Why is Asbestos so Controversial?

Chrysotile is a collective name for serpentine asbestos. Serpentine {Mg6Si4O10 (OH) 8} is a double-octahedral silicate mineral consisting of silicon-oxygen (SiO2) tetrahedron and magnesium hydroxide Mg (OH) 2 octahedron. Due to the inconsistency between the tetrahedral layer and the octahedral layer, three different basic structures are formed, which constitute three minerals, namely, plate-like serpentine with a flat structure; leaf serpentine with an alternating wave-like structure; with curl Serpentine with a cylindrical structure. In the natural world, the fiber serpentine minerals have a wide range of production, and have a high degree of crystallinity, and have good separability. The fiber serpentine with remarkable filamentous characteristics is a useful industrial mineral, and can also be called fiber serpentine asbestos.

Optical properties of chrysotile

Chrysotile asbestos has a variety of physical and chemical properties, excellent splitting performance, can be split into filaments to the greatest extent, and the minimum splitting diameter is 1 to 2 m. For industrial use, the specific surface area is used as a measurement index, generally in the range of 5 to 50 m2 / g. High mechanical strength, the tensile strength value is 120 ~ 350 (unit: 9.8 × 106Pa).

Among them: high-strength fibers are greater than 350, normal-strength fibers are less than 350 and greater than 250, medium-strength fibers are less than 250 and greater than 150, and low-strength fibers are less than 150. temperature

Asbestos has long been known to be carcinogenic, but asbestos is subdivided into chrysotile and amphibole. The comparative experiments of mineral experts, pathologists, and toxicology experts at home and abroad for more than two years have proved that chrysotile asbestos is relatively safe among chrysotile, amphibole, and many other "chrysotile asbestos replacement fibers". Inorganic fiber material. Since 2004, Dr. David Bernstein, a well-known inhalation poison expert in Switzerland and a toxicology consultant for multi-national governments, has released the experimental results of "chrysotile asbestos can be used safely". In the past 2 years, China, Russia, Canada, India, Brazil, Mexico Many experts in mineralogy, pathology, and toxicology from other countries, after their own scientific experiments, have reached a conclusion that is completely consistent with Dr. Bernstein.

However, in March 2001, the WTO made a landmark ruling that since chrysotile asbestos has been identified as a carcinogen, the safe use limit that asbestos manufacturers insist on does not exist. Legalizing the rights of WTO members to ban the use or import of carcinogens such as asbestos, and further confirms that WTO members have the right to believe that protecting lives and health is more important than fulfilling trade obligations.

The carcinogenicity of asbestos has long been known to the academic community, but the domestic industry, especially the construction industry, has not banned it. Although the government has stipulated that protective equipment must be worn for mining and processing chrysotile asbestos, there is no corresponding specification and guidance for the application.

Asbestos is divided into serpentine asbestos (chrysotile) and amphibole asbestos (blue asbestos, ancillary asbestos, amphibole, asbestos, tremolite). Most of China's asbestos resources are chrysotile asbestos, which accounts for more than 95% of total asbestos output. The safety of asbestos use is a controversial topic in the mineral industry. The most serious occupational diseases caused by asbestos are asbestos lung, lung cancer and mesothelioma. Among all types of asbestos, the most pathogenic is bluestone asbestos, and the potential for carcinogenesis and fibrosis of chrysotile is still controversial.

Carcinogenic and fibrotic mechanisms of chrysotile

Chrysotile asbestos has the same pathogenic mechanism as other types of asbestos, and its harm comes from the dust fibers generated during processing. These tiny fibers enter the lungs through breathing, and most of them are excreted through the respiratory clearance system (mucous ciliary clearance mechanism and effective cough). If they cannot be discharged, they can be swallowed by alveolar macrophages or penetrate epithelial cells and enter the lungs. Interstitial, thus staying in the body for a long time. Residual chrysotile asbestos fibers trigger inflammatory and oxidative stress responses, which is an important mechanism for asbestos-induced cell damage. At present, the mechanism of chrysotile asbestos-induced fibrosis and carcinogenesis has not been fully elucidated. It is believed that the following mechanisms are included:

1) Mechanical damage: Most chrysotile asbestos invades the human body in the form of elementary fibers. These fibers are crystalline, sharp and spiked, and can penetrate alveolar epithelial cells and pleural mesothelial cells, causing mechanical interference and damage to chromosomes and DNA , Cause lung cancer and mesothelioma.

