Acrylonitrile ; toxicity ; Carcinogens ; toxicity ; Humans ; Mutagens ; toxicity ; Occupational Exposure

Benzene is classified as Group 1 carcinogen by IARC. It has been found that benzene induces hematotoxicity even in low dose exposure. The identification of key events during benzene induced hematotoxicty leads to adjustment of occupational exposure limits of benzene. In this review, we focus on the exposure, metabolism, target organs, key epigenetic changes, toxicty effects and end points of low-dose chronic benzene exposure induced hematotoxicity and finally discuss the perspectives on the future study of this area.
Benzene ; toxicity ; Carcinogens ; toxicity ; Epigenesis, Genetic ; Humans ; Occupational Exposure

Carcinogens ; chemistry ; toxicity ; Chromium ; chemistry ; toxicity ; Chromium Compounds ; chemistry ; toxicity ; Humans ; Occupational Exposure ; analysis

Benzene ; toxicity ; Carcinogens ; toxicity ; Chromosome Aberrations ; Genetic Predisposition to Disease ; Humans ; Leukemia ; chemically induced ; genetics

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

OBJECTIVETo study the characteristics of occupational exposure of polycyclic aromatic hydrocarbons (PAHs) in coke oven workers.

METHODSSamples were collected individually and PAHs concentration in the ambient air were assayed by high performance liquid chromatography (HPLC) and toxic equivalency factors (TEFs) were introduced to assess the carcinogenic potency.

RESULTSThe levels of PAHs occupational exposure in oven workers at topside was higher than at side oven and bottom oven (P < 0.05). Non-carcinogenic PAHs were more than 70% of total PAHs and benzo[a]pyrene accounted for 65.5% approximately 72.4% of total benzo[a]pyrene equivalents. Total occupational exposure level of PAHs in coke oven workers was positively related to the content of benzo[a]pyrene and pyrene, respectively (r(2) = 0.84, r(2) = 0.94, P < 0.05).

CONCLUSIONCoke oven workers were exposed to a high level of PAHs which possessed some extent of carcinogenic potency, and benzo[a]pyrene is the chief carcinogenic substance.

Benzo(a)pyrene ; analysis ; toxicity ; Carcinogens ; analysis ; toxicity ; Chromatography, High Pressure Liquid ; Coke ; Humans ; Occupational Exposure ; Polycyclic Compounds ; analysis ; toxicity

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

OBJECTIVETo examine maternal and fetal exposure levels to four carcinogenic metals, arsenic (As), cadmium (Cd), nickel (Ni), and beryllium (Be), and to investigate their environmental influences.

METHODSMetal concentrations in maternal and umbilical cord blood were measured by inductively coupled plasma-mass spectrometry (ICP-MS). Environmental factors that might play a role in exposure were analyzed using Mann-Whitney nonparametric U-tests and multiple linear regression.

RESULTSThe concentrations of As, Cd, and Ni in umbilical cord blood (5.41, 0.87, and 139.54 μg/L) were significantly lower than those in maternal blood (6.91, 1.93, and 165.93 μg/L). There were significant positive correlations between the maternal and cord concentrations of each carcinogen. Our results showed that: (i) exposures to potentially harmful occupational factors during pregnancy were associated with high levels of maternal As, Cd, and Ni; (ii) living close to major transportation routes (<500 m) or exposure to second-hand smoke during pregnancy increased the maternal Cd levels and (iii) living close to industrial chimneys induced high maternal Ni levels. Multiple linear regression analysis showed that these environmental factors remained significant in models of the influences of these four carcinogens.

CONCLUSIONBoth mothers and fetuses had been exposed to As, Cd, Ni, and Be. The increased levels of these carcinogens in pregnant women were associated with some detrimental environmental factors, such as occupational exposure, contact with second-hand smoke and living close to major transportation routes or industrial chimneys.

Carcinogens, Environmental ; toxicity ; Environmental Exposure ; Environmental Pollutants ; toxicity ; Female ; Humans ; Maternal-Fetal Exchange ; Metals ; toxicity ; Pregnancy ; Time Factors

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

Recently, Ng et al. reported that the A:T > T:A substitutions, proposed to be a signature of aristolochic acid (AA) exposure, were detected in 76/98 (78%) of patients with hepatocellular carcinoma (HCC) from the Taiwan Province of China, and 47% to 1.7% of HCCs from the Chinese mainland and other countries harbored the nucleotide changes. However, other carcinogens, e.g., tobacco carcinogens 4-aminobiphenyl and 1,3-butadiene, air toxic vinyl chloride and its reactive metabolites chloroethylene oxide, melphalan and chlorambucil, also cause this signature in the genome. Since tobacco smoke is a worldwide public health threat and vinyl chloride distributes globally and is an air pollutant in Taiwan Province, the estimation of the patients' exposure history is the key to determine the "culprit" of the A:T > T:A mutations. Apparently, without estimation of the patients' exposure history, the conclusion of Ng et al. is unpersuasive and misleading.
Aristolochic Acids ; toxicity ; Carcinogens ; toxicity ; Carcinoma, Hepatocellular ; chemically induced ; genetics ; China ; Environment ; Humans ; Liver Neoplasms ; chemically induced ; genetics ; Mutation ; Taiwan ; Tobacco ; toxicity ; Vinyl Chloride ; toxicity