spirometry: race-based values inappropriate

 in the current enlightened approach to reassessing race-based normative values, the MESA Lung Study found that race/ethnicity-neutral spirometry values were appropriately predictive of long-term clinical chronic lower respiratory disease (see spirometry no diff outcomes by race AmJRespCritCare2021 in dropbox, or  DOI: 10.1164/rccm.202107-1612OC )

Details:

-- standardized spirometry done by the Multi-Ethnic Study of Atherosclerosis (MESA) Lung Study, a population-based, prospective cohort study of 3,344 White, Black, Hispanic, and Asian adults from 2004-2006

-- participants were from six US communities with a minimum of two racial/ethnic groups recruited at each site

-- chronic lower respiratory disease (CLRD) was a physician-based diagnosis, and included the categories of COPD, chronic bronchitis, emphysema, and asthma

-- baseline demographics: 

    -- mean age 65, self-reported race/ethnicity was 36% White/25% Black/23% Hispanic/17% Asian, 50% female, height 165 cm, BMI 28, education less than high school varied from 2.5% (White) to 15% (Hispanic), high school 15% (Asian) to 22% (Hispanic), some college 23% (Asian) to 37% (Black), college or more 36% (Black) to 56% (White)

    -- smoking status: never smokers 40% (Black) to 71% (Asian), former smokers 24% (Asian) to 51% (White), current smokers 5% (Asian) to 13% (Black); smoking pack-years overall median 7 (Hispanic) to 15 (White)

        -- ever-smokers were defined as at least 100 lifetime cigarettes, and current smokers as smoking a cigarette in the past 30 days

-- spirometry was done without bronchodilators, with airflow limitation defined as FEV1/FVC <0.70, and with moderate to severe airflow limitation defined as FEV1/FVC <0.70 with percentage predicted FEV1<80%

-- predicted values for spirometry were calculated using race/ethnicity-based equations according to guidelines, vs race/ethnicity-neutral equations

-- participants were followed for chronic lower respiratory disease (CLRD) events and mortality through 2019

    -- clinical events were ascertained by regular follow-up calls through 2019, medical records, and the National Death Index; follow-up on CLRD-related events and mortality was 82% and 92% at 10 years, respectively

-- secondary analyses adjusted for BMI, educational attainment, smoking status, smoking pack-years, blood pressure, HDL, LDL, total cholesterol, and history of hypertension and diabetes

Results:

-- Lung function, mean:

    --FEV1, L: White 2.6L; Black 2.3L; Hispanic 2.5L; Asian 2.2L

    --FVC, L: White 3.6L; Black 3.0L; Hispanic 3.2L; Asian 2.9L

    -- FEV1/FVC: White 0.74; Black 0.76; Hispanic 0.77; Asian 0.76

-- percentage of predicted lung function

    -- using race/ethnicity-based equations:

        -- FEV1: White 93.6; Black 93.7; Hispanic 95.2; Asian 88.8

        -- FVC: White 97.9; Black 96.5; Hispanic 96.5; Asian 92.1

-- percentage of predicted lung function

    -- using race/ethnicity-neutral equations:

        -- FEV1: White 100.4; Black 86.2; Hispanic 102.2; Asian 92.8

        -- FVC: White 106.4; Black 89.2; Hispanic 104.8; Asian 96.8

-- moderate-to severe airflow limitation (FEV1/FVC <0.70 and % predicted FEV1 <80%)

    -- using race/ethnicity-neutral equations:

        -- using race/ethnicity-based equations, number of patients, with % in parentheses: White 116 (10%); Black 66 (8%); Hispanic 42 (6%); Asian 46 (8%) (more people with mod-to-severe airflow limitation in White participants)

        -- using race/ethnicity-neutral equations: White 80 (7%); Black 100 (12%); Hispanic 29 (4%); Asian 37(7%0 (most limitation in the Black population)

 

-- clinical outcomes over 11.6 years:

    -- incident CLRD-related events: total 181 

        -- White 66 (5.6%, event rate/1000=53), Black 57 (6.8%, event rate/1000=66), Hispanic 36 (4.8%, event rate/1000=46), Asian 22 (3.9%, event rate/1000=36); again higher event rate in Black participants

        -- incident CLRD-related event risk was much greater for those with FEV1 <80% of predicted

    -- deaths: total 547

        -- White 203 (17.1%, event rate/1000=160), Black 156 (18.5%, event rate/1000=176), Hispanic 111 (14.7%, event rate/1000=139), Asian 77 (13.8%, event rate/1000=125) [death rate also highest in Black participants]

-- no difference using calculated CLRD-related events or mortality with vs without race/ethnicity-based equations, with striking overlap of results in terms of clinical events 10 years later (this picture is much better than about 1000 words and numbers):

--a few examples from the above:

    --a patient with FEV1 of 80% predicted had 10-yr risk of CLRD-related event of 6% if White and 8% in Black

