|
 Researchers already knew that heavy air pollution makes lung disease
worse in people who already have lung disease. The new study shows
that even among people without lung disease, long-term exposure to
air pollution even in relatively 'clean' areas can lead to signs of
chronic lung disease, said Dr. Joel Kaufman, a co-author of the
study and an environmental health researcher at the University of
Washington in Seattle.
The current study focused on four major pollutants - ozone, an
unstable form of oxygen produced when traffic and industrial fumes
react with sunlight; nitrogen oxide, a byproduct of fossil fuel
combustion that contributes to smog; black carbon, or soot, from
coal-powered factories and traffic; and so-called PM 2.5, a mixture
of solid particles and liquid droplets smaller than 2.5 micrometers
in diameter that can include dust, dirt, soot and smoke.
Researchers assessed levels of these pollutants near the homes of
7,071 people in six U.S. cities: Baltimore; Chicago; Los Angeles;
St. Paul, Minnesota; New York, and Winston-Salem, North Carolina.
Each participant got CT scans to look for the proportion of cells in
the lung that are damaged - described as the percentage of
emphysema. They also underwent lung function tests known as
spirometry at the start of the study and again around 10 years
later.
About 46% of the study group were lifelong nonsmokers, and 22% of
participants had some airflow obstruction at the beginning of the
study period. Over 10 years, the average decline in lung function
for the entire group was a little over 300 milliliters of volume on
inhalation and exhalation tests.
People exposed to higher levels of each of the four pollutants at
the start of the study were more likely to develop emphysema damage
by the end, researchers report in JAMA.
Levels of most of the pollutants declined during the study, but
concentrations of ozone rose. Each 3 parts per billion (ppb) of
ozone in the air was associated with a lung function decline of 18
ml on a test of forced exhalation, and 40 ml on an inhalation test.
Over the 10-year period, each 3 ppb in average daily exposure to
ozone was linked to lung damage equivalent to smoking a pack of
cigarettes a day for 29 years or to an additional three years of
aging, researchers found.
[to top of second column] |
Ever-smokers and people with lung damage at the start of the study
experienced the greatest increases in percentage emphysema and
declines in lung function.
The results suggest that air pollution exposure may help explain why
so many people without any history of smoking still develop chronic
emphysema, the study team concludes.
One limitation of the study is that researchers only examined air
pollution around people's home addresses, and it's unclear how much
time people spent at work or other places away from home or how much
pollution levels might differ at these other locations.
"People don't spend all their time sitting on their front steps, so
while we have a very good idea about their air pollution exposures,
the exposures are a bit different indoors and when they travel to
other places," Kaufman said.
Even so, the results underscore how important it is for people with
chronic lung diseases to take precautions to limit exposure to air
pollution, Kaufman advised.
"Staying indoors on high air pollution days and having a good air
filter at home can be helpful in highly polluted environments,"
Kaufman said.
The results also highlight the importance of public health efforts
to curb pollution.
"Great progress has been made in reducing air pollution
concentrations due to health-based air quality protections and these
need to continue to be strengthened," Kaufman said. "Ozone
concentrations in particular still need attention and reducing use
of fossil fuels and slowing climate change will help reduce these
exposures too."
SOURCE: https://bit.ly/2YUfRrr JAMA, online August 13, 2019.
[© 2019 Thomson Reuters. All rights
reserved.] Copyright 2019 Reuters. All rights reserved. This material may not be published,
broadcast, rewritten or redistributed.
Thompson Reuters is solely responsible for this content. |
