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Why the Rise in Asthma Cases?

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Science  13 Jun 1997:
Vol. 276, Issue 5319, pp. 1645
DOI: 10.1126/science.276.5319.1645

Asthma is a disease of the industrialized 20th century. First described in the mid-1800s, it may have existed before that time, but was very rare. It is still rare in developing countries. But in the developed world in the last 2 decades, asthma rates have skyrocketed—doubling in the United States since 1980. “Asthma and allergies have become representative of the westernization of our society,” says William Busse, an allergist at the University of Wisconsin, Madison.

Asthma ascending.

Researchers are struggling to explain asthma's dramatic increase.


Researchers do not yet know why. They have come a long way in dissecting the sequence of events that leads to individual asthma attacks: the activation by an allergen or other trigger of certain immune cells, which in turn marshal other cells that mount inflammatory attacks on the lungs (see main text). But why some people are predisposed to such attacks—and why their numbers are now increasing—remain mysteries, although researchers have some clues.

Increased exposure to environmental allergens and immune system changes due to fewer childhood infections may play a role, say some. And geneticists are closing in on a host of genes that have been linked to increased asthma susceptibility. The search for a cause is urgent, says Busse, because it might point to ways of preventing children from developing the disease in the first place. For the moment, he says, “we are treating the consequences of the disease, not preventing it from occurring.”

One of the most popular theories holds that asthma has increased partly because of greater exposure to allergens such as house dust mites or cockroaches. Allergist Thomas Platts-Mills of the University of Virginia notes that nowadays children spend more time indoors in front of the television in close contact with carpets and upholstered furniture crawling with dust mites. Still, Platts-Mills says, this “Annette Funicello” effect, as he calls it, “can't explain the rise by itself.” The asthma increase is just too great and has occurred even in dry regions where the dust mite is uncommon.

Another feature of modern life might also be contributing: the fall in childhood infections. Early infections, say proponents of this idea, may stimulate a kind of immune response that suppresses later allergic reactions. Earlier this year, Oxford pulmonologist Julian Hopkin and colleagues at the Wakayama Medical Center in Wakayama, Japan, found that children who responded strongly to a skin test indicating that they had been exposed to tuberculosis are less likely to suffer from asthma or other allergic diseases (Science, 3 January, p. 77). Similarly, in a study of 1600 Italian soldiers, Paolo Matricardi of the Laboratory of Immunology and Allergy in Rome and his colleagues found that soldiers who tested positive for antibodies to hepatitis A virus—a sign of more childhood infections in general, say the authors—had significantly fewer allergies. (The results appeared in the April British Medical Journal.)

Researchers have also turned up other hints that early immunological experience can affect a child's chances of developing asthma—very early experience, if Jill Warner at the University at Southampton in the United Kingdom is right. When she and her colleagues studied immune cells from premature and terminated fetuses, they found that cells from fetuses as young as 22 weeks could multiply when exposed to house dust mites and birch pollen—suggesting that they recognized the allergens from a previous exposure. Warner is currently studying whether limiting a mother's exposure to common allergens can protect her unborn child from later developing allergies and asthma.

Still, environmental influences can't be the full answer, because asthma susceptibility is well known to run in families. A number of all-out hunts are now under way for asthma-susceptibility genes, which might be interacting with environmental factors to drive the rising incidence. So far, only one team—at Sequana Therapeutics Inc. in San Diego—says it has pinpointed a gene, and team members are keeping details of their find under wraps (Science, 30 May 1997, p. 1327). But several more public searches are closing in on genes.

A team led by Carol Ober, a geneticist at the University of Chicago, reported at the recent American Thoracic Society meeting that its work with the South Dakota Hutterites, a religious group of 5000 descended from 64 18th-century ancestors, has linked asthma or asthmalike conditions to specific regions on chromosomes 2, 13, and 21. And in a wider study of the general population, the multicenter Collaborative Study on the Genetics of Asthma reported in the April issue of Nature Genetics that its researchers have linked asthma in various ethnic groups to a half-dozen different chromosome regions. Other studies have found linkages to regions on chromosomes 11 and 12 containing genes known to code for important players in the inflammation that is part of asthma pathology.

The linkages, like all the other clues, are a long way from solving the asthma riddle, but they are a start. “Everyone knew [the gene search] was a black hole,” says Susan Banks-Schlagel, manager of asthma research at the National Heart, Lung, and Blood Institute. “They said, ‘Oh, you'll never find anything.’ But some interesting things are starting to happen.”

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