If you’re one of those people who read about the toxic effects of environmental pollutants or diet and say, bulls***: I know lots of people who breathed or drank or ate that so-called pollutant and are just fine,
then toxicogenomics is for you. This young field examines interactions
between genes and environment, identifying DNA variants that make one
person develop asthma from air pollutants while another breathes free,
for instance, or that make one person develop cancer from cigarettes
while another smokes three packs a day for 70 years with nary a shadow
on his lung x-ray. For a sense of what the field is doing, check out the
“environmental genetics” group at the National Institute of Environmental Health Sciences (the site has a link to publications).
One of the most divisive issues when it comes to pollutants and
health is second-hand smoke. Across the population, passive smoking (as
it’s also called) raises the risk of heart disease, lung cancer and
other things you really should avoid.
But not everyone suffers ill effects. A new study suggests why. A
variation within a single gene can determine how susceptible children
will be to second-hand smoke, even in utero, conclude scientists led by Carrie Breton and Frank Gilliland of the University of Southern California.
For the study, published in the April issue of the American Journal of Respiratory and Critical Care Medicine,
the researchers examined a family of genes called glutathione-s
transferase (GST) genes which defend cells against damage by free
radicals, which are abundant in cigarette smoke.
The genes come in several variants, three of which had a significant
effect on lung function in the 2,100 fourth graders in the study.
One of the variants, present in 30 to 35 percent of the white
population, is correlated with poorer lung function and more
susceptibility to respiratory damage if mom smoked during pregnancy.
Since the GST genes help detoxify free radicals, including those in
cigarette smoke, says Breton, “we speculate that the patterns of genetic
variation we investigated may alter this process, thereby reducing the
lung’s ability to detoxify harmful agents and causing a cascade of other
events that promote inflammation, bronchial constriction, airway
hyper-responsiveness and asthma-like symptoms.”