Background: United States government scientists estimate that COVID-19 may kill between 100,000 and 240,000 Americans. The majority of the pre-existing conditions that increase the risk of death for COVID-19 are the same diseases that are affected by long-term exposure to air pollution. We investigate whether long-term average exposure to fine particulate matter (PM 2.5 ) increases the risk of COVID-19 deaths in the United States.Methods: Data was collected for approximately 3,000 counties in the United States (98% of the population) up to April 04, 2020. We fit zero-inflated negative binomial mixed models using county level COVID-19 deaths as the outcome and county level long-term average of PM 2.5 as the exposure. We adjust by population size, hospital beds, number of individuals tested, weather, and socioeconomic and behavioral variables including, but not limited to obesity and smoking. We include a random intercept by state to account for potential correlation in counties within the same state. Results:We found that an increase of only 1 ߤ g/m 3 in PM 2.5 is associated with a 15% increase in the COVID-19 death rate, 95% confidence interval (CI) (5%, 25%). Results are statistically significant and robust to secondary and sensitivity analyses. Conclusions:A small increase in long-term exposure to PM 2.5 leads to a large increase in COVID-19 death rate, with the magnitude of increase 20 times that observed for PM 2.5 and allcause mortality. The study results underscore the importance of continuing to enforce existing air pollution regulations to protect human health both during and after the COVID-19 crisis. The data and code are publicly available.

Assessing whether long-term exposure to air pollution increases the severity of COVID-19 health outcomes, including death, is an important public health objective. Limitations in COVID-19 data availability and quality remain obstacles to conducting conclusive studies on this topic. At present, publicly available COVID-19 outcome data for representative populations are available only as area-level counts. Therefore, studies of long-term exposure to air pollution and COVID-19 outcomes using these data must use an ecological regression analysis, which precludes controlling for individual-level COVID-19 risk factors. We describe these challenges in the context of one of the first preliminary investigations of this question in the United States, where we found that higher historical PM2.5 exposures are positively associated with higher county-level COVID-19 mortality rates after accounting for many area-level confounders. Motivated by this study, we lay the groundwork for future research on this important topic, describe the challenges, and outline promising directions and opportunities.

Elevated preoperative NLR is an independent predictor of worse RFS for patients with stage IIA colon cancer and a potential biomarker to identify candidates for adjuvant chemotherapy.

ObjectiveTo understand whether ambient air pollutants and meteorological variables are associated with daily COVID-19 incidence. DesignA retrospective cohort during Jan 25 th to Feb 29 th in 2020. SettingCity of Wuhan, XiaoGan and HuangGang. PatientsThe COVID-19 incidence per day. MethodsWe collected daily data of COVID-19 incidence, eight ambient air pollutants (PM2.5, PM10, SO2, CO, NO2, and O3-8h) and three meteorological variables (temperature, relative humidity and wind level) in China's three worst COVID-19 hit cities during the study period. The multivariate Poisson regression was performed to understand their correlation. ResultsOur data showed that daily COVID-19 incidence was positively associated with PM 2.5 and humidity in all cities. Specifically, the relative risk (RR) of PM 2.5 was 1.036 (95% confidence interval [CI], 1.032 -1.039), 1.059 (95% CL, 1.046 -1.072) and 1.144 (95% CL, 1.12 -1.169) for COVID-19 incidence per day in Wuhan, XiaoGan and HuangGang, respectively. The RR of humidity was constantly lower than that of PM2.5, whose difference ranged from 0.027 to 0.111. Moreover, PM 10 and temperature also exhibited a notable correlation with daily COVID-19 incidence, but in a negative pattern The RR of PM 10 raged from 0.915 (95% CL, 0.896 -0.934) to 0.961 (95% CL, 0.95 -0.972) while that of temperature was 0.738 (95% CL, 0.717 -0.759) to 0.969 (95% CL, 0.966 -0.973). Conclusions.Our data suggested that PM 2.5 /humidity and PM 10 /temperature could substantially increase and decrease the risk of COVID-19 incidence, respectively.

