The history, genotoxicity, and carcinogenicity of carbon-based fuels and their emissions. Part 2: solid fuels.

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MUTREV 8087 1–15 Mutation Research xxx (2014) xxx–xxx

Contents lists available at ScienceDirect

Mutation Research/Reviews in Mutation Research journal homepage: www.elsevier.com/locate/reviewsmr Community address: www.elsevier.com/locate/mutres

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Review

The history, genotoxicity, and carcinogenicity of carbon-based fuels and their emissions. Part 2: Solid fuels D. Claxton *

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Q1Larry

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Q2LDC Scientific Services, 6012 Brass Lantern Court, Raleigh, NC 27606, United States

A R T I C L E I N F O

A B S T R A C T

Article history: Received 8 May 2014 Received in revised form 25 July 2014 Accepted 26 July 2014 Available online xxx

The combustion of solid fuels (like wood, animal dung, and coal) usually involves elevated temperatures and altered pressures and genotoxicants (e.g., PAHs) are likely to form. These substances are carcinogenic in experimental animals, and epidemiological studies implicate these fuels (especially their emissions) as carcinogens in man. Globally, 50% of all households and 90% of all rural households use solid fuels for cooking or heating and these fuels often are burnt in simple stoves with very incomplete combustion. Exposed women and children often exhibit low birth weight, increased infant and perinatal mortality, head and neck cancer, and lung cancer although few studies have measured exposure directly. Today, households that cannot meet the expense of fuels like kerosene, liquefied petroleum gas, and electricity resort to collecting wood, agricultural residue, and animal dung to use as household fuels. In the more developed countries, solid fuels are often used for electric power generation providing more than half of the electricity generated in the United States. The world’s coal reserves, which equal approximately one exagram, equal 1 trillion barrels of crude oil (comparable to all the world’s known oil reserves) and could last for 600 years. Studies show that the PAHs that are identified in solid fuel emissions react with NO2 to form direct-acting mutagens. In summary, many of the measured genotoxicants found in both the indoor and electricity-generating combustors are the same; therefore, the severity of the health effects vary with exposure and with the health status of the exposed population. ß 2014 Published by Elsevier B.V.

Keywords: Combustors Mutagenicity Salmonella Coal Wood Cancer

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Contents 1. 2.

3. 4. 5. 6. 7. 8. 9.

Introduction . . . . . . . . . . . . . . . . . . . . . . . Coal as fuel. . . . . . . . . . . . . . . . . . . . . . . . Indoor use of coal . . . . . . . . . . . . . 2.1. Power utility coal emissions. . . . . 2.2. 2.3. Coal waste products . . . . . . . . . . . Liquid fuels from coal . . . . . . . . . . 2.4. Charcoal products . . . . . . . . . . . . . . . . . . Wood . . . . . . . . . . . . . . . . . . . . . . . . . . . . Indoor use of wood. . . . . . . . . . . . 4.1. Dung, crop residues, and other sources . Studies about comparisons of solid fuels Role of environmental transformation . . Summary . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgements . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . .

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* Tel.: +1 919 839 8978. E-mail addresses: [email protected], [email protected] http://dx.doi.org/10.1016/j.mrrev.2014.07.002 1383-5742/ß 2014 Published by Elsevier B.V.

Please cite this article in press as: L.D. Claxton, The history, genotoxicity, and carcinogenicity of carbon-based fuels and their emissions. Part 2: Solid fuels, Mutat. Res.: Rev. Mutat. Res. (2014), http://dx.doi.org/10.1016/j.mrrev.2014.07.002

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L.D. Claxton / Mutation Research xxx (2014) xxx–xxx