2) Free radical and cytokine-mediated damage: Chrysotile asbestos fibers, based on their own chemical properties and by activating alveolar macrophages, can induce the production of reactive oxygen species such as hydrogen peroxide, superoxide anions and hydroxide ions, leading to DNA damage and fibrosis. On the one hand, unsaturated O-Si-O, Si-O-Si, and Mg-O bonds existing on the surface of chrysotile asbestos fibers have strong surface activity, and oxygen-containing free radicals cause chain reactions of cell membrane free radicals; In terms of chrysotile asbestos, it can also stimulate macrophages to cause respiratory bursts and disintegrate to death, releasing a series of lysosomal enzymes, inflammatory cytokines and reactive oxygen free radicals. Under the action of two mechanisms, lipid peroxidation of polyunsaturated fatty acids on the cell membrane causes cell and matrix damage. Chrysotile asbestos fibers cause cell and matrix component damage through lipid peroxidation of cell membranes of macrophages and fibroblasts, promote fibroblast proliferation and collagen synthesis, cause destruction of the entire alveolar structural unit, and form irreversible fibrosis. Asbestos lung and other pulmonary fibrosis diseases. Early changes in genotoxicity caused by chrysotile asbestos fibers are mainly through DNA damage and chromosomal alteration pathways. At the DNA level, cell mutagenicity is mainly caused by DNA single-strand, double-strand breaks, and oxidative damage. At the chromosomal level, chromosomal aberrations or changes in numbers are caused mainly by breaking, deleting, inverting chromosomes or chromosome monomers, and exchanging sister chromosome monomers, resulting in mutagenic effects.

3) Proto-oncogene activation and inactivation of tumor suppressor genes: Chrysotile can change the cell signaling system, activate proto-oncogenes and cause inactivation of tumor suppressor genes, which in turn affects cell proliferation and differentiation, causing the occurrence of lung cancer and mesothelioma. .

Factors affecting the pathogenicity of chrysotile asbestos

Of Concentration on Pathogenicity of Chrysotile Asbestos

Studies at home and abroad suggest that the mass concentration of chrysotile asbestos dust in the air of the working environment (hereinafter referred to as the concentration) has a significant dose-response relationship with the onset of asbestos lungs, and its content in the air must reach a certain level to cause harm to human health. Each study is calculated based on the prevalence of asbestos lung in 1% to 3% and 30 to 40 years of service life. It is predicted that the allowable concentration of asbestos dust should be lower than 2.71 to 3.90 mg / m3 or the allowable concentration of asbestos fiber should be lower than 1.15 to 2.00 f / mL (f is the number of fibers), which indicates that the current occupational exposure limit of asbestos dust in the workplace in China is 0.8 mg / m3 or 0.8 f / mL is reasonable, and the concentration of chrysotile fiber can be controlled within a safe range. At the same time, some scholars believe that the increased carcinogenic risk has been observed in people with low levels of chrysotile asbestos, so there is no certain safety threshold for chrysotile. This is why some researchers believe that chrysotile has no safety threshold.

Effects of Morphology on Pathogenicity of Chrysotile Asbestos

Fiber size affects biological survival, which in turn affects lung respiration, sedimentation, and clearance. The impact of size is considered from two aspects:

1) Whether the fiber is inhalable;

2) If it is inhalable, the effect of fiber size must still be considered after inhalation. Most chrysotile asbestos fibers and dust can be gradually transported upward by the mucus of the trachea-bronchial tree and discharged with cough. According to pathological specimens under electron microscopy, no fibers longer than 200 m were found in the lungs, and most were shorter than 50 m. After entering the lungs, very short fibers, especially those shorter than 5 m, and dust can be completely engulfed by macrophages. They are removed by a mechanism similar to the removal of non-fibrous particles. Longer fibers cannot be macrophages. Completely engulfed, prolonged presence in the lungs will cause disease. And longer, chrysotile fibers longer than 20 m can be quickly cleared from the lungs, not transferred to the pleural cavity, and do not initiate fiber-induced responses. Particularly short ones can be swallowed and dissolved, longer ones can be removed, and pathogenic fibers are concentrated in the middle length. Asbestos fibers with the greatest risk of carcinogenesis to humans are fibers with a length of more than 5 to 8 m, a diameter of less than 1.5 m, or a diameter of more than 0.25 m.

