Abstract
Increased levels of ambient fine particulate matter (PM2.5) air pollution are associated with increased risks for detrimental health outcomes, but risks for patients with kidney transplants (KTs) remain unknown. To investigate the association of PM2.5 exposure with KT outcomes. This retrospective cohort study was conducted using data on patients who received KTs from 2004 to 2016 who were identified in the national US transplant registry and followed up through March 2021. Multiple databases were linked to obtain data on PM2.5 concentration, KT outcomes, and patient clinical, transplant, and contextual factors. Data were analyzed from April 2020 through July 2021. Exposures included post-KT time-dependent annual mean PM2.5 level (in 10 μg/m3) and mean PM2.5 level in the year before KT (ie, baseline levels) in quartiles, as well as baseline annual mean PM2.5 level (in 10 μg/m3). Acute kidney rejection (ie, rejection within 1 year after KT), time to death-censored graft failure, and time to all-cause death. Multivariable logistic regression for kidney rejection and Cox analyses with nonlinear assessment of exposure-response for death-censored graft failure and all-cause death were performed. The national burden of graft failure associated with PM2.5 levels greater than the Environmental Protection Agency recommended level of 12 μg/m3 was estimated. Among 112 098 patients with KTs, 70 522 individuals (62.9%) were older than age 50 years at the time of KT, 68 117 (60.8%) were men, and the median (IQR) follow-up was 6.0 (3.9-8.9) years. There were 37 265 Black patients (33.2%), 17 047 Hispanic patients (15.2%), 48 581 White patients [43.3%]), and 9205 patients (8.2%) of other race or ethnicity. The median (IQR) baseline PM2.5 level was 9.8 (8.3-11.9) μg/m3. Increased baseline PM2.5 level, compared with quartile 1 baseline PM2.5 level, was not associated with higher odds of acute kidney rejection for quartile 2 (adjusted odds ratio [aOR], 0.99; 95% CI, 0.92-1.06) but was associated with increased odds for quartile 3 (aOR, 1.11; 95% CI, 1.04-1.20) and quartile 4 (aOR, 1.13; 95% CI, 1.05-1.23). Nonlinear assessment of exposure-response for graft failure and death showed no evidence for nonlinearity. Increased PM2.5 levels were associated with increased risk of death-censored graft failure (adjusted hazard ratio [aHR] per 10 μg/m3 increase, 1.17; 95% CI, 1.09-1.25) and all-cause death (aHR per 10 μg/m3 increase, 1.21; 95% CI, 1.14-1.28). The national burden of death-censored graft failure associated with PM2.5 above 12 μg/m3 was 57 failures (95% uncertainty interval, 48-67 failures) per year among patients with KTs. This cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with KTs. These findings suggest that efforts toward decreasing levels of PM2.5 concentration may be associated with improved outcomes after KT.
Highlights
Increased levels of ambient air pollution are associated with an increased risk of detrimental health outcomes, including cardiovascular disease, diabetes, and all-cause mortality.[1,2,3,4,5,6] The underlying mechanisms for these associations may include associations of inhaled particulate matter with increased sympathetic vascular modulation, intravascular thrombosis, and promotion of atherosclerosis.[7,8] A dose-response association has been reported.[9]
Increased PM2.5 levels were associated with increased risk of death-censored graft failure and all-cause death
Association of Fine Particulate Matter Air Pollution With Kidney Transplant Outcomes. This cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with kidney transplants (KTs)
Summary
Increased levels of ambient air pollution (ie, fine particulate matter 2.5 μm or less in aerodynamic diameter [PM2.5]) are associated with an increased risk of detrimental health outcomes, including cardiovascular disease, diabetes, and all-cause mortality.[1,2,3,4,5,6] The underlying mechanisms for these associations may include associations of inhaled particulate matter with increased sympathetic vascular modulation, intravascular thrombosis, and promotion of atherosclerosis.[7,8] A dose-response association has been reported.[9]. The etiology of kidney disease may be mediated by an increase in systemic inflammation and oxidative stress associated with air pollutants.[14,15] It has been found that particulate matter inhaled through the respiratory tract and cleared by the kidney may be associated with direct damage to renal tissue.[16] air pollutants and PM2.5 are associated with insulin resistance,[17,18] attenuated flow-mediated arterial dilation,[19] and systemic hypertension,[20,21,22] which are important factors that may be associated with kidney function
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