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1. Introduction

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Solid fuels have been used for hundreds of years. Before the first use of petroleum, solid fuels like wood, animal dung, and coal were used for heating and cooking. Therefore, populations to used solid fuels as countries developed, and most air pollution was from the use of solid fuels. Today, the sources of air pollution depend upon whether air sampling is done in developing countries or in developed populations. For people in developing societies, the majority of indoor exposures are due to solid fuel emissions, which continue for most people throughout their life. In developed countries, the highest indoor pollution levels occur when combustion processes associated with cooking, heating, and/or tobacco smoking are coupled with poor ventilation. When tobacco smoke adds toxicants to other biomass smoke, health concerns are magnified. In both developed and developing countries, pollution exposures indoors may be higher than those outdoors. Desai et al. [1] in a WHO document said, ‘‘Although outdoor sources often dominate air pollution emissions, indoor sources frequently dominate air pollution exposures. Exposure is a function of both the pollutant concentration in an environment, and the persontime spent in the environment. Since most people spend the majority of their time in homes, schools and workplaces, human exposure to air pollution is largely a function of pollutant levels in indoor settings (which can arise from outdoor sources and vice versa).’’ On a global basis, most indoor air pollution results from the burning of solid fuels for household cooking and heating [1]. Approximately 50% of all households and 90% of all rural households, worldwide, use solid fuels for cooking or heating [2]. These populations use stoves that have high emission factors, exposing occupants of residences to high levels of air pollutants. Cooking, a potential problem for people in both developed and developing countries can produce very high concentrations of emissions. In many locations, solid fuels are burnt in inefficient simple stoves under poorly ventilated conditions. In these situations, solid fuel emissions expose individuals to many health-damaging pollutants (e.g., respirable particulates, carbon monoxide, and other toxic compounds) from high levels of indoor air pollution exposures. Therefore, the severity of the health effects will vary with both the intensity and the duration of exposure and with the health status of the exposed population [3]. Investigators are and will continue to use the data of developing societies to identify and understand the health effects of the emissions of solid fuels. Indoor air pollution can be traced to prehistoric times when humans first moved to temperate climates and it became necessary to construct shelters and use fire inside the shelters for cooking, warmth, and light [2,4]. Fire caused exposure to high levels of pollution, as evidenced by the soot found in prehistoric caves [2]. Today, households that cannot afford fuels that are higher on the ‘‘energy ladder’’ (i.e., kerosene, liquefied petroleum gas (LPG) and electricity) often opt for collecting wood, agricultural residue, and animal dung as the household fuels. Po et al. [5] reported that in today’s world the source of energy for cooking and heating is solid biomass fuels for 2.4 billion people. About 0.6 billion people use coal. Therefore, up to 90% of rural households in developing countries still rely on unprocessed biomass fuels [2,6]. These unprocessed fuels typically are burnt indoors in open fires or poorly functioning stoves [4]. As a result, there are high levels of air pollution to individuals responsible for cooking and caring for their young children (i.e., usually women) [4,6]. Solid biomass fuels (typically wood, charcoal, dried animal dung) and agricultural residues (such as straw and sticks) have low combustion efficiency. This incomplete combustion discharges smoke with fine particulate matter, which fills the kitchen and/or living area. In biomassburning households, PM10 or PM2.5 concentration levels often exceed international guidelines [5].

Barnes et al. [7] in a report of the Energy Sector Management Assistance Program (ESMAP) of the World Bank say, ‘‘For people in developed countries, burning fuelwood in an open hearth evokes nostalgia and romance. But in developing countries, the harsh reality is that several billion people, mainly women and children, face long hours collecting fuelwood, which is burned inefficiently in traditional biomass stoves. The smoke emitted into their homes exposes them to pollution levels 10–20 times higher than the maximum standards considered safe in developed countries. And the problem is not out of the ordinary. The majority of people in developing countries at present cannot afford the transition to modern fuels. Today, close to one half of the world’s people still depend on biomass energy to meet their cooking and heating needs.’’ A number of publications [4,8–22] give information on the indoor use of coal and other solid fuels in developing countries. Although these publications do not give information on the genotoxicology of emissions, they are instructive.

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2. Coal as fuel

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Achten and Hofmann [23] noted ‘‘Numerous environmental polycyclic aromatic hydrocarbon (PAH) sources have been reported in literature, however, unburnt hard coal/bituminous coal is considered only rarely.’’ The review of these authors tell us that land plants are buried and converted to coal by prolonged exposure to elevated temperatures and pressures in the subsurface. The physico-chemical changes are complex, with resistant plant biopolymers (e.g., lignin) converted into a highly aromatic, three-dimensional, networked matrix with the order of increasing maturity being: peat ! lignite ! sub-bituminous coal ! bituminous coal ! anthracite coal ! graphite. Ether or methylene bridges and aliphatic side chains mainly consisting of methyl groups commonly link aromatic structures. The average number of aromatic rings per structural unit in most coals is 3–5 with some individual units having up to 10 rings. Therefore, a typical hard coal is characterized by 2–6 PAHs linked by methylene bridges with additional aliphatic side chains and phenol functional groups. In addition to the network structure, a multitude of small molecules (known as the ‘‘mobile phase’’) is present within the network. Because these molecules can be released from the coal network, this mobile phrase is of particular environmental interest. The type of a coal influences the concentration and composition of the mobile phase. This extractable phase may be released to the aquatic environment, be available to organisms, and thus be an important PAH source. During coal heating at manufactured gas plant sites, the linkages between some of the carbon units are cleaved, thereby releasing the conjugated aromatic rings into the mobile fraction (gas and coal tar). Therefore, coal can exhibit native PAH concentrations up to hundreds, in some cases, thousands of mg/kg. PAH concentrations and patterns in coals depend on the original organic matter type, as well as temperature and pressure conditions during coalification. The environmental impact of native unburnt coal-bound PAH in soils and sediments is not well studied. The presence of unburnt coal particles has been reported in some marine sediments, freshwater sediments, and soils. For example, during and after the cleanup of the Exxon Valdez oil spill in Alaska, U.S.A., there were detailed discussions whether the PAHs in sediments of Prince William Sound originated from the spill or from naturally outcroppings of coal seams near the shore [24,25].

