Discussion
Disease activity in our Italian cohort of RA patients was not
significantly affected by short-term air pollutants exposure in urban
and peri-urban areas in Lombardy region in the North of Italy. Notably,
scattered statistical significant associations were observed between
short-term exposure to outdoor air pollutants (PM10,
PM2.5, NO2, and O3) and
RA activity, but the changes observed did not reach the minimal
clinically important difference [20].
A clear comparison with the purpose of establishing whether a difference
exists between our results and the two existing studies on this topic is
not feasible [15, 16]. Firstly, our RA population includes all
consecutive patients referring to the Rheumatology outpatient clinics
and the disease activity was low between remission and low disease
activity (see table 1). By contrast, in the study of Wu, hospital
re-admissions within one year were considered, thus suggesting more
severe flares of disease [16], while the Kuwaiti Colleagues
described an association between DAS28, clinical disease activity index
(CDAI), NO2 and SO2 using data from
their national registry [15]. This latter study, as well as our
results, provided very small variations in outcome measure (i.e. disease
activity), which, even if statistically significant, did not reach the
minimal clinically important difference [20].
Furthermore, accurate measurement of the household and workplace air
pollution was not included in all these studies. These findings are
consistent with studies on cigarette smoking exposure that is recognized
as one of the most influencing environmental factors for RA
susceptibility, but there is no evidence of its influence in a very
short time on disease activity [21]. Moreover, our results are in
line with those on systemic lupus erythematosus disease activity and
short-term air pollution exposure [22].
Notably, strength of our study was to consider different therapeutic
approaches as a potential confounding factor. Therapy seems partially
able to influence the relationship between short-term air pollution
exposure and RA disease activity. It should be noted that this result is
limited to PM2.5 levels and DAS28 at the day of the
visit and O3 levels and disease activity scores (DAS28
and SDAI) for several days with respect to the three groups of
therapies.
Some limitations of our study have to be mentioned. This is a single
center study and data are limited to our tertiary referral center. In
addition, we could not measure all real life exposures, even those
related to daily activities that can also affect results.
As already mentioned, much of our current understanding of the impact of
air pollution on RA pathobiological events has been derived from
long-term retrospective studies using registries or administrative
databases or in vitro studies [4, 5, 13]. Although the environment
seems to play a crucial role in inducing autoimmunity by favouring
disease onset, it seems barely relevant to disease activity once the
loss of tolerance is established in rheumatologic disorders.
In conclusion, despite the strong in vitro evidence that particulate
matter enhances the inflammatory pathways, the evidence of this effect
in real-life RA patients is less impressive. The role of short-term
exposure to air pollutants as a potential contextual factor has not yet
clarified. Further research shall help further elucidate determinants of
RA flare and the implications for disease management.