Air pollution linked to biologic failure in chronic inflammatory arthritis
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Air pollution is a predictor of poor response to biological treatment in patients with rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, according to a poster session at the EULAR 2021 Congress.
“The primary objective our study was to determine the association between the concentration of air pollutants and biological drug retention rates in chronic inflammatory arthritis,” Giovanni Adami, MD, of the University of Verona, in Italy, said during the poster session for the digital meeting.
To accomplish this, Adami and colleagues extracted and analyzed longitudinal data on patients with chronic inflammatory arthritis from the registry of biological therapies at the University of Verona. This registry included data on patient ZIP codes, demographics, and pharmacological and clinical characteristics.
In addition, the researchers collected data on air pollutant concentrations in the Verona area from June 2013 to September 2018, including carbon monoxide, nitrogen oxides such as nitric oxide and nitrogen dioxide, ozone, and particulate matter in diameters of 10 (PM10) and 2.5 microns or less. Altogether, the researchers collected 13,636 daily air pollution records.
In all, Adami and colleagues included 1,257 patients with chronic inflammatory arthritis who resided within 10 km of where the air pollutants were collected. These patients included 863 with RA, 254 with PsA and 138 with AS, who together logged 5,454 follow-up visits. The researchers used a case-crossover study design to compare the exposure to pollutants during the 30- and 60-day periods preceding a drug switch due to disease progression referent to the 30- and 60-day periods preceding a visit with stable treatment for at least 6 months.
All biologic disease-modifying antirheumatic drug failures due to adverse events or intolerance were excluded from the study.
According to the researchers, there was an exposure-dependent relationship between air pollutants and C-reactive protein serum levels in chronic inflammatory arthritis. PM10 exposures greater than 50 and 40 g/m3 were associated with a 150% (OR = 2.564; 95% CI, 2.114-3.11) and 65% (OR = 1.659; 95% CI, 1.44-1.91) higher risk for demonstrating a CRP serum level above 5mg/L, respectively. If the PM10 threshold was set at greater than 30 g/m3— below the European Union health protection limit — the researchers still found a 38% higher risk for altered CRP (OR = 1.383; 95% CI, 1.206-1.588), Adami said.
Among the included patients, 280 — or 22.3% — had at least two follow-up visits where at least one biologic DMARD switch occurred due to drug inefficacy, and at least one visit with stable treatment for no less than 6 months. This population served as the researchers’ sample for the case-crossover study.
According to the researchers, air pollutant concentrations were higher prior a switch due to drug inefficacy. The discriminatory capacity of disease activity alone was the highest (area under receiver operating characteristic curve [AUC] = 0.841). However, when the prediction model included the concentrations of air pollutants during the 60-day period prior to the visit, the discriminatory capacity increased (AUC = 0.879).
“We demonstrated the relationship between environmental air pollution exposure and poor response to biological therapies in chronic inflammatory arthritis,” Adami said. “Approximately five out of 100 biological drug switches were attributable to the sole effect of air pollution.”
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