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2.1. Indoor use of coal

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In 1775, Pott [26] was the first to describe a cancer caused by the soot of coal burning, when he determined that this soot caused cancer of the scrotum of chimney-sweeps. Thus, the first

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carcinogenic substance identified was a complex combustion mixture. When considered closely, the pollution to which chimney sweeps were exposed was both an occupational exposure and a public or personal exposure. The main difference between chimney sweeps and household inhabitants was the level of exposure to sensitive tissues. The experimental production of cancer by this soot was demonstrated much later when in 1922 Passey obtained malignant skin tumors in mice with an ether extract of this type of soot [27]. However, no carcinogenic compound was identified from this domestic soot until 1949 when Goulden and Tipler identified 3,4-benzpyrene (today known as benzo(a) pyrene) as one of its components [28]. In 1952, Waller detected BaP in samples of smoke drawn from the air of eight different towns as did Clemo et al. in 1955 [29,30]. It is generally believed that the most important risk factor for lung cancer is the use of tobacco products. However, this idea may currently be true only in developed countries. In less developed countries, a much larger proportion of lung cancer patients are nonsmokers – especially women. High lung cancer incidence rates among women in China [31,32], Mexico [33], and India [34] are found in non-smokers. For example in China, the odds ratios for lung cancer among women exposed to coal smoke at home (particularly ‘‘smokey’’ coal and not tobacco emissions) were in the range 2–6 [35–37]. Because of the increased lung cancer mortality rates in Xuan Wei County, China, Gallagher et al. [38] compared indoor smoky coal combustion emissions and tobacco smoking emissions by examining exposure levels to benzo[a]pyrene (BaP) and DNA adducts. Human exposures to BaP in smoky coal emissions are 20– 200 times greater than exposure to BaP from smoking 1–2 packs of cigarettes per day. White blood cell DNA was 2.5-fold higher in smokers than in non-smokers. Postlabelling analysis of DNA isolated from placental tissue of smokers revealed multiple adducts as a diagonal radioactive zone. In contrast, discrete adducts unrelated to smoking status were detected, by 32Ppostlabelling analysis, in DNA from multinucleated placental samples from smokers and non-smokers. DNA adduct levels were approximately four-fold higher in bronchoalveolar lavage cells from coal smoke-exposed individuals compared to unexposed individuals. This observation suggested that DNA-reactive intermediates concentrate in the respiratory tract and may not be detectable in whole WBC or placental tissue homogenates. The findings also suggest that the distribution and concentration of placental DNA adducts may be dependent on the site at which the placenta is sampled. DeMarini et al. [39] examined lung tumor tissue from 24 nonsmoking women also from Xuan Wei County, Yunnan Province, China to quantify the levels of mutation in TP53 and KRAS genes. More than 99% of the women in this province are nonsmokers, but they have the highest lung cancer mortality rate in China (25.3/ 100,000). The coal used by these women (for cooking and heating in homes without chimneys) is a low-sulfur (0.2%) mediumvolatile bituminous smoky coal, but the content of the emissions is 43% PAH. Smoky coal emissions are 1000-fold more carcinogenic than cigarette smoke in a skin-tumor assay in mice as shown by Mumford et al. [40], presumably because of their high concentration of PAHs. Consequently, nonsmokers exposed to these emissions inhale 30 times more BaP than do smokers and have urine with high levels of PAH metabolites. Among the 24 women studied by DeMarini et al. [39], 54% had bronchioloalveolar adenocarcinoma and 46% had acinar adenocarcinoma. They determined the TP53 and codon 12 KRAS mutations in lung tumors from these women. Among tumors studied, the data showed the highest percentage of mutations that (a) G ! T transversions at either KRAS (86%) or TP53 (76%), (b) clustered at the G-rich codons of TP53 (33%), and (c) had 100% of the guanines

