Association between ambient air pollution and elevated risk of tuberculosis development.

PMID: 

Infect Drug Resist. 2019 ;12:3835-3847. Epub 2019 Dec 6. PMID: 31827330

Abstract Title: 

Association Between Ambient Air Pollution and Elevated Risk of Tuberculosis Development.

Abstract: 

Background: Broad-scale evidence has shown the significant association between ambient air pollutants and the development of tuberculosis (TB). However, the impact of air quality on the risk of TB in Taiwan is still poorly understood.Objective: To develop a probabilistic integrated population-level risk assessment approach for evaluating the contribution of ambient air pollution exposure to the risk of TB development among different regions of Taiwan.Materials and methods: A Bayesian-based probabilistic risk assessment model was implemented to link exposure concentrations of various air pollutants quantified in a probabilistic manner with the population-based exposure-response models developed by using an epidemiological investigation.Results: The increment of the risk of TB occurred in a region with a higher level of air pollution, indicating a strong relationship between ambient air pollution exposures and TB incidences. Carbon monoxide (CO) exposure showed the highest population attributable fraction (PAF), followed by nitrogen oxides (NO) and nitrogen dioxide (NO) exposures. In a region with higher ambient air pollution, it is most likely (80% risk probability) that the contributions of CO exposure to development of TB were 1.6-12.2% (range of median PAFs), whereas NOand NOexposures contributed 1.2-9.8% to developing TB.Conclusion: Our findings provide strong empirical support for the hypothesis and observations from the literature that poor air quality is highly likely to link aetiologically to the risk of TB. Therefore, substantial reductions in CO, NO, and NOexposures are predicted to have health benefits to susceptible and latently infected individuals that provide complementary mitigation efforts in reducing the burden of TB. Considering that people continue to be exposed to both TB bacilli and ambient air pollutants, our approach can be applied for different countries/regions to identify which air pollutants contribute to a higher risk of TB in order to develop potential mitigation programs.

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Lung cancer deaths attributable to ambient particulate matter exposure in 2016 in China.

PMID: 

Zhonghua Yu Fang Yi Xue Za Zhi. 2019 May 6 ;53(5):475-479. PMID: 31091604

Abstract Title: 

[Lung cancer deaths attributable to ambient PM(2.5) exposure in 2016 in China].

Abstract: 

To analyze the lung cancer deaths attributable to ambient PM(2.5) exposure in China in 2016.All data were from the Global Burden of Disease Study 2016 (GBD 2016). Multiple-source data, including satellite observation, ground measurement, chemical migration model simulation, etc., and the data integration model for air quality (DIMAQ) were used to estimate the grid-level exposure to ambient PM(2.5). Data from the vital registry and cancer registry were used to establish statistical model to estimate the lung cancer deaths by province, age and gender. The lung cancer deaths attributable to PM(2.5) were calculated based on the calculation of population attributable fraction (PAF). The GBD world population age structure was adopted to calculate age-standardized rates for comparison among provinces (including 31 provinces, autonomous regions and municipalities directly under the central government, as well as Hong Kong and Macao special administrative regions, excluding Taiwan of China).In 2016, the lung cancer deaths attributable to ambient PM(2.5) exposure in China were 14.56×10(4) (95% uncertainty interval (): 9.63×10(4)-19.55×10(4)), accounting for 24.66% (95%: 16.38%-33.12%) of total lung cancer deaths. The lung cancer death rate attributable to PM(2.5) increased with age, with the lowest among 25-29 age group (0.25/10(5), 95%: 0.17/10(5)-0.34/10(5)), the highest among≥80 age group (90.70/10(5), 95%: 59.85/10(5)-122.20/10(5)). The lung cancer death rate attributable to PM(2.5) among males (14.84/10(5), 95%: 9.78/10(5)-19.93/10(5)) was higher than that in females (6.21/10(5), 95%: 4.07/10(5)-8.40/10(5)). The age-standardized death rates (ASDR) of lung cancer attributable to PM(2.5) among males and females in China were higher than the global average level. The attributable ASDR of lung cancer varied among provinces, highest in Shandong (13.51/10(5), 95%: 9.14/10(5)-18.20/10(5)) and lowest in Tibet (0.85/10(5), 95%: 0.44/10(5)-1.51/10(5)).In 2016, the lung cancer deaths attributable to ambient PM(2.5) exposure in China was heavy, and varied in different age groups, genders and provinces.

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SV-40, avian leukosis virus, and mouse mammary carcinoma virus are oncogenic viruses.