In addition to length, fiber shape also affects its pathogenicity. The amphibole asbestos fiber is a chain structure, while the chrysotile asbestos fiber is a pleated or rolled sheet silicate, and the curled fiber shape is not easy to inhale into the respiratory tract. In addition, thin and short fibers have a lower mass and stay in the air longer than thick and long fibers. Most asbestos fibers are thicker than the new nanofibers currently under development, indicating that they have a shorter suspension time and are less likely to be inhaled.

Effects of Solubility and Pathogenicity of Chrysotile

When deposited in the lungs, some fibers can be completely dissolved directly, while others cannot be dissolved, but can be broken into short films and successfully swallowed and cleared. Highly soluble fibers show less pathogenicity, while poorly soluble fibers are more pathogenic. Chrysotile asbestos can be broken down by strong acids (such as those produced by macrophages when they are phagocytosed), has better solubility and less biological residencies, which will reduce its pathogenicity to the body. And amphibole asbestos is more stubborn and will not be destroyed in most cases, so it has strong carcinogenicity. Chrysotile asbestos is a flaky silicate with a thin layer and curled shape. It is about 0.8 nm thick and has a sandwich structure composed of magnesium and silica. The acidic environment provided by lung macrophages can quickly destroy this sheet-like structure, breaking down chrysotile asbestos fibers into small pieces, and then these fragments can be easily removed from the lungs.

The amphibole-like asbestos is a solid rod-shaped double-stranded tetrahedral silicate fiber, which makes it very strong and durable. The outer surface of the hornblende-like asbestos crystal structure is like quartz, and has chemical resistance similar to quartz. The amphibole-like asbestos fibers do not dissolve at any pH.

Effects of smoking on the pathogenicity of chrysotile

Tobacco and asbestos are both human carcinogens announced by the International Alliance Against Cancer (IARC), and smoking has a synergistic effect on lung cancer in chrysotile contacts. Smoking reduces the body's ability to remove chrysotile fibers and dust, making asbestos dust easy to deposit in the respiratory system. At the same time, the smoke solution inhibits the phagocytosis of macrophages, making macrophages unable to effectively defend against invasion, thereby directly affecting chrysotile In the target cells, the generation of free radicals is exacerbated, which in turn leads to DNA damage and more serious damage. Surveys have shown that smokers who are not exposed to chrysotile asbestos have a lung cancer relative risk (RR) of 26, and those who are not exposed to chrysotile asbestos have an RR of 12.2, while smokers who are exposed to chrysotile asbestos have an RR of 32.1. The synergy index is 2.2.

Study on reducing pathogenicity of chrysotile

Some studies have found that the composition and content of surface elements of chrysotile asbestos fibers pretreated with three compounds of aluminum citrate, mixed rare earth or sodium selenite have changed, resulting in the effect of this type of chrysotile on In the cell, the acid phosphatase activity of the cell is reduced, the survival rate of human embryonic lung cells is improved, the ultrastructure is changed, the oncogene transcription level is reduced, and finally the cytotoxicity of chrysotile is reduced. Another study found that garlic extract can effectively reduce the genotoxicity of chrysotile asbestos in peripheral blood lymphocytes.

Epidemiological study of occupational tumors caused by chrysotile

A large number of domestic epidemiological investigations have shown that chrysotile asbestos dust has significant pathogenicity when exposed to concentrations exceeding the standard.

