RESUMO
The 2022 wildfires in New Mexico, United States, were unparalleled compared to past wildfires in the state in both their scale and intensity, resulting in poor air quality and a catastrophic loss of habitat and livelihood. Among all wildfires in New Mexico in 2022, six wildfires were selected for our study based on the size of the burn area and their proximity to populated areas. These fires accounted for approximately 90 % of the total burn area in New Mexico in 2022. We used a regional chemical transport model and data-fusion technique to quantify the contribution of these six wildfires (April 6 to August 22) on particulate matter (PM2.5: diameter ≤ 2.5 µm) and ozone (O3) concentrations, as well as the associated health impacts from short-term exposure. We estimated that these six wildfires emitted 152 thousand tons of PM2.5 and 287 thousand tons of volatile organic compounds to the atmosphere. We estimated that the average daily wildfire smoke PM2.5 across New Mexico was 0.3 µg/m3, though 1 h maximum exceeded 120 µg/m3 near Santa Fe. Average wildfire smoke maximum daily average 8-h O3 (MDA8-O3) contribution was 0.2 ppb during the study period over New Mexico. However, over the state 1 h maximum smoke O3 exceeded 60 ppb in some locations near Santa Fe. Estimated all-cause excess mortality attributable to short term exposure to wildfire PM2.5 and MDA8-O3 from these six wildfires were 18 (95 % Confidence Interval (CI), 15-21) and 4 (95 % CI: 3-6) deaths. Additionally, we estimate that wildfire PM2.5 was responsible for 171 (95 %: 124-217) excess cases of asthma emergency department visits. Our findings underscore the impact of wildfires on air quality and human health risks, which are anticipated to intensify with global warming, even as local anthropogenic emissions decline.
Assuntos
Poluição do Ar , Incêndios Florestais , Poluição do Ar/estatística & dados numéricos , New Mexico , Nível de Saúde , Incêndios Florestais/estatística & dados numéricos , Material Particulado/análise , Monitoramento Ambiental , Exposição por Inalação/estatística & dados numéricos , Modelos Estatísticos , Humanos , Mortalidade PrematuraRESUMO
Functional constipation (FC) is one of the most common gastrointestinal disorders characterized by hard stools and infrequent bowel movements, which is associated with dysfunction of the enteric nervous system and intestinal motility. Luteolin, a naturally occurring flavone, was reported to possess potential pharmacological activities on intestinal inflammation and nerve injury. This study aimed to explore the role of luteolin and its functional mechanism in loperamide-induced FC mice. Our results showed that luteolin treatment reversed the reduction in defecation frequency, fecal water content, and intestinal transit ratio, and the elevation in transit time of FC models. Consistently, luteolin increased the thickness of the muscular layer and lessened colonic histopathological injury induced by loperamide. Furthermore, we revealed that luteolin treatment increased the expression of neuronal protein HuC/D and the levels of intestinal motility-related biomarkers, including substance P (SP), vasoactive intestinal polypeptide (VIP), and acetylcholine (ACh), as well as interstitial cells of Cajal (ICC) biomarker KIT proto-oncogene, receptor tyrosine kinase (C-Kit), and anoctamin-1 (ANO1), implying that luteolin mediated enhancement of colonic function and contributed to the anti-intestinal dysmotility against loperamide-induced FC. Additionally, luteolin decreased the upregulation of aquaporin (AQP)-3, AQP-4, and AQP-8 in the colon of FC mice. In summary, our data showed that luteolin might be an attractive option for developing FC-relieving medications.
Assuntos
Constipação Intestinal , Loperamida , Luteolina , Animais , Camundongos , Acetilcolina , Colo , Constipação Intestinal/induzido quimicamente , Constipação Intestinal/tratamento farmacológico , Luteolina/farmacologia , Luteolina/uso terapêuticoRESUMO
Functional constipation (FC) is one of the most common gastrointestinal disorders characterized by hard stools and infrequent bowel movements, which is associated with dysfunction of the enteric nervous system and intestinal motility. Luteolin, a naturally occurring flavone, was reported to possess potential pharmacological activities on intestinal inflammation and nerve injury. This study aimed to explore the role of luteolin and its functional mechanism in loperamide-induced FC mice. Our results showed that luteolin treatment reversed the reduction in defecation frequency, fecal water content, and intestinal transit ratio, and the elevation in transit time of FC models. Consistently, luteolin increased the thickness of the muscular layer and lessened colonic histopathological injury induced by loperamide. Furthermore, we revealed that luteolin treatment increased the expression of neuronal protein HuC/D and the levels of intestinal motility-related biomarkers, including substance P (SP), vasoactive intestinal polypeptide (VIP), and acetylcholine (ACh), as well as interstitial cells of Cajal (ICC) biomarker KIT proto-oncogene, receptor tyrosine kinase (C-Kit), and anoctamin-1 (ANO1), implying that luteolin mediated enhancement of colonic function and contributed to the anti-intestinal dysmotility against loperamide-induced FC. Additionally, luteolin decreased the upregulation of aquaporin (AQP)-3, AQP-4, and AQP-8 in the colon of FC mice. In summary, our data showed that luteolin might be an attractive option for developing FC-relieving medications.