PMID: 

Cancer Genet Cytogenet. 1984 Oct ;13(2):167-79. PMID: 6090006

Abstract Title: 

Mutagenic effects of DNA-containing oncogenic viruses and malignant transformation of mammalian cells.

Abstract: 

It was discovered in the 1970s that oncogenic viruses could induce gene mutations in mammalian cells. The phenomenon seems to be widespread: it was observed with all groups of DNA-containing viruses and some retroviruses. The mutagenic effects of the tested viruses at gene level are not locus specific. The viruses induce point mutations, including base substitutions, as well as deletions and insertions. The mutagenic effect of SV40 is controlled by the activity of the early A gene, which encodes the T antigen. Presumably, the process of integration creates the possibility for occurrence of mutations early after infection. Mutagenesis seems to be induced by an integrated virus, though to a much smaller extent. Virus-induced mutagenesis may be connected with an activation of the cell error-prone repair systems. The sum total of the experimental data shows that virus-induced mutagenesis and transformation are interrelated: (A) viruses, like other carcinogenes, display mutagenic activity; (B) viruses that are far removed from each other systematically, whose only similarity lay in being oncogenic and capable of integration, simultaneously showed the ability to induce gene mutations; (C) agents changing the rate of transformation also changed the rate of gene mutations: (D) The function of mutagenicity was mapped in the oncogene of SV40 (gene A); and the DNA of (E) mouse mammary carcinoma virus (MMTV) and avian leukosis virus (ALLV) induced tumors has been found to contain nucleotide sequences that transform 3T3NIH cells but do not carry any viral genetic information. Mutagenesis induced by oncogenic viruses may play a part in the multistage process of malignant transformation, though its contribution may be different in various specific cases and for different groups of viruses. Further studies of the uncommon mutagens, which viruses seem to be, may greatly increase our knowledge of the virus-cell relationship. An understanding of the extent of genetic danger inherent in viruses and live viral vaccines is necessary for practical medicine.

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Mortality risk and fine particulate air pollution in a large, representative cohort of U.S. adults.

PMID: 

Environ Health Perspect. 2019 07 ;127(7):77007. Epub 2019 Jul 24. PMID: 31339350

Abstract Title: 

Mortality Risk and Fine Particulate Air Pollution in a Large, Representative Cohort of U.S. Adults.

Abstract: 

BACKGROUND: Evidence indicates that air pollution contributes to cardiopulmonary mortality. There is ongoing debate regarding the size and shape of the pollution–mortality exposure–response relationship. There are also growing appeals for estimates of pollution–mortality relationships that use public data and are based on large, representative study cohorts.OBJECTIVES: Our goal was to evaluate fine particulate matter air pollution ([Formula: see text]) and mortality using a large cohort that is representative of the U.S. population and is based on public data. Additional objectives included exploring model sensitivity, evaluating relative effects across selected subgroups, and assessing the shape of the [Formula: see text]–mortality relationship.METHODS: National Health Interview Surveys (1986–2014), with mortality linkage through 2015, were used to create a cohort of 1,599,329 U.S. adults and a subcohort with information on smoking and body mass index (BMI) of 635,539 adults. Data were linked with modeled ambient [Formula: see text] at the census-tract level. Cox proportional hazardsmodels were used to estimate [Formula: see text]–mortality hazard ratios for all-cause and specific causes of death while controlling for individual risk factors and regional and urban versus rural differences. Sensitivity and subgroup analyses were conducted and the shape of the [Formula: see text]–mortality relationship was explored.RESULTS: Estimated mortality hazard ratios, per [Formula: see text] long-term exposure to [Formula: see text], were 1.12 (95% CI: 1.08, 1.15) for all-cause mortality, 1.23 (95% CI: 1.17, 1.29) for cardiopulmonary mortality, and 1.12 (95% CI: 1.00, 1.26) for lung cancer mortality. In general, [Formula: see text]–mortality associations were consistently positive for all-cause and cardiopulmonary mortality across key modeling choices and across subgroups of sex, age, race-ethnicity, income, education levels, and geographic regions.DISCUSSION: This large, nationwide, representative cohort of U.S. adults provides robust evidence that long-term [Formula: see text] exposure contributes to cardiopulmonary mortality risk. The ubiquitous and involuntary nature of exposures and the broadly observed effects across subpopulations underscore the public health importance of breathing clean air. https://ift.tt/2FyOsyP.

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Influenza vaccinees had significantly higher F1 IgE-specific antibodies following vaccination, suggesting a contamination of vaccine products with allergens of egg origin.

