last systematic review  of this topic with an attempt to supply causal thinking to the evidence on indoor air pollution and asthma. You can see that this  slide gets at the development of asthma. There is sufficient evidence  for a causal relationship for dust mites. For second-hand smoke, there is good evidence, not for causation, but for association.  Regarding second-hand, the literature on exacerbation of asthma  is very clear, but the evidence on onset of asthma related to second-hand  smoke is a little more difficult and not quite as convincing.

 The next slide shows factors that are said to cause the exacerbation  of asthma. Second hand smoke, here called ETS, has a causal relationship,  along with biological agents: cat, cockroach and dust mite. In addition, there is evidence for an association of the exacerbation  of asthma with other biological agents (dog, fungi or mold, rhinovirus),  and chemical agents (NO2 and NOX).

 The slide labeled “ETS and Childhood Asthma” comes  from meta-analysis by Cook and Strachan (1997), looking at cross-sectional  studies. There is a clear increase in the prevalence of asthma  and wheeze in second-hand smoke exposure.

 I’d like to flip to the very last slide and skip over the  elegant work you heard about from Rob McConnell. The very last  slide shows the emerging literature on residents’ location  and respiratory disease, in children in particular. There is a  substantial body of literature now, say 10-15 studies looking at  various childhood outcomes including asthma and allergy and proximity  to traffic. This is interesting literature with potentially very  important implications for transportation, urban planning, and  public health. The literature shows that children who live near  traffic are more likely to have respiratory symptoms or perhaps  to have allergic sensitizations and there are some biological reasons  for that which seem plausible. I think that if this literature  bears out to be true, one of the important issues will be penetration  of traffic related pollutants into homes. Homes are very important  because that is where the majority of time is spent.

Jeanette Swafford: I think that we have time for one question.

Question: What about mouse and mouse urine?

Jonathan Samet: The MUS antigen has been looked at, and George  may be the right person to talk about this from the Inner City  Asthma Study. My understanding is that in inner city housing this  antigen can be very widespread and important, and it’s a  well-known sensitizer in work situations. A good example is the  Jackson Laboratory, the world’s largest raiser of laboratory  mice, where sensitization occurs in 25-30% of people. I think the  same phenomenon is replicated in high density housing that has an infestation, and this is a potentially controllable exposure.

Jeanette Swafford: Thank you very much, Jonathan. Let’s shift  gears and hear from Dr. George O’Connor, again he is at Boston  University School of Medicine and one of the Principle Investigators  of the Boston Inner City Asthma Study. When we get to the Q & A  section, please make sure to identify yourself and make sure that  your question is on topic, which today is indoor air quality and  respiratory health. For Dr. O’Connor’s presentation,  please refer to his New England Journal of Medicine article on  the CHE website.

George O’Connor, Boston University School of Medicine, Principle  Investigator, Inner-City Asthma Study:

I will be discussing a specific  study, the inner city asthma study, and in particular a component  of the study, a randomized clinical trial of a home-based environmental  intervention among inner-city children with asthma. One of the  slides that Jon showed from the “Clearing the Air” report  showed a table of indoor exposures that had been linked, either  with a causal degree of evidence or at least an association with  the exacerbation of asthma. If you remember that slide, it listed  cat, cockroach and dust mite allergens as well as dog, fungi, and  rhinovirus infection on the biological side. On the chemical side,  it listed environmental tobacco smoke (ETS) and NO2. Those are  all exposures which have been pretty clearly linked with exacerbations  of asthma and, frankly, most of them are ones which clinicians  caring for patients with asthma can observe very directly with  their patients to bring on asthma attacks.

 When we designed the inner city asthma study, we wanted to come  up with a home-based environmental intervention which was feasible  for a limited amount of money. We were willing to spend up to a  couple thousand dollars per participant for the year-long survey.  We didn’t want an intervention that was going to involve  major renovations to homes, which would be even more costly, and  there has been some work like that done for other studies. We wanted  ours to be a little bit more cost-limited than what would be involved  in ripping out rugs, putting in ventilation, and other major structural  renovations. We wanted our intervention to be multi-faceted, and  to deal with these multiple exposures that I just mentioned, at  least as many of them as we could. Our argument was that since  asthma is aggravated by multiple exposures, that if we dealt with  only one or two of the exposures while leaving the other exposures  un-remediated, we might not be able to accomplish an improvement.  Simply put, if you’re allergic to cats and dogs, and you  get rid of the cat, but leave the dog, can you really expect to  see an improvement? We felt we needed to have a multi-faceted intervention  to deal with the variety of allergens as well as environmental tobacco smoke.

 There is a disadvantage to that design decision, in that our intervention  became a bit of a black box. We had multiple components and a multi-faceted  intervention, so the design does not leave us the ability to disentangle  the different components of the intervention. Our thinking was  that “that’s okay.” If a fairly comprehensive,  multi-faceted intervention isn’t working, then we should  turn our attention elsewhere. On the other hand, if the multi-faceted  intervention let to improvements in asthma morbidity, then future research could try to figure out which component of the intervention  was most important.

