Genetics, long-term air pollutant exposure combine to increase lupus risk
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Key takeaways:
- Exposure to particulate matter and other air pollutants was linked to increased risk for SLE.
- High genetic risk and high air pollutant exposure were associated with the greatest SLE risk.
Long-term exposure to air pollutants, including particulate matter, increases the risk for developing systemic lupus erythematosus, according to data published in Arthritis & Rheumatology.
Individuals with high genetic risk and high air pollution exposure demonstrated the greatest risk for SLE, the researchers added.
“Accumulating evidence illustrates that air pollution is a risk factor for SLE,” Meiqi Xing, MASc, of the Huazhong University of Science and Technology, in Wuhan, China, and colleagues wrote.
“Several studies have illustrated the current knowledge of gene-environment interactions and SLE risk, which may have the potential to elucidate SLE pathogenesis and its clinical heterogeneity,” they added. “However, no study to date has examined the interactions of genetic factors and air pollutants on SLE.”
To investigate the relationship between air pollution and SLE risk, as well as the impacts of genetic lupus risks, Xing and colleagues conducted a prospective cohort study of U.K. Biobank data. The first stage of the analysis included 459,815 adults and assessed the relationship between air pollution and SLE using a Cox proportional hazards model. The second stage, a gene-related analysis excluding non-white Europeans (n = 418,028), used a polygenic risk score to assess interaction of genetic risk and air pollutants.
The study employed a land-use regression model to estimate concentrations of air pollutants, including PM2.5, PM10, nitrogen dioxide and nitrogen oxides. Participants were followed until death, follow-up loss or Dec. 31, 2020, whichever came first.
Over a median follow-up period of 11.77 years, 399 study participants developed SLE. Analysis revealed positive associations between incident SLE and exposure to each of the evaluated air pollutants, according to the researchers. For each interquartile-range increase in each pollutant, the adjusted HRs were:
- PM2.5: 1.18 (95% CI, 1.06-1.32);
- PM10: 1.23 (95% CI, 1.1-1.39);
- nitrogen dioxide: 1.27 (95% CI, 1.14-1.41); and
- nitrogen oxides: 1.13 (95% CI, 1.03-1.23).
According to the researchers, SLE risk was greatest among those with high genetic risk and high air pollutant exposure vs. those with low genetic risk and low exposure to air pollutants. Compared with participants who had low genetic risk and low air pollution exposure, HRs for those with high genetic risk and high exposure to each pollutant were as follows:
- PM2.5: 4.16 (95% CI, 2.67-6.49);
- PM10: 5.31 (95% CI, 3.3-8.55);
- nitrogen dioxide: 5.61 (95% CI, 3.45-9.13); and
- nitrogen oxides: 4.8 (95% CI, 3-7.66).
Adding a multiplicative term to the model revealed a statistically significant interaction between nitrogen dioxide and genetic risk for SLE (P = .021), the researchers added.
“Our current study provided crucial insights into the environmental factors contributing to autoimmune diseases,” Xing and colleagues wrote. “Findings can inform the development of stricter air quality regulations to mitigate exposure to harmful pollutants, thereby reducing the risk of SLE.
“Additional cohort studies are needed to elucidate the relationship between specific air pollutants and the development of SLE,” they added. “In addition, the underlying biologic mechanisms linking air pollution exposure to SLE pathogenesis need to be further explored. Given that a meaningful correlation analysis result does not imply a causal association, more studies are needed in the future to confirm the causal link between air pollution and incident SLE.”
Perspective
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Daniel J. Wallace, MD, FACP, MACR
A Chinese group studied 460,000 patients in a European databank and found 400 with systemic lupus erythematosus. They compared the influence of pollution, genetic susceptibility and risk for SLE incidence. The results showed that approximately 1 in 1,000 participants had the disease. Long term exposure to air pollutants was associated with a slightly increased HR for developing incident SLE, and only two out of many comparisons were statistically significant. A putative association was hypothesized.
There are several problems with this paper. First, no charts were reviewed to confirm the diagnosis of SLE fulfilling criteria. In addition, the ethnicities of the 400 patients were not stated. It is known that people of color in Europe tend to reside in more polluted, industrial regions of the continent and this could confound the data.
That being said, there is very slight evidence that pollution and genetic susceptibility could be one of many factors associated with incident SLE.
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