Even At Low Levels, Long-term Air Pollution May Increase COPD Risk

Marta Figueiredo, PhD avatar

by Marta Figueiredo, PhD |

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Long-term exposure to air pollution, even at relatively low concentrations, is associated significantly with reduced lung function and may increase the risk of chronic obstructive pulmonary disease (COPD), according to a population-based study in Canada.

“Few studies have examined the relationship between air pollution and the lung health of adults in areas where air pollution concentrations are low, such as in Canada,” Jean Bourbeau, MD, the study’s senior author, said in a press release.

“Our study shows that even in this setting, long-term exposure to outdoor air pollution has significant negative impacts on lung function,” added Bourbeau, who is a senior scientist at the Research Institute of the McGill University Health Center (RI-MUHC) and a professor in the department of medicine at McGill University in Montreal.

A link between increasing air pollution and higher COPD risk was found to be statistically significant for people who had the smallest airways relative to lung size.

These findings not only support previous data highlighting air pollution and smaller airway-to-lung ratios as potential independent COPD risk factors, but suggest people with smaller airways may be more susceptible to COPD-induced air pollution.

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“For the first time, common differences in lung structure that arise early in life were shown to increase susceptibility to the harmful effects of air pollution later in life,” Dany Doiron, PhD, one of the study’s authors and a research associate at RI-MUHC, said.

The study, “Ambient Air Pollution and Dysanapsis: Associations with Lung Function and COPD in the CanCOLD Study,” was published in the American Journal of Respiratory and Critical Care Medicine.

While tobacco smoke “is recognized as the single most important risk factor for the development and progression of COPD, 25% to 45% of individuals with COPD have never smoked,” the researchers wrote.

Given COPD’s global burden, “identifying risk factors beyond tobacco smoking and determining interactions amongst them are of utmost importance to inform preventive strategies, clinical diagnosis and management,” they wrote.

Both air pollution and dysanapsis — a mismatch of airway-to-lung size — appear to be significant risk factors of COPD, but whether they also interacted with each other was unclear until now.

A collaborative Canadian research network led by RI-MUHC scientists evaluated whether low levels of air pollution, such as those typically seen in Canada, had a significant effect on lung function and COPD development, as well as potential interactions with dysanapsis.

They analyzed lung function and structural data from 1,452 people enrolled in the Canadian Cohort Obstructive Lung Disease (CanCOLD; NCT00920348), a population-based study with the main goal to identify risk factors of COPD development and progression other than smoking.

Estimates of air pollution — fine particulate matter (PM2.5) and nitrogen dioxide (NO2) — for participants’ residential areas were provided by the Canadian Urban Environmental Health Research Consortium.

The most commonly studied air pollutant, PM2.5, is made up of tiny inhalable particles that can travel deep into the respiratory tract. Key sources include industrial emissions, residential wood heating and cooking, agriculture, and vehicle traffic. NO2 is a result of fossil fuel burning and an indicator of traffic-related air pollution.

Participants had a mean age of 66.6 years, 56% were men, and just less than half had COPD, most often mild.

Analyses accounted for several potential influencing factors, such as age, sex, body size, socioeconomic status, tobacco use and intensity, environmental tobacco and biomass smoke, and respiratory medication intake.

Results showed that higher concentrations of both PM2.5 and NO2 air pollution were significantly associated with poorer lung function.

“We saw that small increases in fine particulate matter and nitrogen dioxide air pollution led to clinically relevant decreases in lung function,” Bourbeau said.

A similar link was found for COPD frequency, but this failed to reach statistical significance, which contrasts with several prior studies reporting a significant association.

However, a link between PM2.5 and COPD was detected for people with the strongest dysanapsis, or smallest airway-to-lung ratio. Specifically, with similar exposure to air pollution, people with smaller airways in relation to lung size were 87% more likely to develop COPD relative to those with larger airways.

This group also showed poorer lung function, suggesting they were more susceptible to the impacts of PM2.5 exposure on lung function and COPD development.

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These findings highlight “PM2.5 and NO2 air pollution exposure were associated with lower [lung function], even at low concentrations relative to many countries across the world,” the researchers wrote.

They also suggest that “a relatively important proportion of the Canadian population is particularly susceptible to inhaled air pollutants,” said Benjamin Smith, MD, another of the study’s authors at the RI-MUHC and an associate professor in the department of medicine at McGill University. “While exposure to air pollution during childhood has been shown to adversely affect lung function and lung development, our study suggests that early-life lung development could in turn play a key role in protecting from, or increasing susceptibility to, air pollution-induced reductions in lung function and COPD in adulthood.”

“For the first time, our results show that in addition to being a COPD risk factor, dysanapsis might also modify the impact of inhaled outdoor air pollutants on lung function and COPD,” the researchers wrote.

These data “highlight the need to further reduce ambient air pollution concentrations and can help inform clinical management by identifying individuals with increased susceptibility to air pollutants,” the researchers concluded.

They noted, however, that longer studies are needed to confirm these findings.