 We also decided that we would not have a “sham” control  intervention group. It was a randomized clinical trial, but we  decided that the control arm would not have “sham” devices,  as have sometimes been used in other studies. We didn’t want  to have a HEPA (high-efficiency particulate air) filter lacking  the filter. We didn’t want to do any harm, for example by  having vacuums with fans and no filters blowing air around the  house, conceivably raising dust in the air that could be harmful.  We also didn’t want to dilute the effect of the intervention  by having the control group have a lot of partial environmental  interventions due to the “shams.” For example, some  studies have used mattress covers that are porous and not fully allergen impermeable so that changing covers could lead to a partial  effect diluting the difference. Our decision was that we’d  have a rigidly designed, randomized clinical trial, but without  attempting to come up with a “sham” intervention.

 Our sample consisted of 937 children in seven cities around the  US. They were 5-12 years old, and they all lived in census tracts  where at least 20% of the families were below the federal poverty  level. They all had to have one or more positive allergy skin-test  to an indoor allergen. Of all the children we screened as potentially  eligible, only 6% of the children screened failed to have at lease  one positive allergy skin-test to an indoor allergen, which is  not a surprise because it’s well known that the vast majority  of children with asthma are atopic and will tend to have a positive  reaction to one of these allergens.

 If people are on the website and can go to the PDF of the New  England Journal of Medicine article and can scroll down a few pages until  you get to Table 1, you’ll see the characteristics of the  sample’s allergy skin test sensitivity patterns. Again, these  are inner city children and 68-70% of them had a positive allergy skin test to cockroaches, about 63% were allergic to dust mites,  about half to one or more molds. You can see the prevalences for  the different skin tests: if you go down a little further to the  environmental exposures, you’ll see that about 62% of the  homes had some evidence of cockroach infestation, about 50% of  the homes had one or more current smokers. Water, dampness or leaks  were observed or reported in about 45% of the homes. About 20%  of the homes had a dog, a little less than that had a cat. You  can see that these children are sensitized, to these common indoor  allergens, and many of the kids are multiply sensitized. There’s  a high prevalence of exposure to indoor environmental conditions  leading to exposure to these allergens as well as environmental  tobacco smoke.

 Our intervention was both multi-faceted and tailored to the given  individual. For example, we would do an allergy skin test at the  beginning, and if we found that the child was not allergic to cockroaches,  we didn’t focus on that. However, if the child tested positive  to skin allergy to roaches, then we made sure when we designed  the intervention that cockroaches would be included. Our intervention  included education which was delivered in a number of modules spaced  over five home visits during the year. We designed the modules  based on social learning theory to maximize the benefit that they  would have. We provided HEPA vacuum cleaners and instructions and  demonstration on how they should be used and their role in environmental  intervention for asthma. HEPA filters for the child’s bedroom  were provided whenever there was smoking in the home, or the child  was allergic to pets and there had been a pet in the home recently,  or the child was allergic to mold. It turned out that when we applied  those conditions almost all of the homes got a HEPA air filter  for the child’s bedroom. We provided covers for the mattress,  box spring, and pillows. For children with positive skin tests  to cockroaches, we provided pest control.

 In table 2, we show some of the key results of the study. We collected  symptom results by computer-assisted telephone interviews done  by an anonymous firm that we hired to do this. They had no knowledge  of the intervention group, and did telephone interviews every two  months over the course of the year when we got information on symptoms.  When we looked at symptoms over the twelve-month intervention,  we saw that the number of days per two weeks with symptoms, maximal  symptom days, was 3.39 in intervention group, 4.2 in the control  group, a difference of 0.8 days, nearly a day per two weeks. Reduced  symptoms in intervention, school days missed reduced by .17 days  per two weeks for the intervention compared to the control group.  Unscheduled visits to the emergency room were reduced by 0.35.  Unscheduled visits per year for the intervention group compared  to the control group. These were statistically significant reductions.

 Not every outcome showed an impact of the intervention. For example,  hospitalizations did not show a significant difference, but the  number of hospitalizations was quite small to begin with, and our  study was designed to focus on symptom days over two-week periods.  Similarly, pulmonary function, which was not studied over the whole  year, but at six-month intervals we did two-week epics of pulmonary  testing, and didn’t see any differences in pulmonary function  epics measured every six months.

 What’s interesting is that in looking at year two, we see  that symptom reductions are maintained over the entire second year  of the study, even after the intervention was concluded. The intervention  was a twelve-month intervention, and the reduction in symptoms  persisted for another year. Scroll down to another figure showing  the primary outcome of the study, maximum number of days with symptoms  per two weeks. You can see that the reduction in symptoms occurred  fairly quickly—by two months into it, we could see that reduction,  and then that reduction was maintained over the 12-month intervention,  and for another year after the intervention had ended.

