air pollution: still causing emphysema

A recent article found that long-term exposure to air pollution was significantly associated with increasing emphysema, as assessed using quantitative CT imaging and lung function (see air pollution and copd jama2019 in dropbox, or doi:10.1001/jama.2019.10255)

Details:

-- 7071 participants in the Multi-Ethnic Study of Atherosclerosis (MESA study) from 6 US metropolitan areas (Winston-Salem, NC; New York City; Baltimore, MD; St. Paul, MN, Chicago, IL; Los Angeles, CA), from 2000-2018

-- age at recruitment 60, 47% men; others varied by site (eg 10% white/37% Chinese/12% black in LA, 50% white/50% black in Baltimore, 20% white/35% black/45% Hispanic in NY), some college in 60%, never smoker 45%/former smoker 40%/current 15%, BMI <30 in 70%

-- pollutant exposures measured: ground-level ozone (O₃), PM_2.5 (fine particular matter < 2.5 microns), NO_x (nitrogen oxides) and black carbon

    --baseline: O₃ 15-25 parts per billion, PM_2.5 13-18 mcg/m³, NO_x 24-83 parts per billion and black carbon 0.4 to 1.4 mcg/m³

-- Main outcomes: percent emphysema (percent of lung pixels <-950 Hounsfield units, a number based on pathologic comparisons and prognosis) was assessed up to 5 times by cardiac CT scans (2000-2007) and equivalent regions on lung CT scans (2010-2018); spirometry done up to 3 times (2004-2018)

Results:

-- CT-based percent emphysema: 3% at baseline, increased 0.58 percentage points per 10 years

-- PFTs: 22% had airflow obstruction at baseline, and mean decline in FEV1 of 309 ml and FVC 331 ml over 10 years

-- median ambient concentrations of PM_2.5 and NO_x decreased substantially during the follow-up period, not so for O₃

-- O₃, PM_2.5, NO_x, and black carbon were significantly associated with the following percent progression of emphysema over 10 years:

    -- O₃: 0.13 per 3 parts per billion at baseline; increasing to 0.18 per 3 ppb percent progression in followup

        --of note, this increase is equal to that associated with 29 pack-years of smoking (each 10 pack-yrs of smoking was associated with a 0.06 percentage point increase in emphysema progression)

    -- PM_2.5: 0.11 per 2mcg/m³ at baseline; decreasing 0.04 per 2mcg/m³ percent progression in followup

    -- NO_x: 0.06 per 10 parts per billion at baseline; increasing to 0.12 per 10  ppb percent progression in followup

    -- black carbon: 0.10 per 0.2 mcg/m³ at baseline

-- multiple air pollutant exposures resulted in a greater increased percent emphysema vs individual ones, though ground-level ozone remains the most destructive single agent

-- there was a greater progression of emphysema in those who had airflow limitations at baseline, increase of 0.35 percentage points vs 0.15 percentage points in those without baseline airflow obstruction

-- ambient O₃ and NO_x concentrations during follow-up, but not PM_2.5 concentrations, were also significantly associated with greater increases in percent emphysema

-- ambient O₃ concentrations, but not other pollutants, at both baseline and during follow-up were significantly associated with greater decline in FEV₁ for 10 years at 18.15 mL per 3 ppb; and for FVC at 40.19 ml greater decline per 3 ppb.  There were greater declines in those who were current smokers [note: there were fewer people getting spirometry, with half the observations than for CT, and these spirometry occured later in the study when many of the ambient pollutant levels had already decreased, so the statistical power for the spirometry observations is less than for CTs]

Commentary:

-- emphysema is 4^th leading cause of death in the US and 3^rd worldwide

-- percent emphysema, quantitated with CT scans, is associated with dyspnea and mortality

-- in other studies both O₃, and PM_2.5 are associated with faster decline in lung function in those exposed to traffic-related air pollution

-- mechanistically, ground-level ozone is associated with lung inflammation, and in a mouse model is associated with increased protease expression, epithelial apoptosis, and alveolar enlargement and apoptosis. PM_2.5  is associated with increased systemic inflammation, pulmonary inflammation and oxidative stress (and human studies link this to heart disease: see http://gmodestmedblogs.blogspot.com/2016/06/air-pollution-and-heart-disease.html for an evaluataion of the MESA study (the same one as above) but finding increased coronary artery calcium associated with increased PM_2.5 , and cad air pollution jacc 2012 in dropbox, or DOI: 10.1161/CIRCRESAHA.118.313948 for a Chinese study

-- this is an important article for several reasons:

    -- it is a rigorous longitudinal study that reinforces and extends the results of prior observational studies over the past several decades that found that air pollution levels are associated with lung disease

    -- the study quantitates lung deterioration, finding a pretty linear relationship with the levels of the different pollutants; and, it provides a quantitative relationship with a history of smoking exposure

    -- it confirms the effect of pollutants on lung disease in an era when major pollutants in urban settings have decreased substantially. It is notable that ground-level ozone has not decreased over time and still has the highest rate of lung deterioration. And this ground-level ozone is not expected to get better with climate change

    -- we are in a political climate in the US now where regulations are being reversed and the increased use of pollutants is being encouraged (eg from attempts to increase the use of fossil fuels).  So, the prior found benefits of regulations to decrease air pollution are in jeopardy

-- as noted by the authors, limitations of this study include the fact that community-based evaluations of air pollutants are unlikely to apply to individuals equally (ie, some living in similar conditions may in fact have significantly different actual individual exposures); the CTs used to measure the percent emphysema just looked at the lower 2/3 of the lung, though this does seem correlate with whole lung measurements, CT scanners have changed significantly over the course of this 18 year study (though they did use analyses of advanced image processing to try to account for scanner variation).

-- ground-level ozone arises when NO_x and volatile organic compounds react in sunlight and stagnant air, which are produced by gasolene combustion and dispensing facilities, vehicles and other combustion engines (lawnmowers, garden equipment, aircraft, trains), wood combustion, evaporation of liquid fuels and solvents, paints/insectides, cleaners/industrial solvents. Temperature, wind speed, and driving patterns affect ozone development (see https://www3.epa.gov/region1/airquality/oz_prob.html ). The major way to lower ground-level ozone is by decreasing burning fossil fuels.

so, an important article, especially in light of the current political climate. it is great that most of the ambient pollutants have decreased over the years, but ground-level ozone remains a significant problem. And governmental rollbacks, especially for fossil fuel regulations, are likely to aggravate the emphysema problems, as above, but also other medical problems (esp cardiovascular), and, no doubt a tad more importantly, climate change and the ability of the world to sustain life as we know it....

geoff

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