Genes, Air Pollution Combine to Raise Lupus Risk
British studies suggest that environmental and genetic elements contribute to
By John Gever
The exposure to high levels air pollutants is a significant increase in the risk of developing new-onset systemic lupus and erythematosus (SLE) and significantly more so for those with identified genetic risk factors, U.K. Biobank data revealed.
The study of 460,000 people in the British health database showed an increase between 18% and 27 percent of the risk of developing SLE for every step in the quartiles of exposure estimates to particulate matter and nitrogen oxides, according to Jian Yang, PhD, of China Three Gorges University in Yichang, China, and colleagues.
Additionally it is for those who are deemed to be high risk genetically, and with high levels of four major pollutant -PM2.5 and PM10 PM2.5 and PM10 (particulate matter 2.5 millimeters or less, as well as 10 millimeters less or less) (NO2) and PM2.5 (NO2) and any nitrogen oxides (NOx) (NOx) (NOx)The increase in SLE risk ranged between 316% and 461% in comparison to people who have a lower exposure to environmental factors and genetic risk. The study was released by researchers from Arthritis as well as Rheumatologyopens in a new tab or in a separate window.
The massive increases in risk were triggered mostly by genetic risk factors. The individuals who were at risk for this risk factor were in danger of having a quadruple risk of developing lupus having a low exposure to particles and nitrogen oxides. On the other hand, the risk increases of 30 to 70% were determined for those with a lower genetic risk as well as more exposure to pollution. The results were not significantly significant statistically or even borderline.
Its confidence intervals were quite large, and from 460,000 patients, only 399 were diagnosed with SLE with an average of 11.8 years of follow-up.
Thus, Yang and colleagues were prudent in their interpretation of these results. “Additional cohort studies are needed to elucidate the relationship between specific air pollutants and the development of SLE,” they wrote.
“In further, the biological mechanisms linking air pollution exposure and SLE pathogenesis require to be further investigated. Since a significant correlation analysis result doesn’t necessarily mean a causal link and that more research is needed in the near future to establish the causal connection with air pollutants and onset SLE. “
The researchers believed that their findings ought to be taken seriously. “Our current study provided crucial insights into the environmental factors contributing to autoimmune diseases,” they wrote. “Findings could guide the development of more stringent air quality standards to reduce the exposure of harmful contaminants, thus decreasing the chance of developing SLE. “
Their findings add to many studies that have identified environmental factors such as air pollution, as an underlying reason for SLE. However, Yang and co-workers noted that the bulk of their studies relied on the information about exposure and its outcomes such as hospitalizations or activity related to disease rather than on new-onset Lupus. Research regarding this condition is currently being conducted within Taiwan. “It is essential to evaluate this association in Europe, where the air pollution level is significantly lower,” the authors of the study claimed.
Yang’s group was influenced to work by U.K. Biobankopens in an entirely new window or tab it could be a project that collects health records of millions people living in Britain and that was registered between 2006 and 2010. The biobank also conducts periodic physical exams as well as questionnaires. The tissues samples are used to facilitate the genetic analysis.
Average exposures for one year to all four pollutants were determined for 2010, based on data from monitoring from previous years prior to that period. This was the basis of the statistical analysis conducted by the research team. Biobank people who reside in areas not regularly monitored weren’t included. The amount of each pollutant were divided by segments. The medians of each pollutants were follows:
- PM2.5: 9.93 mg/m3
- PM10: 19.16 mg/m3
- NO2: 28.11 mg/m3
- NOx: 42.26 mg/m3
Polygenic risk scores were calculated for all participants. The risk scores were later divided into tertiles that are characterized as moderate, low, and high risk for SLE as derived from previous studies of genome-wide interactions.
Statistics were re-adjusted to account for a variety of possible covariates, including race/ethnicity/sex, sex, and income, in addition to smoking and employment status as well as the body mass index.
The median age of the participants at baseline was approximately 57 (a possibility of a limitation given that SLE typically begins around the age of early adulthood.) A little more than half participants were females and over 90 percent were white.
Yang and colleagues have also studied the pollution exposure in terms of a continuous variable, which showed that the relationship between pollution exposure and SLE risks was non-linear in 2 of four pollutant types. No x as well as the PM 2.5 along with NO x both showed the effects of a plateau. They also showed strong correlations were observed with SLE risk at moderate to low exposures however, there were no additional increases as exposures increase. Linear correlations were found with PM10 and NO2 and NO 2 on the contrary.
The study’s weaknesses aside from the small number of identified SLE patients, which is mainly an older sample, are the individuals’ decision of joining the Biobank (meaning they may be more concerned about their health than others) and the possibility that the exposure of individuals to pollutants to be different from what was estimated in estimates of exposures per year. Additionally, there are a myriad of variables that could cause confusion, such as pollution from other sources like silica dust, or ground-level ozone, aren’t taken into consideration.
Disclosures
Yang as well as co-authors declared that they do not have any financial interests.
Primary Source
Arthritis & Rheumatology
Source Reference opens in a new tabXing M and other “Air pollution, genetic susceptibility, and risk of incident systemic lupus erythematosus: a prospective cohort study” Arthritis Rheumatol 2024; DOI 10.1002/art.42929.