    -- BUT a patient with FEV1 of 50% of predicted had observed 10-yr risk of 56% if White and 27% if Black

    -- no similar underestimation was evident for Hispanic patients and too few Asian participants to have stable assessment

    -- overall very similar results for all-cause mortality

-- no significant differences by sex, if pre-baseline CLRD or if nonsmokers, or if using different prediction equations (NHANES III vs GLI equations)

Commentary:

-- an interesting article traced the history of race as a differentiator of lung function, noting that Thomas Jefferson himself commented on "a difference of structure in the pulmonary apparatus" between slaves and white colonists, as a justification for the condition of slaves in the Republic. And, this conception remained until the mid-1800s. Studies in the later 1800s did find that Black individuals had a lower lung capacity by spirometry than their White counterparts. One of the early investigators (John Hutchinson) in the 1840s, however noted that other factors were important: height was an important predictor of lung function and occupation mattered. Not surprisingly, the racial differences reinforced the ideology of inferiority of several ethnicities to the White population. Most of the more current studies (e.g. in the 1970s) still did not take into account social conditions as potential confounders (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631137/ )

-- current measurements of lung function with the race/ethnicity-based "correction factor", an example:

    -- using the race/ethnicity-based algorithm: a 65yo man with height of 168 cm and FEV1 of 2.1L and FVC of 2.8L has a percentage predicted FEV1 of 70% (moderate lung disease) if White but 82% if Black (normal lungs); and a percentage of predicted FVC of 72% if White and 85% if Black!!!

-- this study basically found no evidence that including race/ethnicity improved upon race/ethnicity-neutral in predicting CLRD-related events or mortality

-- these results from the MESA study above are so profound for a number of reasons:

    -- the initial cohort had a mean age of 65, at which time many in the racial/ethnic groups had had decades of exposures that would decrease lung function, including low birth weight, lower respiratory tract infections, secondhand smoke, air pollution both inside and outside the house, higher-risk occupations

    -- underclassification of lung dysfunction in Black persons (ie, having results look okay only by the race/ethnicity-based evaluation) might well lead to:

        -- decreased helpful pulmonary medications, which could lead to more hospitalizations since their lung disease may not have been diagnosed and treated appropriately

            -- and, other studies have found that Black patients are already undertreated for pulmonary disease

        -- decreased referral to pulmonary rehab programs (which also is documented to happen less often with Black patients); pulmonary rehab can lead to important benefits, including decreased mortality

        -- not evaluating the type and cause of the lung disease (which could potentially lead to better preventative measures or different meds to decrease disease progression)

        -- not assessing and therefore not ameliorating the important social risk factors for lung disease (e.g. the importance of occupational lung diseases, which tends to be more prevalent amongst poor Black and White people, though studies have suggested that Black workers also tend to have less personal protective equipment)

        -- directing more resources to White patients, exacerbating racial inequities

        -- and, just the existence of race-based medical criteria reinforces implicit racial biases

-- Another recent study accessed the NHANESIII database of 5294 White and 3743 Black participants conducted from 1988-1994, assessing FVC in Black versus White participants, also finding that race-based FVC determinations were not justified: Race-based assessments were not independently predictive of higher mortality (see spirometry NHANES racial inequities EClinMed2021 in dropbox, or doi: 10.1016/j.eclinm.2021.101073). This was a much younger cohort, mean age around 40, and death specifically attributable to respiratory causes were infrequent in this younger group

Limitations:

-- no information about important social issues: occupation, occupational exposures, use of personal protective equipment at work, housing density, outdoor air pollution (which should include proximity to major highways/bus routes), passive smoking exposure, other chemical exposures (including hobbies), etc

    -- though, there is a very high probability that non-White people as a group by age 65 have accumulated many more lung injuries related to these social factors than White people

-- some of the data were based on reports by the patients (e.g. race/ethnicity) or physicians (CLRD), both of which could be biased

-- there were too few Asian patients to have meaningful results

so, pretty powerful study challenging the accepted very long-standing "truth" that there were important racial differences in assessing pulmonary function, thereby leading to major differences in correctly classifying and prescribing optimal treatment for Black patients, who may well have more lung disease because of their living/working situations, as noted above. This is similar to current studies finding that race should not be a factor in assessing renal function (see http://gmodestmedblogs.blogspot.com/2021/10/eliminating-race-in-calculating-renal.html ). And, of course, the real issue is that race is a social and not a physiological construct, and the measured differences found between Black and White individuals has much more to do to with structural racism which exposes Black individuals more than White ones to lower paying/more menial jobs with more occupational/environmental exposures, poorer quality housing (thanks to redlining, higher mortgages/rents and other inequities), decreased access to healthy foods (food deserts), decreased access to health care, etc.  So to the extent that pulmonary disease may well be more rampant in Black communities, it is not race/ethnicity that is causing that.....

geoff

 

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