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TOPLINE:
Chronic exposure to air pollutants such as fine particulate matter ≤ 2.5 μm in diameter (PM2.5), particulate matter ≤ 10 μm in diameter (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) increased the risk for systemic lupus erythematosus (SLE) onset. The risk was highest among those with high genetic risk and high air-pollution exposure.
METHODOLOGY:
- Researchers prospectively investigated the association between long-term exposure to air pollutants and incident SLE in 459,815 participants from the UK Biobank.
- A land-use regression model was used to quantify the annual average air pollution concentrations, including PM2.5, PM10, NO2, and NOX.
- The genetic susceptibility to lupus was assessed using polygenic risk scores (PRS), and the participants were classified into low–, intermediate–, or high–genetic-risk groups based on the tertiles of PRS.
- The joint effect of air pollutants and genetic susceptibility to lupus on the risk for incident SLE was evaluated, with the reference group consisting of participants with a low genetic risk and low exposure to air pollution.
TAKEAWAY:
- Over a median follow-up period of 11.77 years, 399 new cases of SLE were identified.
- The odds of developing SLE were higher among participants with high genetic risk than among those with low genetic risk (hazard ratio [HR], 3.45; P < .001 for trend).
- The risk for developing SLE was even higher among participants with a high genetic risk and high exposure to PM2.5 (adjusted HR [aHR], 4.16; 95% CI, 2.67-6.49), PM10 (aHR, 5.31; 95% CI, 3.30-8.55), NO2 (aHR, 5.61; 95% CI, 3.45-9.13), and NOX (aHR, 4.80; 95% CI, 3.00-7.66) than among with those with a low genetic risk and low exposure to air pollutants.
IN PRACTICE:
“Findings can inform the development of stricter air quality regulations to mitigate exposure to harmful pollutants, thereby reducing the risk of SLE,” the authors wrote.
SOURCE:
The study was led by Meiqi Xing, MASc, Huazhong University of Science and Technology, Wuhan, China. It was published online in Arthritis & Rheumatology.
LIMITATIONS:
The study participants were enrolled voluntarily, which may have led to selection bias because they might have been healthier or more health conscious. The study did not consider the specific components of air pollutants, particularly particulate matter, which may have varying effects on the incidence of SLE. Other air pollutants such as ozone, sulfur dioxide, and carbon monoxide were not included in the analysis.
DISCLOSURES:
This study did not disclose any funding source. The authors declared no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Chronic exposure to air pollutants such as fine particulate matter ≤ 2.5 μm in diameter (PM2.5), particulate matter ≤ 10 μm in diameter (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) increased the risk for systemic lupus erythematosus (SLE) onset. The risk was highest among those with high genetic risk and high air-pollution exposure.
METHODOLOGY:
- Researchers prospectively investigated the association between long-term exposure to air pollutants and incident SLE in 459,815 participants from the UK Biobank.
- A land-use regression model was used to quantify the annual average air pollution concentrations, including PM2.5, PM10, NO2, and NOX.
- The genetic susceptibility to lupus was assessed using polygenic risk scores (PRS), and the participants were classified into low–, intermediate–, or high–genetic-risk groups based on the tertiles of PRS.
- The joint effect of air pollutants and genetic susceptibility to lupus on the risk for incident SLE was evaluated, with the reference group consisting of participants with a low genetic risk and low exposure to air pollution.
TAKEAWAY:
- Over a median follow-up period of 11.77 years, 399 new cases of SLE were identified.
- The odds of developing SLE were higher among participants with high genetic risk than among those with low genetic risk (hazard ratio [HR], 3.45; P < .001 for trend).
- The risk for developing SLE was even higher among participants with a high genetic risk and high exposure to PM2.5 (adjusted HR [aHR], 4.16; 95% CI, 2.67-6.49), PM10 (aHR, 5.31; 95% CI, 3.30-8.55), NO2 (aHR, 5.61; 95% CI, 3.45-9.13), and NOX (aHR, 4.80; 95% CI, 3.00-7.66) than among with those with a low genetic risk and low exposure to air pollutants.
IN PRACTICE:
“Findings can inform the development of stricter air quality regulations to mitigate exposure to harmful pollutants, thereby reducing the risk of SLE,” the authors wrote.
SOURCE:
The study was led by Meiqi Xing, MASc, Huazhong University of Science and Technology, Wuhan, China. It was published online in Arthritis & Rheumatology.
LIMITATIONS:
The study participants were enrolled voluntarily, which may have led to selection bias because they might have been healthier or more health conscious. The study did not consider the specific components of air pollutants, particularly particulate matter, which may have varying effects on the incidence of SLE. Other air pollutants such as ozone, sulfur dioxide, and carbon monoxide were not included in the analysis.
DISCLOSURES:
This study did not disclose any funding source. The authors declared no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Chronic exposure to air pollutants such as fine particulate matter ≤ 2.5 μm in diameter (PM2.5), particulate matter ≤ 10 μm in diameter (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) increased the risk for systemic lupus erythematosus (SLE) onset. The risk was highest among those with high genetic risk and high air-pollution exposure.
METHODOLOGY:
- Researchers prospectively investigated the association between long-term exposure to air pollutants and incident SLE in 459,815 participants from the UK Biobank.
- A land-use regression model was used to quantify the annual average air pollution concentrations, including PM2.5, PM10, NO2, and NOX.
- The genetic susceptibility to lupus was assessed using polygenic risk scores (PRS), and the participants were classified into low–, intermediate–, or high–genetic-risk groups based on the tertiles of PRS.
- The joint effect of air pollutants and genetic susceptibility to lupus on the risk for incident SLE was evaluated, with the reference group consisting of participants with a low genetic risk and low exposure to air pollution.
TAKEAWAY:
- Over a median follow-up period of 11.77 years, 399 new cases of SLE were identified.
- The odds of developing SLE were higher among participants with high genetic risk than among those with low genetic risk (hazard ratio [HR], 3.45; P < .001 for trend).
- The risk for developing SLE was even higher among participants with a high genetic risk and high exposure to PM2.5 (adjusted HR [aHR], 4.16; 95% CI, 2.67-6.49), PM10 (aHR, 5.31; 95% CI, 3.30-8.55), NO2 (aHR, 5.61; 95% CI, 3.45-9.13), and NOX (aHR, 4.80; 95% CI, 3.00-7.66) than among with those with a low genetic risk and low exposure to air pollutants.
IN PRACTICE:
“Findings can inform the development of stricter air quality regulations to mitigate exposure to harmful pollutants, thereby reducing the risk of SLE,” the authors wrote.
SOURCE:
The study was led by Meiqi Xing, MASc, Huazhong University of Science and Technology, Wuhan, China. It was published online in Arthritis & Rheumatology.
LIMITATIONS:
The study participants were enrolled voluntarily, which may have led to selection bias because they might have been healthier or more health conscious. The study did not consider the specific components of air pollutants, particularly particulate matter, which may have varying effects on the incidence of SLE. Other air pollutants such as ozone, sulfur dioxide, and carbon monoxide were not included in the analysis.
DISCLOSURES:
This study did not disclose any funding source. The authors declared no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.