 One final aspect of the study is shown in Table 3. I’m not  going into all the lines of the data. The gist of this is that  when we look at whether the reduction in symptoms was correlated  with reduction in allergens, some measured in the bed, some measured  in the floor, the reduction in symptoms was correlated with the  degree of reduction in the allergen that was obtained. That doesn’t  necessarily constitute proof that it was the reduction in allergen  component of our intervention that caused the clinical benefit.  Keep in mind that it could simply be a marker of how well intervention  was implemented in the specific home. For example, could the HEPA  air filters have been the major component leading to the health  benefits? Maybe the HEPA filters in the children’s bedroom  by reducing exposure to the environmental tobacco smoke was the  major factor, or maybe the major factor was the reduction in the  cockroach allergen? Our study cannot tease that apart with any  certainty. That will remain for future research to see if one can  unravel which component of the intervention was most important.  Our conclusion is that this multi-faceted intervention tailored  to the individual child’s exposures at home and skin test  profile, led to a significant reduction in symptoms and a significant  reduction in unscheduled visits for asthma. Again, there was not a significant reduction in hospitalizations, but we were quite  underpowered to analyze that outcome. Are there any questions?

Question and Answer Period:

Jeanette Swafford: Thank you very much, George. We’d like to  open up the lines. We have about twenty minutes for discussion.

Sandy Ross, Health and Habitat in California: George, could you please  give a general percentage of which symptoms were reduced?

George O’Connor: Yes, I can. If you look at Table 1: at baseline,  based on one interview. Max number of days with symptoms during the  last two weeks was six in both the intervention and the control group  at the time that they were enrolled into the study. Subsequently,  on average, during the course of the twelve months, symptoms were  reduced to 3.39 days in each intervention group, also down to 4.2  in control group. The reduction difference between control and intervention  was about 0.8 days per two weeks, or about one-seventh of the original  six days of symptoms. Probably a more reasonable comparison is the  number of symptoms in the intervention group as compared to the control  group—then that 0.8 days reduced becomes more like a 20% reduction  in the days per year with symptoms.

Richard Kreutzer, California Department of Health Services: Were  you able to do any qualitative assessment of the school environment  as a way to potentially control for a difference in environment that would affect the outcome of the intervention in the home?

George O’Connor: We didn’t attempt to undertake that—it  would be an interesting study, but our focus was on the home environment.

Polly Hoppin, University of Massachusetts,  Lowell: Could you comment  a little bit on what you think your data show regarding cost-effectiveness?

George O’Connor: We have a formal analysis in the works right  now that will eventually be a paper. We estimated the cost of the  intervention to be about $1500-2000 per child. However, we saw the  effects of symptom reduction over two years, so the cost goes down  to about $750-$1000 per year for each year of the follow-up, based  on the lasting effects of the intervention. To look at cost-benefit,  note that hospitalizations were relatively unusual in our study,  but we reduced unscheduled visits for asthma by 1/3 of an unscheduled  visit per child per year. For every three children on whom you spend  $750-$1000 per year, you save one unscheduled visit, which doesn’t  cost $3000. Our study doesn’t demonstrate that you would  save any money by doing this. However, if in addition to healthcare  costs  alone, you factor in quality of life, waking up at night, etc.,  then the gap begins to narrow a little bit. Not sure you could  show the  intervention saves money to direct healthcare costs, but the indirect,  societal costs tell a different story.

Polly Hoppin: Could you also mention the issue of comparability of  costs of this intervention with other pharmaceutical costs?

George O’Connor: An inhaled steroid medication might run $100  per month or more, so if you think of an inhaled, cortico-steroid  medication as costing you $1200 per year, then our intervention,  per year, costs less per year than that. The figure of $750-$1000  per year assumes that the intervention impact lasts only two years.  If the impact of the intervention persisted to three or four years  because people get to keep the HEPA filter and the HEPA vacuum cleaner  and they’ve internalized what you’ve taught them, and  continue to use them. If the benefits occur not just over two years,  but even longer, then the per-year costs continue to decrease in  comparison with year’s prescription of inhaled steroids. Certainly  the cost is less than a year’s worth of inhaled steroids. One  can’t necessarily compare the benefits of the two, as inhaled  steroids have been shown to reduce hospitalizations and mortality,  among other things, whereas our study shows reductions in symptoms  and unscheduled visits, but not necessarily hospitalizations.

Ted Schettler, Science  and Environmental Health Network: Can you  speculate a little bit about the potential interaction of various  factors rather than our tendency to want to disentangle and tease  apart and figure out what the most important contributor is. There  is some data on outdoor air pollutants, how for example, they changed  the allergenicity of the pollen proteins. Is there anything similar  that might be going on in the indoor environment where we need to  look at interactions and multiple factors collectively?

George O’Connor: I think there certainly could be an interaction  between smoking and allergen exposure, for example. Smoking damages  the airway of the epithelium and it leads to a higher risk of the negative effects of allergen inhalation. I think these things are  certainly possible. From a research point of view, that makes life  challenging, if one wants to do some research to tease these things  apart—it becomes all the more difficult to do, looking at effect  modification and so forth. From the point of view of healthcare:  what do we do for our patients and how do we intervene? It makes  intuitive sense that there may well be interactions, but that even  without getting into those details, we know that a multiplicity of things are bad for patients. It stands to reason that an effective  intervention should deal with all of them or as many of them as possible.  It raises an interesting question: armed with data like this, are  we prepared to go out there and implement interventions? Can we go  out there and say, well, we don’t know how it works, know all  the interactions between these exposures, but here’s one study  that shows that if you do a multi-faceted intervention and reduce  multiple exposures, it seems to have some benefit? Should we go ahead  and implement that and let the scientists worry later about how these  things might be interacting? It’s a great question, and there  must be some interactions as you suggest.