PMID: 

Epidemiol Infect. 1988 Apr ;100(2):291-9. PMID: 3356225

Abstract Title: 

Serological examination of IgE- and IgG-specific antibodies to egg protein during influenza virus immunization.

Abstract: 

The concentrations of serum IgE (PRIST) and IgE- and IgG-specific antibodies to egg protein were determined in paired sera taken from students who had received influenza virus vaccine. Although persons who gave a history of allergy to egg or to chicken feathers were excluded, 10-16% of vaccinees possessed higher titres of serum IgE and IgE-specific antibody (RAST) to egg white (F1) allergen before vaccination. The titres of IgG-specific antibody to egg protein (ovalbumin and ovomucoid antigens) were negligible, and did not show any significant response after vaccination. In contrast, IgE-specific antibody to F1 allergen rose significantly in a considerable number of the vaccines. The results obtained indicate possible contamination of vaccine products with allergens of egg origin and a potential risk of allergic manifestation after influenza vaccination.

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Of vaccines derived from different cell types, avian leukosis viruses and SV-40 viruses have been found.

PMID: 

Dev Biol Stand. 1991 ;75:9-15. PMID: 1794634

Abstract Title: 

Regulatory philosophy and acceptability of cells for the production of biologicals.

Abstract: 

The issue of what types of cells should be considered acceptable for use in manufacture of biologicals dates back to the early 1950s. One of the central points in the discussions and debates over the past 35 years has been the possibility that the use of a given type of cell would result in unsafe products. Of the possible sources of risk, the presence of endogenous viruses in cell substrates has been the only one with realistic and practical implications for public health. The discovery of SV-40 in polio vaccines derived from primary Rhesus kidney cells made the issue of viral contaminants a very real one. Avian leukosis viruses have also been identified as endogenous agents that were carried over into products derived from chicken eggs. It is now important for regulatory policy to continue to be flexible, and to be guided by our technological capabilities in addressing safety issues associated with endogenous viral contaminants.

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These findings suggest that short-term exposure to air pollution may be associated with elevated blood pressure.

PMID: 

Sci Rep. 2019 Dec 30 ;9(1):20298. Epub 2019 Dec 30. PMID: 31889065

Abstract Title: 

Short-term effects of air pollution on blood pressure.

Abstract: 

Elevated blood pressure (BP) has been proposed as a possible pathophysiological mechanism linking exposure to ambient air pollution and the increased risk of cardiovascular mortality and morbidity. In this study, we investigated the hourly relationship between ambient air pollutants and BP. BP measurements were extracted from the electronic health record database of the Seoul National University Bundang Hospital from February 2015 to June 2017. A total of 98,577 individual BP measurements were matched to the hourly levels of air pollutants. A generalized additive model was constructed for hour lags of 0-8 of air pollutants adjusting for age, sex, meteorological variables, and time trend. Systolic BP was shown to be significantly lower at 2-4 hours and 3-5 hours after increased levels of SOand CO, respectively (0.24 mmHg and 0.26 mmHg for an interquartile range, respectively). In contrast, Oand NOwere associated with significantly increased systolic BP at 3-5 lag hours and at 0-2 lag hours, respectively. BP elevation in association with Oand NOwas shown to be significantly greater in hypertensive patients than normotensive subjects. Our findings suggest that short-term exposure to air pollution may be associated with elevated BP.

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Long-term exposure to ambient hydrocarbons increases dementia risk in people aged 50 years and above in Taiwan.

PMID: 

Curr Alzheimer Res. 2020 Jan 2. Epub 2020 Jan 2. PMID: 31902365

Abstract Title: 

Long-Term Exposure to Ambient Hydrocarbons Increases Dementia Risk in People Aged 50 years and above in Taiwan.

Abstract: 

BACKGROUND: Alzheimer's disease, the most common cause of dementia among the elderly, is a progressive and irreversible neurodegenerative disease. Exposure to air pollutants is known to have adverse effects on human health, however, little is known about hydrocarbons in the air that can trigger a dementia event.OBJECTIVE: We aimed to investigate whether long-term exposure to airborne hydrocarbons increases the risk of developing dementia.METHOD: The present cohort study included 178,085 people aged 50 years and older in Taiwan. Cox proportional hazards regression analysis was used to fit the multiple pollutant models for two targeted pollutants, including total hydrocarbons and non-methane hydrocarbons, and estimated the risk of dementia.RESULTS: Before controlling for multiple pollutants, hazard ratios with 95% confidence intervals for the overall population were 7.63 (7.28-7.99, p

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