Air Pollutants, Occupational ; analysis ; Carcinogens, Environmental ; analysis ; Chromium ; analysis ; Environmental Monitoring ; methods ; Workplace

Objective: To analyze the level of PCDD/Fs exposure of occupational workers in the waste incineration industry and explore the risk of occupational exposure. Methods: In September 2021, literature on environmental PCDD/Fs exposure in waste incineration plants published from the establishment of the database to February 10, 2021 was retrieved from CNKI database. A total of 1365 literatures were retrieved, and 7 met the criteria for inclusion. The US Environmental Protection Agency (EPA) inhalation risk model was used to assess and analyze carcinogenic and non-carcinogenic risks of PCDD/Fs exposure among occupational workers in the waste incineration industry. Results: A total of 86 sampling sites were included in incineration plants in 7 regions. The study of Wuhan area showed that the concentration of working environment near the waste incinerator in the same factory was the highest, followed by the rest and office area in the factory. The concentration of PCDD/Fs in waste incinerators was the highest in Southwest China (4880.00-24880.00 pg TEQ/m(3)), and the lowest in Shenzhen (0.02-0.44 pg TEQ/m(3)). According to the cancer risk assessment, with the increase of exposure years, the risk of cancer increased. The highest risk of cancer was found in the waste incineration plants in Southwest China. When the exposure period was 1 year, the risk was moderate (22.40×10(-6)-114.20×10(-6)). When the exposure time was more than 5 years, the risk of cancer was high. In Jinan, workers working near the incinerator had a moderate risk of cancer after five years of exposure. In Zhejiang, workers were at medium risk of cancer after exposure for more than 20 years. Workers in Wuhan, Shanghai, Zhejiang Province, Shenzhen and the Pearl River Delta were still at low risk of cancer after 40 years of occupational exposure. HQ>1 of workers working near the waste incinerators in Jinan, Zhejiang Province and Southwest China, and the qualitative evaluation results showed that the non-carcinogenic risk was unacceptable. Conclusion: There are great differences in PCDD/Fs of occupational exposure in waste incineration industry, and the occupational exposure exceeding the occupational exposure limit has higher carcinogenic and non carcinogenic risks.
Humans ; Dibenzofurans ; Polychlorinated Dibenzodioxins/analysis* ; Air Pollutants/analysis* ; Incineration ; Dibenzofurans, Polychlorinated/analysis* ; China/epidemiology* ; Benzofurans ; Occupational Exposure/analysis* ; Carcinogens ; Risk Assessment ; Neoplasms ; Environmental Monitoring/methods*

Recently, the International Agency for Research on Cancer (IARC) has classified outdoor air pollution and the particulate matter component of outdoor air pollution as class I carcinogen. Air pollution is consistently associated with lung cancer in epidemiologic and experimental studies. The IARC assessment is specifically designed as hazard identification, and it does not quantify the magnitude of the cancer risk. This article addresses the magnitude of the lung cancer risk in the population due to ambient air pollution exposure.
Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Carcinogens, Environmental ; toxicity ; Humans ; Lung Neoplasms ; etiology ; Particulate Matter ; toxicity ; Risk Factors

The International Agency for Research on Cancer (IARC) has classified outdoor air pollution and the particulate matter (PM) in outdoor air pollution as carcinogenic to humans, as based on sufficient evidence of carcinogenicity in humans and experimental animals and strong support by mechanistic studies. The data with important contributions to the evaluation are reviewed, highlighting the data with particular relevance to China, and implications of the evaluation with respect to China are discussed. The air pollution levels in Chinese cities are among the highest observed in the world today and frequently exceed health-based national and international guidelines. Data from high-quality epidemiologic studies in Asia, Europe, and North America consistently show positive associations between lung cancer and PM exposure and other indicators of air pollution, which persist after adjustment for important lung cancer risk factors, such as tobacco smoking. Epidemiologic data from China are limited but nevertheless indicate an increased risk of lung cancer associated with several air pollutants. Excess cancer risk is also observed in experimental animals exposed to polluted outdoor air or extracted PM. The exposure of several species to outdoor air pollution is associated with markers of genetic damage that have been linked to increased cancer risk in humans. Numerous studies from China, especially genetic biomarker studies in exposed populations, support that the polluted air in China is genotoxic and carcinogenic to humans. The evaluation by IARC indicates both the need for further research into the cancer risks associated with exposure to air pollution in China and the urgent need to act to reduce exposure to the population.
Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Animals ; Asia ; Carcinogens, Environmental ; toxicity ; China ; Environmental Exposure ; Humans ; International Agencies ; Lung Neoplasms ; etiology ; Neoplasms ; etiology ; Particulate Matter ; toxicity ; Risk Factors