Lodie Lambright, Rhode  Island: The conundrum that  I’ve always  faced for the five years that I’ve been in asthma control is, “what  has changed over the past 10-15 years?” Urban children have  always lived in the same environment—why the change in asthma  prevalence rates?

George O’Connor: I can’t answer the question, and I don’t  think anyone else can because I’ve been in the research field  for 20 years since I was a pulmonary fellow. Every year, this is  the big question that Jon raised earlier. Cockroaches haven’t  changed in twenty years. In many ways air pollution is getting better,  smoking doesn’t seem to be becoming more common over the last  twenty years—we don’t know for sure. One thing that may  have changed is things related to “hygiene hypothesis,” early  life respiratory infections are treated with antibiotics. Could this  be an important factor, that kids now are less likely to experience  untreated respiratory infections. Is it indoor allergens, something  about indoor tobacco smoke, diesel exhaust particles? I tend to suspect,  and Jon hinted at this in his talk, that we’ll never know what  the cause of the longitudinal asthma increase over twenty or thirty  years because we can’t go back in time and do a prospective  study starting thirty years ago. That’s why I’ve always  thought that it makes more sense to look at discrepancies like inner  city asthma versus suburban asthma. If there is variation in asthma  occurrence rates that we can see now, we have a better chance to  explain those discrepancies because they’re present now,  and if we can understand why one population has a higher prevalence  of asthma morbidity than another, that may give us a clue as to why  asthma is going up.

 For example, the obesity story—evidence shows that obesity  may be associated with asthma…does it explain the increase  of asthma over last 30 years? We can’t study it directly over  the last thirty years, but we can study what’s going on right  now in ongoing birth cohort studies or other study designs and we show that obesity is related to asthma occurrence, and we see that  obesity has gone up over the last twenty years, then maybe we have  a good story linking the two and we can try to avoid future problems. The key is to look for studies we can do now comparing different  groups to try to explain the discrepancies to re-construct what has  happened over the last thirty years—or maybe we’ll  never know and we can focus on how to avoid asthma in the future.

Kevin Doering, Vermont  Department of Health: I have  a comment on air pollution—I used to work for the EPA as an air pollution  meteorologist, and now I’m at the Department of Health. I think  that there are parameters in air pollution that are on the increase.  National ambient air quality standards notwithstanding (only six  pollutants), things that we’re not measuring appropriately  are on the increase: air toxics, diesel exhaust and particulates,  fine particulates (pm 2.5); in certain urban areas and street canyons,  the amount of vehicle miles traveled has increased incredibly over  the last 10-15 years. The mobile source component of air pollution,  which we are not measuring in EPA or at the state-level, are possibly  impacting or perhaps compounded by, at least in New England, the  tightening up of homes for energy conservation and the increased  use of products that may have an EPA label on them but are not necessarily  passing health muster before they are being used in homes. I think  that there is some increase in environmental exposure not being measured  and it would be hard to go back and measure those differences. One  major thing driving it is the increase in vehicle miles traveled,  and that’s nation-wide.

George O’Connor: That’s a great point. I agree with everything  you said. I also agree that if we can get at that now and look at  differences in asthma occurrence as they are occurring now in relationship  to pm 2.5 or toxics or diesel, or other things that have not been  measured as part of the criteria pollutants over the last thirty  years, we can get very important info that we need to know with respect  to risk factors for asthma. We might be able to apply that to find  out how prevalence has increased in the last thirty years, or maybe  not—but we will have learned something very important. I  can well believe that toxics or diesel or pm 2.5 are playing a  role here.

Greg Reiser, New York  State Department of Health: You didn’t  see any statistically significant changes in your objective lung  function measures. Was there any challenge testing of the children  for Bronchial hyper-responsiveness?

George O’Connor: No, we did not include that. Our focus for  this study in inner-city children was not to try to make this a study  that involved lots of trips with families coming into the study centers.  We had them in for a baseline exam at the beginning of the study,  we tried to get them in for another exam at 12-months, and those  are the only times the children and families had to come in. The  rest was done in their homes or with telephone contact. We tried  to limit it in that regard and as it was, the baseline exam was very  long with a number of questionnaires, spirometry and allergy skin  testing. We felt that methacholine was going to “break the  bank” and I think it would have, in terms of participant  burden. So we tried not to go that way, and our outcomes are mostly  telephone-derived  outcomes.

Susan Kegley, Pesticide  Action Network: Have you looked at all at  home pesticide use? As someone mentioned just a minute ago, air toxics  are known to contribute to asthma when there are occupational exposures.  There are a lot of chemicals people are using, not just pesticides,  but plug-in air fresheners and cleaning products as well.

