In this national cohort of non-hypertensive Spanish adults, we found a positive association between the concentrations of PM (both PMten and PM2.5) and the incidence of hypertension after a mean follow-up of 7.4 years. The association remained after multivariate weighted analysis of the data, showing a significant dose-response relationship, and was consistent across various subgroups.
To our knowledge, this report provides the first data on the impact of air pollutants on hypertension in Spain from the perspective of a national study, while previous evidence was limited to local studies in the northeast of Spain. ‘Spain.18, also included in multicenter studies12.
Our data are consistent with a large body of evidence suggesting that air pollution may contribute to the pathogenesis of hypertension8, also arguing that the particulate component of air pollution is the most significant threat to the cardiovascular system3,4,5,6. In this regard, although previous associations between exposure to gaseous pollutants and hypertension have shown some discrepancies, the majority of studies reporting long-term exposure to PM and incident hypertension have reported associations positive ones that are consistent with our findings.9,10,11,12,13,14,15,16.
Interestingly, these associations have now been observed in studies conducted in countries with relatively low concentrations of PM in North America (mean PM2.5 of 10.7 g / m3ten, 13.9 g / m311 and 13.2 g / m313 and Europe, (average PM2.5 between 6.6 and 15 g / m312 and 10.8 g / m3 in the present study), as well as in heavily polluted regions of Asia (average PM2.5 26.5 g / m314, 77.7 g / m315 and 92.1 g / m316. This strongly suggests that the relationship between particulate exposures and the development of hypertension is likely a general phenomenon in different populations and across the range of pollution. In fact, the increased incidence of hypertension that we describe in our study occurs in PMten and PM2.5 concentration ranges well below the existing target values of the European Ambient Air Quality Directive (PM10 3 and PM2.5 3)19. On the other hand, our results are online and reinforce the validity of the maximum annual concentrations for the protection of health proposed by the WHO (PMten3and PM2.53)20.
The mechanism by which PM could contribute to the development of hypertension includes inflammation and oxidative stress and triggering an imbalance in the autonomic nervous system affecting vascular tone and responsiveness3. Epigenetic changes that occur during exposure may also play a role in the interaction between air pollution and hypertension21,22,23.
Interestingly, controlled studies in humans have confirmed observational results showing that acute inhalation of concentrated particles can trigger a rapid and sustained rise in blood pressure.24.
Additionally, the use of air filtration to lower PM concentrations has been shown to have rapid effects on lowering blood pressure, further strengthening this biological relationship.25,26,27.
Our study has several limitations:
First, our sample size is relatively small, which may affect the precision of the estimates. Due to the experimental design, the time between the event and the result was not available for analysis. We therefore used logistic regression models to calculate the fitted odds ratios, which are known to overestimate the relative risks.28.
Second, our food frequency questionnaire did not include data on participants’ salt intake, so we could not adjust our analyzes accordingly.
Third, nationwide noise maps of Spain are also not currently available, so we were unable to adjust our analyzes for ambient noise. Nevertheless, although long-term noise exposure has been linked to incident hypertension in some studies12.29, the results are inconsistent30. In addition, the associations between PM and hypertension in both31.32.33, and longitudinal studies9.12 did not change substantially after adjusting for noise.
Finally, as in other studies, we used outdoor ambient measurements modeled at participants’ residential addresses as a proxy for air pollution exposure, while no information on time-activity models or on PM concentrations. inside was available. This is, however, a limitation common to most studies evaluating the health effects of air pollution and, in fact, the air quality guidelines focus primarily on air pollution. ‘ambient air (outside) for their recommendations.20.
As strengths of the study, we included a population-based design with measurements of each participant’s BP during baseline and follow-up exams so that we could identify both diagnosed and non-diagnosed hypertension cases. diagnosed.
We also included extensive data at the individual level, including clinical, demographic, and lifestyle variables, which allowed us to perform a robust multivariate fit of the data.
Finally, our perspective at the national level, first in the Spanish population, allows us to extrapolate our results more widely than local or regional studies, increasing the implications of the results for public health.
In conclusion, our study helps to assess the impact of particulate pollution on the incidence of hypertension in Spain. Our results reinforce the need to improve air quality as much as possible to decrease the risk of hypertension in our population, as even moderate levels like those in this study significantly increase the risk.