Air pollution in China comes from multiple sources, including coal consumption, construction and industrial dust, and vehicle exhaust. Coal consumption in particular directly determines the emissions of three major air pollutants: dust, sulfur dioxide (SO(2)), and nitrogen oxide (NOx). The rapidly increasing number of civilian vehicles is expected to bring NOx emission to a very high level. Contrary to expectations, however, existing data show that the concentrations of major pollutants [particulate matter-10 (PM10), SO(2), and nitrogen dioxide (NO(2))] in several large Chinese cities have declined during the past decades, though they still exceed the national standards of ambient air quality. Archived data from China does not fully support that the concentrations of pollutants directly depend on local emissions, but this is likely due to inaccurate measurement of pollutants. Analyses on the cancer registry data show that cancer burden related to air pollution is on the rise in China and will likely increase further, but there is a lack of data to accurately predict the cancer burden. Past experience from other countries has sounded alarm of the link between air pollution and cancer. The quantitative association requires dedicated research as well as establishment of needed monitoring infrastructures and cancer registries. The air pollution-cancer link is a serious public health issue that needs urgent investigation.
Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Carcinogens, Environmental ; toxicity ; China ; Coal ; Humans ; Neoplasms ; etiology ; Nitrogen Dioxide ; toxicity ; Particulate Matter ; toxicity ; Sulfur Dioxide ; toxicity ; Vehicle Emissions ; toxicity

Air Pollutants, Radioactive ; adverse effects ; Environmental Exposure ; adverse effects ; Humans ; Lung Neoplasms ; etiology ; genetics ; Neoplasms, Radiation-Induced ; etiology ; genetics ; Radon ; adverse effects

A substantial literature demonstrates that the main ultrafine particles found in ambient urban air are combustion-derived nanoparticles (CDNP) which originate from a number of sources and pose a hazard to the lungs. For CDNP, three properties appear important-surface area, organics and metals. All of these can generate free radicals and so induce oxidative stress and inflammation. Inflammation is a process involved in the diseases exhibited by the individuals susceptible to the effects of PM- development and exacerbations of airways disease and cardiovascular disease. It is therefore possible to implicate CDNP in the common adverse effects of increased PM. The adverse effects of increases in PM on the cardiovascular system are well-documented in the epidemiological literature and, as argued above, these effects are likely to be driven by the combustion-derived NP. The epidemiological findings can be explained in a number of hypotheses regarding the action of NP:-1) Inflammation in the lungs caused by NP causes atheromatous plaque development and destabilization; 2) The inflammation in the lungs causes alteration in the clotting status or fibrinolytic balance favouring thrombogenesis; 3) The NP themselves or metals/organics released by the particles enter the circulation and have direct effects on the endothelium, plaques, the clotting system or the autonomic nervous system/ heart rhythm. Environmental nanoparticles are accidentally produced but they provide a toxicological model for a new class of purposely 'engineered' NP arising from the nanotechnology industry, whose effects are much less understood. Bridging our toxicological knowledge between the environmental nanoparticles and the new engineered nanoparticles is a considerable challenge.
Air Pollutants/*toxicity ; Carcinogens, Environmental/*toxicity ; Cardiovascular Diseases/etiology ; Endothelium/drug effects ; Humans ; Lung/*drug effects ; Nanoparticles/*toxicity ; Nanotubes, Carbon/toxicity ; Particle Size ; Quantitative Structure-Activity Relationship

OBJECTIVETo investigate the possible effects of long-term exposure to dust containing thorium and thoron progeny on dust-exposed miners.

METHODSA negative, high voltage, exhaled thoron progeny measurement system was used to estimate the miners' thorium lung burden.

RESULTSThe highest thorium lung burden of 638 miners was 11.11 Bq. The incidence of stage 0(+) pneumoconiosis was higher among dust-exposed miners. Lung cancer mortality of the dust-exposed miners was significantly higher than that of controls (P < 0.005).

