**Occupational Exposure to Coal, Genotoxicity, and Cancer Risk**

Grethel León-Mejía , Milton Quintana Sosa , Paula Rohr , Katia Kvitko, João Antonio Pêgas Henriques and Juliana da Silva

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/62486

#### **Abstract**

Coal is a heterogeneous mixture containing large quantities of organic and inorganic matter, including carbon, hydrogen, oxygen, sulfur, nitrogen, and organometallic forms. The presence of mineral matter in coal may result in a number of environmental and human health problems related to its mining, preparation, and combustion. During coal mining activities, large quantities of coal dust, ashes, polycyclic aromatic hydrocarbons (PAHs), and heavy metals are released into the environment, forming a complex mixture. This mixture becomes one of the most important occupational risks for the health and safety of workers due to its synergistic, additive, and enhancing effects. Once inside the organism, this cocktail-like mixture can interact with cellular mechanisms related to the production of reactive oxygen species (ROS) and can cause damage in important macromolecules such as DNA, lipids, and proteins. In this review, human populations exposed to coal and coal burning were analyzed. Data from different studies were evaluated in relation to the effect of complex mixture exposure on DNA damage and mechanisms, and the background factors, such as gender, age, or smoking habit. The high temperatures that occur in combustion processes affect the characteristics of the resulting particles. The coal fly ash is released by combustion and its composition varies depend‐ ing on the coal type and the method of collection used such as electrostatic precipita‐ tors. Compounds such as PAHs once activated by the organisms have been shown to have mutagenic and carcinogenic activity due to its ability to form adducts with purines. Moreover, metals that commonly are evaporated during the cooling process increase its toxicity. The particles when inhaled can pass from the alveoli into the bloodstream and affect extrapulmonary organs. Several studies have described the inflammatory cascade that triggers exposure to coal and coal fly ash particles; they have a complex composi‐ tion capable of generating a persistent inflammatory process, resulting in diseases widely described as emphysema, bronchitis, pneumoconiosis, asthma, and cancer. Several human biomonitoring studies have been conducted evaluating the inflammatory process and

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the release of cytokines, polymorphisms involved in detoxification mechanisms, different biomarkers associated with occupational exposure, DNA damage, and the influence of oxidative stress in disease development. The relationship between chronic exposure to coal and coal ash particles and cancer is still widely debated. This review gave us a broad assessment about the associated mechanisms between cancer and exposure to coal and different findings around the world.

**Keywords:** coal, biomonitoring, DNA damage, ROS, PAHs, diseases

### **1. Introduction**

In the last decades, the human population genetics integrity has been compromised by the great industrial activity, which exposes people to a variety of chemicals and genotoxic agents. As a result, it is important to determine what is considered as an "acceptable" level of genetic damage in a concrete population, carry out assay genotoxicity as a routine and also monitor those who, by their occupation or lifestyle, are more exposed or with a bigger risk of having alterations on their genetics stability [1].

One method to quantify the exposure to those substances, as well as its possible impact on the organism, is the use of biological monitoring procedures, or biomonitoring, through biomark‐ ers. Biomonitoring studies try to establish a connection between the environmental factors and the diseases. They detect first alterations in nonmalignant phases, so as to prevent health problems by recognizing the environmental cause of them.

The biological markers, or biomarkers, are the measurable changes (biochemical, physiologi‐ cal, or morphological) that associate to a toxic exposure or any early biochemical alteration, whose study on the biological fluids, tissues, or exhaled air that allow to assess the health risk exposure intensity. The identification of genotoxicity markers believed to cause genome damage is useful, since it can define a prepathogenesis state, such as cancer. It is of vital importance for different diseases prevention, which is the final goal of biomonitoring. In order to achieve it, there must be two stages: 1) detecting human exposure to environment carcino‐ genic agents; 2) determining genotoxic effects *in vivo* [2].

The combined use of genetic biomarkers and classic epidemiology tools (clinic history and questionnaires) has enabled the identification of early effects to the occupational exposure to distinct pollutant around the world [2–4]. Many biomarkers are used to assess genotoxic effects on human populations exposed to complex mixtures of chemicals. Although there are different possibilities, micronuclei (MN) frequency, chromosomal aberrations (CAs), and comet assay are the most commonly chosen biomarkers. MN originates from chromosome fragments or whole chromosomes that are not included in the main daughter nuclei during nuclear division [5, 6]. MN induction reflects clastogenic and aneugenic damage and is a predictive biomarker of cancer risk [7]. Comet assay detects DNA lesions in individual cells obtained under a variety of experimental conditions; the technique can also be used to evaluate DNA repair [8, 9].

The large inter-individual variability in the capacity to activate or inactivate potential geno‐ toxic and carcinogenic compounds is probably influenced by polymorphisms of the genes encoding the metabolizing enzymes. Genes and proteins involved in metabolization/detoxi‐ fication of xenobiotics, as well as those involved in DNA repair, are usually used as potential markers of susceptibility for the development of several diseases in which the etiology is related to exposure to environmental hazards. Polymorphisms in such genes have been linked with an increased risk of cancer in several case-control studies [10].

Biomonitoring studies in populations exposed to complex mixtures of chemicals considering individual susceptibility are quite complicated due to inadequate toxicity data, and the unpredictable nature of interaction effects that may be synergistic, additive, or enhancers.