George O’Connor: We didn’t collect any data on that either.  It’s another interesting area. We wanted to focus on those  things that were identified by the Institute of Medicine, for example,  and by the literature as being the things that were most clearly  related to exacerbation of asthma, especially in our inner-city population.  I’m sure that there are many other things that could potentially  be related to asthma, but we’re not as clear about them. Even  now, I’d say that the science is not clear that the things  you mentioned are exacerbating asthma. We tried to focus on things  that were more known. Those are all potentially things that could  be important though.

Lavinia Weissman, WorkEcology: Did you look at where  the child was located at the time of asthma attack—whether  it was school or home?

George O’Connor: No, asthma symptoms are occurring throughout  the year, on average 3-4 days per week throughout the year of follow-up.  Symptoms happening at home, school, outside, we didn’t try  to pin down location of symptoms.

Carolyn Wysocki, Ecological  Health Organization: What kinds of interventions  were used for cockroaches, rats, and mold?

George O’Connor: For the mold, we instructed families on how  to clean visible mold with a weak bleach solution. We also instructed  them in the importance of dampness as a risk factor for aggravating  asthma. We couldn’t fix leaks that occurred in their homes,  but advised them that if there were leaks it was important to get  them fixed to eliminate dampness and offered to write letters to  their landlords to help get things fixed. We didn’t take  on fixing leaks or structural problems like leaky windows, so that  was mostly education. But also, in terms of mold, HEPA filters reduced  airborne mold spores, and we provided them to any child who had  a positive allergy skin test to mold, so that the mold spores in  the  air could be continuously filtered out. For cockroaches, any child  who was allergic to roaches, and had any evidence of roach infestation  in the home, was provided with Terminex pest control for 12-months  at no cost to the family. We worked with Teminex, a nationwide  company and came up with a protocol that we had them implement,  involving  gel baits, and a few other chemicals that were applied. We tried  to teach families about integrated pest control, storing food in  sealed containers, eliminating access points, etc.

Marie Chan, San Francisco  Bay Area: Can you please talk about the  reason that the control group also showed reduction in incidence?

George O’Connor: Sure, we see that in most asthma studies.  We believe that is an attention effect, sometimes called a Hawthorne  effect. Once people start paying more attention to their disease  because they are in a study and getting phone calls about their symptoms,  they are paying a little more attention to the disease, and symptoms  tend to come down. Another part of it could be regression to the  mean. You enroll people on the basis of the fact that within the  last six months they have experienced some degree of asthma utilization  in last six months. We required that all of our children had been  hospitalized or had two or more unscheduled visits for asthma. When  you recruit a group of asthmatics because they have recently been  rather symptomatic, they will tend to go down once the study starts  as a matter of statistical regression to the mean. Because of these  two effects that take the incidence of symptoms down, it’s  very important to do any study as a randomized control trial with  ongoing check-ins. Pre-post analysis is ineffective, and you need  a control group to judge the intervention.

Jeanette Swafford: Thank you, George, for a very  interesting and informative presentation. Thanks to everyone else  for a very interesting  discussion. Our next call will be July 13 at 9am Pacific, noon  Eastern, and as Polly mentioned, the call topic will be “Putting Science  Into Action,” and will feature case studies of useful ways  to apply the science that we’ve been hearing. Notes and a  participant list will be distributed. Thank you everyone for joining  us today.

[session end]

Participant List:

Carol A. Allen
busylaidy@cablespeed.com

Connie Barker
 President
 Health Council of Marin
 Ecology House
 P.O.1033
 San Rafael, CA 94912
 415-385-9907
 cjbarker@lmi.net

 Myriam Laura Beaulne
 Biologist and Environmental Health Organizer
 Clean Water Fund and Clean Water Action
 The Alliance for a Healthy Tomorrow
 262 Washington Street, Room 301
 Boston, MA 02108
 978-544-3774
 myriam_bio@earthlink.net

 David Brown ScD.
 Environment and Human Health Inc.
 Westport, Connecticut.
 NPAWLET@aol.com

 Phil Brown, Ph.D.
 Professor
 Sociology and Environmental Studies Brown University
 Box 1916 Providence RI 02912
 401-863-2633
 phil_brown@brown.edu

 Marie Chan
 IAQ Steering Committee Member
 Novato Unified School District
 9 Pioneer Court
 Novato, CA 94945-2119
 415-892-4655
 my.ch@comcast.net

 Sue Chiang, M.P.H., M.P.P.
 Safe Playgrounds Project
 Center for Environmental Health
 528 61st Street, Suite A
 Oakland, CA 94609
 510-594-9864
 sue@cehca.org

 Sandra Conant, R.N., M.S.
 Environmental Public Health Tracking Program
 Center for Environmental Health
 Massachusetts Department of Public Health
 250 Washington St., 7th floor
 Boston, MA 02108
 617-624-5757

 Anthony J. DeLucia, Ph.D.
 Board of Directors
 Kingsport Tomorrow
 214 Commerce Street, Suite 103
 Kingsport, TN 37614-0575
 423-246-2017
 delucia@mail.etsu.edu