CONCLUSIONThere is a difference in cancer rates between those who have long-term exposure to dust containing thorium (in which carcinogenic ThO(2) and SiO(2) exist) and thoron progeny and those who have not.

Air Pollutants, Radioactive ; adverse effects ; Body Burden ; China ; epidemiology ; Dust ; Follow-Up Studies ; Humans ; Lung Neoplasms ; epidemiology ; Mining ; Occupational Diseases ; epidemiology ; Occupational Exposure ; adverse effects ; Thorium ; adverse effects

Inhibition of cyclooxygenase(COX), and thus prevention of the formation of prostaglandins, provided a unifying explanation of the therapeutic and toxic actions of nonsteroidal anti-inflammatory drugs(NSAIDs). Recently, the discovery of the two isoforms of COX was made by molecular biologists studying neoplastic transformation in chick embryo cells. The constitutive enzyme, COX-1, is obviously responsible for the production of prostaglandins involved in housekeeping functions such as maintenance of integrity of the gastric mucosa, renal blood flow and platelet aggregation. The inducible form of COX(COX-2) is responsible for the formation of prostaglandins that pathologic effects of inflammation, pain and fever. Clearly, all the experimental and clinical data support the hypothesis that the beneficial effects of NSAIDs are due to inhibition of the COX-2 enzyme, whereas the gastrotoxicity is due to inhibition of COX-1. The COX-2/COX-1 ratios of the NSAIDs in common use have been measured and compared with epidemiological data on their side effects. there is little evidence to suggest that one NSAID is clearly more efficacious than another and substantial individual variability is present with respect to the pharmacology and pharmacokinetics of these drugs, it is essential to adjust the dosage and choose specific drug to the patient`s response.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Chick Embryo ; Fever ; Gastric Mucosa ; Housekeeping ; Inflammation ; Pharmacokinetics ; Pharmacology ; Platelet Aggregation ; Prostaglandins ; Protein Isoforms ; Renal Circulation ; Toxic Actions

Antioxidants oppose the toxic actions of lipid peroxides and oxygen radicals, and they limit the amount of lipid peroxides formed. Women with normal pregnancies have an increase in oxidative stress and lipid peroxidation when compared with nonpregnant women. The antioxidants also increase progressively with advancing gestation, and the antioxidants in the fetus also increase with advancing gestation, especially during late gestation. The purpose of this study is to investigate the diefference of antioxidant status in maternal and neonatal plasma according to the delivery type. So, we investigated the status of antioxidant in the maternal and neonatal plasma when compared normal vaginal delivery with Cesarian section without labor. This study was done under the hypothesis that labor pain is originated from the hypoxic state of myometrium during uterine contraction. The number of women who were studied was total 56, 24 women were delivered by normal vaginal delivery and 32 women were done by Cesarean section without labor. The blood was sampled during active labor and postpartum 24 hour in the case of normal vaginal delivery, the women who were done Cesarean section being sampled before operation and 24 hours after operation. The neonatal blood was sampled from cord, birth 1 day and 3 day. The antioxidant levels were measured by Total Antioxidant Status (Randox Laboratory Ltd., UK) kit. The results were as follows. 1. The mean maternal plasma antioxidant status was not significantly different according to delivery types and not significantly different when compared antepartum with postpartum (vaginal delivery; antepartum: 1.54+/-0.31 mM/L, postpartum: 1.58+/-0.32 mM/L, Cesarean section; antepartum: 1.55+/-0.29 mM/L, postpartum: 1.56+/-0.33 mM/L). 2. The neonatal antioxidant status was not significantly different between the neonates who were born by vaginal delivery and the neonates who were born by Cesarean section. The neonatal plasma antioxidant status was increased progressively after birth (cord: birth 1 day: birth 3 day=1.46+/-0.25 mM/L: 1.59+/-0.25 mM/L: 1.79+/-0.37 mM/L). Therefore, labor pain was not seems to be significantly affect the maternal and neonatal plasma antioxidant status. And the neonatal antioxidant status was increased for adaptation to the external environment after birth.
Animals ; Antioxidants ; Cesarean Section ; Female ; Fetus ; Humans ; Infant, Newborn ; Labor Pain ; Lipid Peroxidation ; Lipid Peroxides ; Mice ; Myometrium ; Oxidative Stress ; Parturition ; Plasma* ; Postpartum Period ; Pregnancy ; Reactive Oxygen Species ; Toxic Actions ; Uterine Contraction