Albuterol (ProAir, Proventil, Ventolin; salbutamol (international)) and Black patients

Albuterol is one of the most consequential examples of race-specific pharmacogenomics in asthma:

• Pharmacogenomics. The ADRB2 gene encodes the beta-2 receptor. The Arg16Gly polymorphism (and the Arg16Arg genotype) affects response to regular beta-agonist use. Arg16Arg is more common in African-ancestry populations (~25–30 percent) than European (~10–15 percent) and has been associated with reduced bronchodilator response and, with regular (non-rescue) use, potentially worse asthma control — the SOCS and BAGS trials (Israel et al., Lancet 2004;364:1505–12) explored this interaction.
• SMART / PALISADE / FLEX trials and NAEPP 2020 focused update support as-needed albuterol-plus-ICS (rather than as-needed albuterol alone) for mild asthma — reducing total beta-agonist exposure. This approach is especially important for Black patients with the Arg16Arg genotype.
• Disparities in asthma outcomes. Black children have 5x the asthma mortality of white children; Black adults have roughly 3x the mortality. These gaps are not primarily pharmacologic — they reflect exposures (air pollution, housing mold, cockroach allergen), access to specialty care, and inhaler-technique support. But pharmacogenomics compounds these environmental disparities.
• Rescue overuse is a red flag. Using albuterol more than twice a week indicates uncontrolled asthma and should trigger a controller (ICS) review. Black patients are less likely to be stepped up to appropriate controller therapy (Gamble et al., Pediatrics 2015;136:e1014–21).