 Kevin P. Doering
 Environmental Health Program Chief
 Vermont Department of Health
 108 Cherry Street
 Burlington, VT 05401
 802-652-0358
 kdoerin@vdh.state.vt.us

 Steffi Domike
 Coordinator
 CHE Pennsylvania
 c/o PennFuture
 425 6th Avenue, Suite 2770
 Pittsburgh, PA 15219
 412-258-6687
 steffidomike@earthlink.net

 Sara Donahue
 Program Associate
 Environmental Health Program
 Lowell Center for Sustainable Production
 University of Massachusetts, Lowell
 1 University Avenue
 Lowell, MA 01854
 617-848-9253
 sdonahue@envhealth.net

Rhonda J. Duerst, R.R.T.-N.P.S., A.E.-C.
 Asthma Program Coordinator
 Children’s Hospital of Wisconsin
 P.O. Box 1997, MS 736
 Milwaukee, WI 53201-1997
 414-266-2729
 rduerst@chw.org

 Julia Earl, M.S.
 Preventing Harm Minnesota, Coordinator
 C/O Women's Cancer Resource Center
 4604 Chicago Ave. South
 Minneapolis, MN 55407
 612-746-4892
 Julia@wcrcmn.org

 Pamela H. Elizabeth
 Project Director, 'Beating Asthma'
 Neighborhood Health Plan of RI
 299 Promenade Street
 Providence, RI 02908
 401-459-6652
 pelizabeth@nhpri.org

 Monique Ferguson
 Program Director
 Community Toolbox for Children1s Environmental Health
 999 Sutter Street, 4th Floor
 San Francisco, CA 94109
 415-614-9533
 monique@communitytoolbox.org

 Neil Gendel
 Project Director
 Healthy Children Organizing Project Consumer Action
 717 Market Street, Suite 310
 San Francisco, CA 94103
 415-777-9648
 neil.gendel@consumer-action.org

 Michelle Garcia
 Program Director
 Improving Life, One Breath at a Time
 4948 N. Arthur
 Fresno, CA 93705
 559-222-4800 x 13
 mgarcia@amerilungcencal.org

 Jim Glauber, M.D.
 Medical Director
 Neighborhood Health Plan
 253 Summer Street
 Boston, MA 02210
 617-428-7434
 jim_glauber@nhp.org

 Robert Gould, M.D.
 President
 San Francisco Bay Area Physicians for Social Responsibility
 311 Douglass Street
 San Francisco, CA 94114
 408-972-7299
 rmgould1@yahoo.com

 Ani Gupta
 Community Health Program Coordinator
 Center for Environmental Health
 528 61st Street, Suite A
 Oakland, CA 94609
 510-594-9864
 ani@cehca.org

 Mary Jo Harris, R.N., M.S.
 Program Director
 Baltimore City Health Department
 Childhood Asthma Program
 4 South Frederick St.,3rd Floor
 Baltimore, MD 21202
 410-361-9645
 maryjo.harris@baltimorecity.gov

 Michael A. Heumann
 Environmental and Occupational Epidemiology
 Department of Human Services
 800 NE Oregon St., # 827
 Portland, OR 97232-2162
 503-731-4573
 michael.a.heumann@state.or.us

 Cory Holmes, D.P.H.
 Environmental Analyst
 Massachusetts Department of Public Health
 Center for Environmental Health
 Emergency Response/Indoor Air Quality Program
 250 Washington St, 7th Floor
 Boston, MA 02108
 617-624-5757
 Cory.Holmes@state.ma.us

 Polly Hoppin, Sc.D.
 Program Director
 University of Massachusetts, Lowell
 1 University Avenue
 Lowell, MA 01854
 978-934-4941 / 617-524-2365
 phoppin@envhealth.net

 Andrea Hricko, M.P.H.
 Director
 Community Outreach and Education Program
 Southern California Environmental Health Sciences Center for Environmental  Health 1540 Alcazar Street, CHP 236
 Los Angeles, CA 90033
 323-442-3077
 ahricko@usc.edu

 Molly Jacobs, M.P.H.
 Environmental Health Initiative
 University of Massachusetts Lowell
 600 Suffolk St., 5th Floor
 Lowell MA 01854
 978-934-4943
 mjacobs@envhealth.net

 Peggy L. Jenkins
 Manager
 Indoor Exposure Assessment Section
 Research Division
 CA Air Resources Board
 PO Box 2815
 1001 I Street, 5th floor
 Sacramento, CA 95814
 916-323-1504
 mjenkins@arb.ca.gov

 Susan Kegley, Ph.D.
 Staff Scientist/Program Coordinator
 Pesticide Action Network North America
 49 Powell Street, #500
 San Francisco, CA 94102
 415-981-6205 ext. 316
 skegley@panna.org

 Janice J. Kim, M.D., M.P.H.
 Air Toxicology and Epidemiology Section
 Office of Environmental Health Hazard Assessment
 1515 Clay Street 16th Floor
 Oakland, CA 94612
 510-622-3198
 jkim@oehha.ca.gov