A 25-year longitudinal cohort study of Chongqing asbestos factories exposed to pure asbestos workers showed that the dust concentration in the raw material room and the textile room was 7.6 f / mL and 4.5 f / mL, respectively. 8.1 times. A 27-year follow-up study of 515 workers exposed to chrysotile asbestos in another large asbestos plant in China found that the average concentration of chrysotile asbestos before the 1960s was 146.2 mg / m3 and decreased to 10 mg / m after the 1990s. m3, the incidence of lung cancer was significantly higher in workers exposed to chrysotile asbestos (P <0.05).

Another 41-year investigation of Zhejiang home chrysotile asbestos textile industry found that the concentration of chrysotile asbestos dust in the operating environment in the 1960s was 38.00 to 73.00 mg / m3, and it was reduced to an average of 1.25 mg / m3 in the 1970s. However, it still exceeded the standard. A total of 858 deaths occurred among 5,681 female workers, of which 213 died of cancer. Lung cancer ranked first (87 cases, 40.85%). The standardized death rate for lung cancer was 3.88, which was significantly higher than the age-standardized death rate of local women. ratio. A study on a large chrysotile asbestos mine found that exposure to chrysotile can increase the mortality of lung cancer, asbestos and other diseases in miners. However, foreign studies believe that chrysotile fiber dust below the limit concentration will not cause health risks. Studies by David Bernstein, PhD in toxicology, show that chrysotile and amphibole are different in kinetics and pathology, and other similar studies have shown that low-level exposure to chrysotile does not pose a detectable safety risk.

Evidence shows that high concentration and long-term exposure to chrysotile asbestos can cause lung cancer, and low concentrations of chrysotile asbestos do not have detectable health risks, and even if exposed to high concentrations of chrysotile asbestos for a short period of time, the risk of health risks is not high. A 39-year study of cement workers exposed to pure chrysotile asbestos in Greece shows that occupational exposure to pure chrysotile asbestos has nothing to do with the significant increase in lung cancer and mesothelioma. Studies in Brazil have found that reducing asbestos exposure can significantly reduce the incidence of asbestos lung, parenchymal, and / or benign pleural disease.

Epidemic difference in pathogenicity of chrysotile asbestos asbestos

Chrysotile and amphibole are different in inhalation toxicity and pathogenicity. According to David Bernstein, chrysotile asbestos is significantly different from other amphibole asbestos in terms of chemical and mineralogical properties and can be cleared from the lungs more quickly.

Multicentre controlled studies in six Central and Eastern European countries and the United Kingdom found that occupational exposure to asbestos does not appear to promote the incidence of lung cancer in men, and that the risk of lung cancer induced by chrysotile is less than that of chrysotile asbestos combined with amphibole. Another study counted the number of asbestos fibers longer than 5 m in the lung tissue specimens of 133 patients with mesothelioma and 262 patients with lung cancer, and found that chrysotile fibers accounted for only 2%. A study by the British Health Security Council showed that chrysotile asbestos and the other two types of amphibole asbestos differ in the risk of mesothelioma by 1: 100: 500. Summarizing extensive epidemiological studies of 71 asbestos populations shows that there is no evidence to support the hypothesis that chrysotile asbestos that is not contaminated with amphibole can cause mesothelioma.

Research Direction and Prospect of Pathogenic Mechanism of Chrysotile Asbestos

The mechanism of carcinogenesis and fibrosis of chrysotile asbestos is very complicated, and there are still many unclear researches. For example, what is the complete pathogenic mechanism of chrysotile asbestos at the level of cell signal transmission? The composition of chrysotile asbestos in different regions is different, and how does it affect the pathogenicity of chrysotile? Chrysotile has both carcinogenicity and fibrosis. What is different from other carcinogens or fibrotic substances? At the cellular level, what are the differences in the pathogenic mechanisms of chrysotile asbestos and other types of asbestos? Are there effective methods and applications for reducing the pathogenicity of chrysotile asbestos? A complete study of the chrysotile asbestos pathogenic mechanism, influencing factors and methods of reducing toxicity can help people to more fully understand the hazards of chrysotile asbestos, and based on this, develop appropriate protective measures and protective methods for safer and healthier application Chrysotile. ^[3]