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Summary Background Accumulating evidence links fine particulate matter (PM 2·5 ) to premature mortality, cardiovascular disease, and respiratory disease. However, less is known about the influence of PM 2·5 on neurological disorders. We aimed to investigate the effect of long-term PM 2·5 exposure on development of Parkinson’s disease or Alzheimer’s disease and related dementias. Methods We did a longitudinal cohort study in which we constructed a population-based nationwide open cohort including all fee-for-service Medicare beneficiaries (aged ≥65 years) in the contiguous United States (2000–16) with no exclusions. We assigned PM 2·5 postal code (ie, ZIP code) concentrations based on mean annual predictions from a high-resolution model. To accommodate our very large dataset, we applied Cox-equivalent Poisson models with parallel computing to estimate hazard ratios (HRs) for first hospital admission for Parkinson’s disease or Alzheimer’s disease and related dementias, adjusting for potential confounders in the health models. Findings Between Jan 1, 2000, and Dec 31, 2016, of 63 038 019 individuals who were aged 65 years or older during the study period, we identified 1·0 million cases of Parkinson’s disease and 3·4 million cases of Alzheimer’s disease and related dementias based on primary and secondary diagnosis billing codes. For each 5 μg/m 3 increase in annual PM 2·5 concentrations, the HR was 1·13 (95% CI 1·12–1·14) for first hospital admission for Parkinson’s disease and 1·13 (1·12–1·14) for first hospital admission for Alzheimer’s disease and related dementias. For both outcomes, there was strong evidence of linearity at PM 2·5 concentrations less than 16 μg/m 3 (95th percentile of the PM 2·5 distribution), followed by a plateaued association with increasingly larger confidence bands. Interpretation We provide evidence that exposure to annual mean PM 2·5 in the USA is significantly associated with an increased hazard of first hospital admission with Parkinson’s disease and Alzheimer’s disease and related dementias. For the ageing American population, improving air quality to reduce PM 2·5 concentrations to less than current national standards could yield substantial health benefits by reducing the burden of neurological disorders.

BackgroundAlthough an abundance of evidence has indicated that tumor-associated macrophages (TAMs) are associated with a favorable prognosis in patients with colon cancer, it is still unknown how TAMs exert a protective effect. This study examined whether TAMs are involved in hepatic metastasis of colon cancer.Materials and methodsOne hundred and sixty cases of pathologically-confirmed specimens were obtained from colon carcinoma patients with TNM stage IIIB and IV between January 1997 and July 2004 at the Cancer Center of Sun Yat-Sen University. The density of macrophages in the invasive front (CD68TFHotspot) was scored with an immunohistochemical assay. The relationship between the CD68TFHotspot and the clinicopathologic parameters, the potential of hepatic metastasis, and the 5-year survival rate were analyzed.ResultsTAMs were associated with the incidence of hepatic metastasis and the 5-year survival rate in patients with colon cancers. Both univariate and multivariate analyses revealed that the CD68TFHotspot was independently prognostic of survival. A higher 5-year survival rate among patients with stage IIIB after radical resection occurred in patients with a higher macrophage infiltration in the invasive front (81.0%) than in those with a lower macrophage infiltration (48.6%). Most importantly, the CD68TFHotspot was associated with both the potential of hepatic metastasis and the interval between colon resection and the occurrence of hepatic metastasis.ConclusionThis study showed evidence that TAMs infiltrated in the invasive front are associated with improvement in both hepatic metastasis and overall survival in colon cancer, implying that TAMs have protective potential in colon cancers and might serve as a novel therapeutic target.

BackgroundExpansions of myeloid-derived suppressor cells (MDSCs) have been identified in human solid tumors, including colorectal cancer (CRC). However, the nature of these tumor-associated MDSCs and their interactions with tumor cells in CRC are still poorly understood.MethodsThe percentages and phenotype of MDSCs in peripheral blood and tumorous and paraneoplastic tissues from CRC patients, as well as the clinical relevance of these MDSCs, were assessed. Age-matched healthy donors were included as controls. The interaction between MDSCs and T cells or tumor cells was investigated in a coculture system in vitro, and the molecular mechanism of the effect of MDSCs on T cells or tumor cells was evaluated.ResultsWe discovered that CRC patients had elevated levels of CD33+CD11b+HLA-DR− MDSCs in primary tumor tissues and in peripheral blood, and the elevated circulating MDSCs were correlated with advanced TNM stages and lymph node metastases. Radical resection significantly decreases the proportions of circulating MDSCs and CD4+CD25highFOXP3+ regulatory T cells. In vitro, CRC cells mediate the promotion of MDSC induction. Moreover, these tumor-induced MDSCs could suppress T cell proliferation and promote CRC cell growth via cell-to-cell contact. Such effects could be abolished by the inhibition of oxidative metabolism, including the production of nitric oxide (NO), and reactive oxygen species (ROS).ConclusionsOur results reveal the functional interdependence between MDSCs, T cells and cancer cells in CRC pathogenesis. Understanding the impact of MDSCs on T cells and tumor cells will be helpful to establish an immunotherapeutic strategy in CRC patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-015-0410-7) contains supplementary material, which is available to authorized users.