 Jane Q Koenig, Ph.D.
 Professor
 Environmental Health
 School of Public Health and Community Medicine
 University of Washington
 206-543-2026
 jkoenig@u.washington.edu
 Mary Frances Kornak, M.P.H.
 DC Department of Health
 Primary Care and Prevention Administration
 202-442-9167
 Mary.kornak@dc.gov

 Mary Kreger
 Project Director
 CAFA Initiative
 UCSF Institute for Health Policy Studies
 3333 California St., Suite 265
 San Francisco, CA 94118
 415-502-4544
 mkreger@itsa.ucsf.edu

 Richard Kreutzer, M.D.
 Chief
 Environmental Health Investigations Branch
 California Department of Health Services
 1515 Clay Street, #1700
 Oakland CA 94612
 510-622-4500
 rkreutze@dhs.ca.gov

 Amy D. Kyle, Ph.D. M.P.H.
 Research Scientist and Lecturer
 School of Public Health, University of California Berkeley
 SPH EHS, 140 Warren Hall MC 7360, Berkeley CA 94720 USA
 510-642-8847
 adkyle@berkeley.edu

 Rebecca Love
 Associate, Health & Environment Programs
 National Environmental Education & Training Foundation
 1707 H StreetNW, Suite 900
 Washington, DC 20006
 202-261-6475
 love@neetf.org

 Sonya Lunder
 Environmental Working Group
 1904 Franklin Street, Suite 703
 Oakland, CA 94612
 510-444-0973
 sonya@ewg.org

 Daniel Luttinger, Ph.D.
 Director
 Bureau of Toxic Substance Assessment
 Center for Environmental Health
 New York State Department of Health
 Flanigan Square, 547 River Street
 Troy, NY 12180-2216
 518 402-7800
 dal02@health.state.ny.us

 Barbara Maco
 U.S. EPA, Pacific Southwest Region
 Environmental Justice Coordinator
 Communities and Ecosystems Division, CED-1
 75 Hawthorne Street
 San Francisco, CA 94105
 415-972-3794
 Maco.Barbara@epa.gov

 Virginia Souders-Mason (Ginger)
 Chair, Marin Beyond Pesticides Coalition
 Health Council of Marin
 Board of Marin Cancer Project
 Grassroots Leadership Network, Environmental Justice Grant
 10 Ash Avenue
 Kentfield CA 94904
 415-456-2849
 ginger@seajay.org

 Rina Mehta
 Project Director
 Health and Environmental Justice Project
 Silicon Valley Toxics Coalition
 760 North First Street
 San Jose, CA 95112
 (408) 287-6707, ext. 316
 rmehta@svtc.org

 Diane L. Matuszak, M.D., M.P.H.
 Director of Community Health Administration
 Maryland Department of Health and Mental Hygiene
 201 W. Preston St., Room 320
 Baltimore, Maryland 21201
 410-767-6742
 dmatuszak@dhmh.state.md.us

 Leyla Erk McCurdy
 Senior Director, Health and Environment Programs
 The National Environmental Education & Training Foundation
 1707 H Street NW, Suite 900
 Washington DC 20006-3915
 202-261-6488
 mccurdy@neetf.org

 Molly Miklosovic, M.P.H.
 Project Coordinator
 Asthma Health Outcomes Project
 University of Michigan School of Public Health
 109 South Observatory Street
 Ann Arbor, MI 48109-2029
 734-764-7136
 mmikloso@umich.edu

 Rachel Morello-Frosch, Ph.D., M.P.H.
 Assistant Professor
 Center for Environmental Studies & Department of Community  Health
 School of Medicine
 Brown University
 Box 1943
 Providence, RI 02912
 401-863-9429
 Rachel_Morello-Frosch@brown.edu

 Sherlina Nageer, M.P.H.
 Environmental Health and Justice Program Manager
 Literacy for Environmental Justice
 800 Innes Ave, Unit 11
 San Francisco, CA 94124
 415-282-6840
 superfundschools@lejyouth.org

 Elena Nicolella
 Centers for Medicare & Medicaid Services
 Boston Regional Office
 JFK Bldg. Room 2250
 Government Center
 Boston, MA 02203
 617-565-1243
 Elena.Nicolella@cms.hhs.gov

 Frieda Nixdorf
 Administrative Specialist
 Collaborative on Health and the Environment
 Commonweal
 P.O. Box 316
 Bolinas, CA 94924
 415-868-0970 ext. 649
 frieda@healthandenvironment.org

 Laura Oatman
 Environmental Research Scientist
 Minnesota Department of Health
 Asthma Program
 717 Delaware Street SE
 P.O. Box 9441
 Minneapolis, MN 55440-9441
 612-676-5049
 laura.oatman@health.state.mn.us

 George O'Connor, M.D.
 Associate Professor
 Pulmonary Epidemiology
 Boston University, School of Medicine
 715 Albany Street, R-304
 Boston, MA 02118
 617-638-4470
 goconnor@bu.edu

