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Call Notes

Moderator: Polly Hoppin, Sc.D., Program Director, University of Massachusetts, Lowell

Featured Presentations:
1) Ted Schettler, MD, MPH, Science Director, Science and Environmental Health Network
2) John Balmes, MD, Professor of Medicine, School of Medicine, Division of Occupational and Environmental Medicine, University of California, San Francisco
3) Megan Sandel, MD, MPH, Pediatrician and Researcher, Boston Medical Center at Boston University, and member of the Executive Committee of the New England Asthma Regional Council

1) Ted Schettler, MD, MPH, Science Director, Science and Environmental Health Network

Ted Schettler provided us with an overview of the science, the pathophysiology of asthma and some important definitions.

Asthma: A disease of the airways, characterized by airway inflammation, caused by a complex interplay of environmental, genetic and other host factors. If untreated, asthma inflammation may lead to irreversible changes in lung structure, called “airway remodeling.” Once asthma develops, the lungs may be sensitized to a variety of stimuli.

Asthma may be classified as allergic or irritant/non-allergic asthma.

Environmental substances that cause or exacerbate asthma:
1.    Specific Sensitizers – Cause allergic asthma, which can result from a predisposition combined with exposure over time to biological agents (mold, etc.) or non-biological agents/specific sensitizers (pharmaceuticals, heavy metals, and other chemicals).
2.    Non-Specific Sensitizers / Irritants – Cause asthma not mediated by the immune system, so non-allergic asthma. Exposure to lung irritants can result in Reactive Airways Dysfunction Syndrome (RADS), which can occur after a single exposure to a high concentration of a strong irritant gas vapor or fume, although can also be caused by repetitive low-level exposure to susceptible groups of people. A person without prior problems with asthma may develop asthma from an irritant over several weeks.
3.    Adjuvants – Do not specifically up-regulate immune response, resulting in augmented response to specific allergens to people who have allergic asthma (ex. diesel exhaust).

Sources of these substances include ambient air pollution, building related indoor air pollution, occupational exposures, an in-utero exposures (i.e. tobacco smoke).

Mechanisms:
•    The allergic asthma mechanism is an antibody-mediated reaction.
•    Irritant asthma shows the same symptoms as allergic asthma, but not an immune system mechanism.

4 Hypotheses:
1. Following extensive inflammation associated with acute exposure, subsequent repair of the epithelial lining of airways and nerves may result in a significantly altered receptor threshold, resulting in non-specific bronchial hyper-responsiveness.
2. Damage to bronchial mucosa may lead to increased airway permeability, allowing easier access of inhaled materials to irritant receptors.
3. High-level toxic exposure and subsequent inflammation may result in a mass release of mediators that alter smooth muscle responsiveness for a prolonged period of time.
4. Airway inflammation persists in some people.

Nonspecific sensitizers / irritants can be found in hairsprays, perfumes, bleaches, tobacco smoke, etc. Reactions can also be caused by cold air.

2) Dr. John Balmes, MD, Professor of Medicine, School of Medicine, Division of Occupational and Environmental Medicine, University of California, San Francisco

Dr. Balmes discussed occupational asthma & implications for other settings, policy, & research.

Occupational asthma is a serious condition. Good epidemiological data exists that shows that about 15-20% of the adult asthma burden has an occupational component. There is sound evidence for about 250 chemicals, and probable evidence for about 100.

Many of these studies involve non-allergen sensitizers. An important area of research has to do with low molecular weight chemicals that are highly reactive and used in polymerization processes to make plastics and foam. Some of these are the most common causes of occupational asthma in the developed world.

More research is also needed on the mechanism of irritant-induced asthma, and the epidemiological research also needs more work. It is very important to do this research because irritant-induced asthma in the workplace is probably the same disease process as irritant-induced asthma in the environment. The science of low level exposures in particular, would have broad implications.

There is an increasing interest and concern about irritants because air fresheners, carpets, cleaning materials, etc. all release low levels of Volatile Organic Compounds (VOC’s), which can be oxidized in the indoor environments of homes, public buildings, and industrial settings, and cause low level irritant exposure.

There are also policy implications of research – if polymorphisms are identified, workplaces may begin to screen workers for genetic polymorphisms and may potentially deny access to certain jobs.

Air pollution research – we used to think criteria of air pollutants didn’t actually cause, but would exacerbate asthma, but now we have increasing evidence that some exposures can actually cause the initially onset of asthma, and workers tend to not get better with treatment, but only with removal or significant reduction of exposure.

3) Megan Sandel, MD, MPH, Pediatrician and Researcher, Boston Medical Center at Boston University, and member of the Executive Committee of the New England Asthma Regional Council

Dr. Sandel spoke about implications of asthma research in the clinical setting.

It is difficult to differentiate between patients with extrinsic or intrinsic asthma - to separate children who wheeze when they have colds and may likely grow out of it, kids with allergic signs (like hay fever, eczema, etc.), and kids with irritant-induced asthma. These are important distinctions for prescribing the right environmental changes, behavior changes, and medications.

Dr. Sandel tries to minimize harm and increase primary prevention, by educating patients on avoiding pesticide bombs, air fresheners, mixing chemicals and any other products or behaviors that might cause or exacerbate asthma, while promoting integrated pest management solutions and safer mold cleaning. 30-40% of her patients are using some form of air freshener on a regular basis.

Q&A / Discussion

We discussed pesticide drift, co-morbidities such as obesity and asthma, the NAAEP guidelines, diesel engine exhaust, REACH, cleaning products, the lack of information on alternatives, and pesticides near schools.