Ownby and his team have seen it in follow-up tests with the Detroit study subjects, who are now 18 years old, and his team is currently immersed in another population study, also out of Detroit, that includes both infants and the infants’ mothers. His preliminary data are consistent with the European farm findings that a woman’s microbial exposure while pregnant is significant to her child’s ability to switch to the Th1 mode.
“We were kind of surprised to find that pets actually had an effect through the mother on the fetus even before birth,” Ownby says. The mechanism of protection, however, remains unclear. “One of the prevailing theories on pets is that they increase the level of endotoxin in the home,” says Ownby. Like von Mutius, however, he has his doubts that endotoxin will prove to be the key. Pets, he notes, “are not changing the levels of endotoxin [in homes] very much, so the effect of pets seems to be separate from that.”
Allergy and the Big City
Pets, cows and pigs, farm bacteria, good microbes in the gut, big families and day cares, their protective qualities all fit with the hygiene hypothesis. But the theory does have holes. With the growth in allergy, many people are living with immune systems programmed in the Th2 mode, but at the same time, there has also been a surge in Th1 diseases such as diabetes.
What’s also not easy to reconcile with the theory is the link between exposure to traffic pollution, that unhygienic chemical stew, and high rates of asthma. Perhaps no scientific theory can encompass a range of situations as opposite as the European family farm and the giant American city (the latter of which Turvey could sub-divide into hundreds of environments). But this much is certain: a link among asthma, allergies and traffic exhaust has emerged.
In population studies from Europe to Southern California, the proximity to busy roadways and increased levels of vehicle exhaust have been related to the onset of asthma in school kids. But whether the inflammation seen in the airways of participating children relates to outdoor allergens as well as the exhaust itself has been a matter for debate.
However, Dr. Joachim Heinrich, head of environmental epidemiology at Munich’s Heimholtz Center, was part of a team of scientists that assessed allergic sensitization among 2,600 children living in high-traffic areas of metropolitan Munich. The resulting study, published in 2008, clearly finds that “living on busy roads is associated with a higher risk for sensitization to pollen.”
It says this might show “interaction between pollen and air pollutants and the effect of this interaction on the human immune response.” Other studies have mentioned the greater likelihood of allergic response to pollen and other airborne allergens when inhaled alongside diesel fuel. All this appears to suggest that components of smog are working alongside pollen triggers, that they are the “facilitators” of allergy.
Yet, University of Southern California scientists at the Keck School of Medicine caution that it’s too soon to say exactly what happens in polluted air to cause children to develop asthma. With at least 13 million cars and trucks on the road every day, and a reputation as a smog capital, Los Angeles has become a natural environment of study. The USC scientists are now drawing findings from a second large population study on the effects of exhaust pollution on children’s lungs.
So far, they’ve shown that the closer a young child lives to a major roadway, and the more sports an older child plays outside in smog, the more likely the onset of asthma. They’ve even been able to make this radical contention: “We have evidence that pollution may actually cause the asthma, not just make it worse,” says Ed Avol, a professor at USC and co-author on this research.
Whether the development of the disease is “an immune response or whether that’s something else that’s going wrong or whether it’s a genetic component – it’s hard to know,” Avol says. His team has recently identified some gene dispositions in children that make them more susceptible to asthma in a polluted environment. As well, smog includes several types of gases and particulates, so sifting through the answers in this area is not a quick process.
Von Mutius doesn’t pretend to be an expert on the inner city; the farm is her lab. But on the pollution question, she advises bearing in mind again what’s meant by the term ‘environment’. “Is the allergen seen [by the immune system] along with chemicals or along with microbes?” she asks. That might either promote or protect against allergy. “My idea is that the context of the allergen exposure matters,” she says.
The context of the exposure. That is something which will change from farm to city and its toxic substances, from one part of the world to another. “I don’t think there’s going to be one factor [to explain allergy] that you can generalize about all the way around the world,” von Mutius says.
“It’s a context of different mixtures, and it’s also in the related background of genetics that will then develop into asthma and allergies.” When it comes to the causes of allergies, she is “pretty sure it’s going to be many things.”
Sears would agree. He notes that the immune system of a child born in rural Africa would probably be different to the immune system of a child born in downtown Manhattan, and explains that “you see enormously high IgE levels without asthma, where the IgE is directed against the parasites in certain parts of the world. So if you don’t have parasites to deal with, then the theory is that the IgE deals with other things – like cats or dust mites.”
Interestingly, in the developing world, a transition in immune system responses can be studied in real time since there has been considerable migration from agrarian life to the big city. Von Mutius points to a recent medical paper about Mongolia. The people in the study “had been living in tents and among camels and there was very little allergy. The more they move toward the larger city, the more the risk of becoming allergic. So there is something in this more affluent lifestyle, this more Westernized lifestyle.” She thinks that previous protection was farm related.
There is no neat bow to put on the complex question of why there are so many allergies today. We have been changing our world, our environments, our contexts and we apply those to our particular sets of genes. Now our immune systems are speaking up – or acting out. The scientists filling in the pieces of the puzzle do hope for answers for the longer term, which won’t just be academic, but will allow them to offer prevention strategies.
Von Mutius is optimistic that if she can identify those protective qualities on the European farms, maybe a vaccine could be produced. The CHILD study is still a work in progress, but Sears and Turvey are also thinking ahead to results.
“We hope there will be recommendations that count in terms of what mothers can do or how houses should be built or how you avoid or encourage exposures such as to animals,” says Sears. By seeing the fundamental differences between kids in Westernized cities who do and do not develop allergies and asthma, this sets the scene for future intervention.
“What ultimately we all care about,” says Turvey, “is being able to prevent or modify these diseases for future generations.” That’s worth all the sampling and analyzing, the late hours in the labs and the intrusions on study participants’ lives. Meantime, Sears gives advice that’s only partly tongue-in-cheek: “On the way home from the maternity hospital,” he suggests, “buy a dog.”
Updated in August 2010 from the Fall 2008 issue of Allergic Living magazine.
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