 Brenda Olsen, R.N.
 Assistant CEO/Director of Governmental Affairs
 American Lung Association of Florida, Inc.
 539 Silver Slipper Lane, Ste A
 Tallahassee, FL 32303
 850-386-2065
 bolsenalaf@earthlink.net

 Julie Osgood, M.S.
 Program Manager, Clinical Integration
 MaineHealth
 465 Congress Street, Suite 301
 Portland, ME 04101
 207-541-7515
 osgooj1@mmc.org

 Glen Patrick
 Epidemiologist
 Office of Environmental Health Assessments
 Division of Env. Health Programs
 Washington State Dept. of Health
 P.O. Box 47846
 Olympia, WA 98504-7846
 360-236-3177
 g.patrick@doh.wa.gov

 Elise Pechter, M.P.H., C.I.H.
 Industrial Hygienist
 Occupational Health Surveillance Program
 Massachusetts Department of Public Health
 250 Washington Street
 Boston, MA 02108
 617-624-5681
 Elise.pechter@state.ma.us

 Susan Pizzi
 Research Analyst
 Environmental Public Health Tracking Program
 Center for Environmental Health
 Massachusetts Department of Public Health
 250 Washington St., 7th floor
 Boston, MA 02108
 617-624-5757
 Susan.pizzi@state.ma.us

 Stephen C. Redd, M.D.
 CAPT, USPHS
 Acting Deputy Director for Program
 National Center for Environmental Health /
 Agency for Toxic Substances and Disease Registry
 scr1@cdc.gov

 Margaret Reid, R.N.
 Director
 Asthma and Diabetes Prevention and Control
 Boston Public Health Commission
 1010 Massachusetts Avenue, 2nd floor Boston, MA 02118
 617-534-2673
 Margaret_Reid@bphc.org

 Arlene Rodriguez
 Program Officer, Environment and
 Environmental Health and Justice Initiative
 The San Francisco Foundation
 225 Bush Street, Suite 500
 San Francisco, CA 94104
 415-733-8517
 amr@sff.org

 Sandra Miller Ross, Ph.D.
 Health and Habitat
 76 Lee Street
 Mill Valley, CA 94941
 415-383-6130
 healthhab@igc.org

 Ruthann Rudel
 Silent Spring Institute
 29 Crafts Street
 Newton, MA 02458
 617-332-4288 x14
 rudel@silentspring.org

 Ronald H. Saff, M.D.
 College of Medicine, Florida State University
 Allergy & Asthma Diagnostic Treatment Center 2300 Centerville  Road
 Tallahassee, FL 32308
 850-386-6680
 rsaff@aol.com

 Jonathan M. Samet, M.D., M.S.
 Professor and Chairman
 Department of Epidemiology
 Johns Hopkins University
 Bloomberg School of Public Health
 615 N. Wolfe Street, Suite W6041
 Baltimore, MD 21205
 410-955-3286
 jsamet@jhsph.edu

 Lauren Sassoubre
 Research Assistant
 Institute for Health Policy Studies
 University of California, San Francisco
 415-514-0426
 laurens@itsa.ucsf.edu

 Eleni Sotos, M.A.
 National Coordinator
 Collaborative on Health and the Environment
 Commonweal
 P.O. Box 316
 Bolinas, CA 94924
 415-759-1637
 eleni@healthandenvironment.org

 Ted Schettler, M.D., M.P.H.
 Science Director
 Science and Environmental Health Network
 39 Bromfield Street, #2
 Newburyport, MA 01950
 978-462-4092
 tschettler@igc.org

 Greg Siwinski, M.S., C.I.H.
 PI: Indoor Environment and Asthma Intervention Study- Syracuse
 CNY Occupational Health Clinical Center SUNY
 Upstate Medical University Syracuse, NY
 315-432-8899
 siwinskg@upstate.edu

 Jeanette Swafford, M.H.Ed.
 Director of Health Initiatives
 Collaborative on Health and the Environment
 Commonweal
 P.O. Box 316
 Bolinas, CA 94924
 415-868-0970 ext. 792
 jeanette@healthandenvironment.org

 Judith C. Taylor-Fishwick
 Assistant Professor
 Department of Pediatrics
 Center for Pediatric Research
 Eastern Virginia Medical School
 Children's Hospital of The King's Daughters
 855 W. Brambleton Ave
 Norfolk, VA 23510
 757-668-6459
 TaylorJ@CHKD.COM

 Pam Tsai, Sc.D., DABT
 Toxicologist
 US Environmental Protection Agency Region IX
 75 Hawthorne Street (Air-6)
 San Francisco, CA 94105
 415-947-4196
 tsai.pam@epa.gov

 Mily Trevino-Saucedo
 Líderes Campesinas
 611 S. Rebecca St.
 Pomona, CA 91766
 909-865-7776
 liderescampesinas@hotmail.com

 Diana Vanek
 Outreach Coordinator
 Center for Environmental Health Sciences
 University of Montana, Skaggs 155
 Missoula, MT 59812
 406-243-4030
 diana.vanek@umontana.edu
 Maricela Velásquez, B.S.
 Community Health Worker
 CMC-Asthma Educatio