Background　Although　the　impact　of　ambient　air　pollution　on　mortality　in　cardiovascular　and　pulmonary　diseases　is　well　documented,　its　specific　link　to　pulmonary　arterial　hypertension　remains　unclear.　This　study　investigated　the　association　between　ambient　particulate　matter　(PM)　exposure　and　all-cause　death　or　lung　transplantation,　as　well　as　pulmonary　hemodynamics　in　patients　with　pulmonary　arterial　hypertension.Methods　This　retrospective　cohort　study　included　1327　participants　with　pulmonary　arterial　hypertension　who　underwent　right　heart　catheterization　(RHC).　Ambient　PM2.5　and　PM10　levels　were　estimated　using　the　China　High　Air　Pollutants　data　set,　with　a　3-year　average　exposure　before　diagnosis　as　the　primary　exposure　metric.　All-cause　death　or　lung　transplantation　was　the　primary　end　point.　Cox　proportional　hazard　models　assessed　the　association　between　PM　exposure　and　primary　outcomes,　and　generalized　linear　models　evaluated　pulmonary　hemodynamics.　Mediation　analysis　explored　potential　mediating　factors.Results　The　median　age　of　the　participants　was　33.0　years,　with　73.2%　being　women.　Median　PM2.5　and　PM10　levels　were　58.0　[43.6-76.1]　and　103.0　[80.4-129.3]　mu　g/m3,　respectively.　Over　a　median　follow-up　of　3.1　years,　149　patients　died　or　underwent　lung　transplantation.　Each　10　mu　g/m3　increase　in　PM2.5　and　PM10　was　associated　with　a　14.5%　and　7.9%　increased　risk　of　primary　outcomes,　respectively.　PM　exposure　was　linked　to　worsened　pulmonary　hemodynamics,　such　as　pulmonary　vascular　resistance　and　cardiac　index.　Mediation　analysis　suggested　lipid　metabolism,　uric　acid,　and　lymphocytes　may　partially　mediate　these　effects.Conclusions　Long-term　PM2.5　and　PM10　exposure　is　not　only　associated　with　increased　risk　of　death　or　lung　transplantation　in　patients　with　pulmonary　arterial　hypertension　but　also　affects　disease　severity　and　pulmonary　hemodynamics.