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Air pollution as a contributing factor of relapses and cases of multiplesclerosis

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The role of air pollution exposure in multiple sclerosis (MS) incidence and relapse worldwide has not yielded a consensus; some studies have reported positive associations, which have failed to reject the null hypothesis. Potential reasons for these contradictory results can in part be explained by differences in study designs and their associated limitations. Of note, rat and canine studies in 2010 and 2013, respectively, have shown that expression of HO-1 enzyme and inflammatory factors increased due to PM10 and diesel engine exhaust (DEE) exposure. Of the eight non-null epidemiological studies scrutinized, the majority included a retrospective study design with air pollution monitoring data, which may be an advantage due to large number of study participants and a disadvantage with possible air pollution measurement error for personal exposure. The studies included analyses of PM10, PM2.5, SO2, NO2, NOx and/or O3 with PM10 as the common denominator between all of them. Studies from 2003, 2014–2019 from Finland, France, Iran, Italy, and Serbia all provide evidence of an association between PM10 and incidence or relapse of MS. Though one 2018 study likewise described associations between exposures to NO2, O3, and PM10 and MS relapses using a case-crossover design, the multi-pollutant model only associated O3. Of the epidemiological studies that fail to reject the null hypothesis, there was no evidence of an association between PM10 exposure and MS relapse or incidence. Though air pollution has not been conclusively proven to be a cause of MS, evidence from multiple studies have associated incidence and relapse with exposure to pollutants, particularly PM10.
Federal Scientific Center for Medical and Preventive Health Risk Management Technologies
Title: Air pollution as a contributing factor of relapses and cases of multiplesclerosis
Description:
The role of air pollution exposure in multiple sclerosis (MS) incidence and relapse worldwide has not yielded a consensus; some studies have reported positive associations, which have failed to reject the null hypothesis.
Potential reasons for these contradictory results can in part be explained by differences in study designs and their associated limitations.
Of note, rat and canine studies in 2010 and 2013, respectively, have shown that expression of HO-1 enzyme and inflammatory factors increased due to PM10 and diesel engine exhaust (DEE) exposure.
Of the eight non-null epidemiological studies scrutinized, the majority included a retrospective study design with air pollution monitoring data, which may be an advantage due to large number of study participants and a disadvantage with possible air pollution measurement error for personal exposure.
The studies included analyses of PM10, PM2.
5, SO2, NO2, NOx and/or O3 with PM10 as the common denominator between all of them.
Studies from 2003, 2014–2019 from Finland, France, Iran, Italy, and Serbia all provide evidence of an association between PM10 and incidence or relapse of MS.
Though one 2018 study likewise described associations between exposures to NO2, O3, and PM10 and MS relapses using a case-crossover design, the multi-pollutant model only associated O3.
Of the epidemiological studies that fail to reject the null hypothesis, there was no evidence of an association between PM10 exposure and MS relapse or incidence.
Though air pollution has not been conclusively proven to be a cause of MS, evidence from multiple studies have associated incidence and relapse with exposure to pollutants, particularly PM10.

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