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of the G ! T transversions on the nontranscribed strand. This mutation spectrum is consistent with an exposure to PAHs. These results show that mutations in the TP53 and KRAS genes also reflect a specific environmental exposure. Keohavong et al. [41] analyzed mutations in codon 12 KRAS within lung tumors or sputum samples from 41 nonsmoking women and 61 smoking men also from Xuan Wei County. In addition, they examined specimens from lung cancer patients from Beijing and Henan (14 nonsmoking women, 33 smoking men, and 3 nonsmoking men). For the control, they used individuals expose to natural gas (the main domestic fuel in Beijing and Henan). KRAS mutations (mainly G to T transversions) were found in 9 women and 14 men from Xuan Wei. Among Beijing and Henan patients, 1 woman and 6 men had KRAS mutations, with G to T transversions. Therefore, the frequency and type of KRAS mutations in Xuan Wei nonsmoking women are similar to those of KRAS mutations found in Xuan Wei and Beijing and Henan smoking men. In addition, the mutation frequency in Xuan Wei women is higher than (although not statistically) Beijing and Henan nonsmoking women. In these results, an association between exposure to coal smoke and the increased KRAS mutation frequency in Xuan Wei nonsmoking female lung cancer patients was seen. The results imply that the mutagens and the mechanisms for mutation induction in these nonsmoking women is similar to the ones responsible for KRAS mutations in cigarette smoking lung cancer patients. Because of the known smoky coal exposure in Xuan Wei County, Yunnan Province, China, Granville et al. [42] examined nonsmoking women. Because these women used smoky coal for cooking and heating in poorly ventilated homes, their lung cancer is linked epidemiologically to their use of smoky coal. The emissions from their cook stoves contain 81% organic matter, of which 43% is PAHs. Exposure assessment and molecular analysis for these nonsmoking women, who use smoky coal, strongly indicate that the associated PAHs are a primary cause of the elevated lung cancer in this population. Granville et al. [42] determined the mutation spectra of an extract of smoky coal emissions in Salmonella TA98 and TA100. The extract was 8.7 more mutagenic in TA100 with S9 than without S9 and was >3 more mutagenic in TA100 than in TA98. PAHs are generally more mutagenic in the base-substitution strain TA100 than in the frameshift strain TA98. In TA100, the mutation spectra of the emission extract was primarily (78–86%) GC ! TA transversions and were not significantly different in the presence or absence of S9. The frequency of GC ! TA transversions induced in Salmonella (78–86%) was similar to the frequency of this mutation in the TP53 (76%) and KRAS (86%) genes of lung tumors from nonsmoking women exposed to smoky coal emissions. The mutation spectra of extracts from smoky coal emissions reflect the presence of PAHs in the mixture and maintain a role for PAHs in the induction of the mutations and tumors related to exposure to smoky coal emissions [42].

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2.2. Power utility coal emissions

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According to Bauer [43], coal was the nation’s (U.S.) most plentiful and lowest-cost fuel for electric power generation and provided more than half of the electricity generated in the United States. The world’s coal reserves equal approximately 1 exagram (1 1015 kg). The energy content equals 290 zettajoules (2.9 1023 J) [44]. Using a value of 15 terawatt as the global energy consumption, the coal supply could last for 600 years [44]. In terms of energy value, coal constituted approximately 95% of total U.S. domestic fossil energy reserves (coal, oil, and natural gas). Coal provides the energy equivalent of about 1 trillion barrels of crude oil, which is comparable to all the world’s known oil reserves [43]. Many other fuels come from coal. Because coal is the starting

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material for other fuels, these other fuels will be discussed in this paper and in Part 4 of this series [45]. Because most coals contain significant amounts of water that interfere with its combustion, coal usually is ground and dried to kerosene LPG. The results show that burning biomass-based fuels increase the frequency of cytogenetic alterations in blood lymphocytes of exposed populations. In 2005, Pandey et al. [109] used the comet assay to measure the DNA damage in a population of women cooking with biomass fuels (fire wood and cow dung cakes). Out of 144 volunteers, 70 used wood or dung (biomass-based fuels, BMFs) for domestic cooking, while the remaining 74 used LPG. The women exposed to LPG served as a reference population. Higher levels of DNA damage were observed for BMF users than for LPG users. Similar significant differences were found when the groups were stratified by age and length of exposure. Realizing that PAHs

Table 2 Mutagenicity for biomass combustion aerosols based on the Salmonella assay (tester strains TA98 and TA100). Stove

S. typhimurium TA98 S3, traditional U-shaped mud stove

Fuel

S9 revertants X 107 per kg fuel

+S9 revertants X 107 per kg fuel

Wood Dung Biofuel briquettes

1.39 2.22 2.45 2.02

2.32 1.66 4.31 2.76


1.18 1.91 na 1.185

0.84 2.36 na 1.600


0.87 2.14 2.00 1.67

0.87 2.24 2.59 1.90


0.90 2.31 na 1.605

1.17 2.26 na 1.715


1.32 4.80 3.84 3.32

2.16 5.95 4.54 4.217


2.23 2.71 na 2.47

2.89 3.19 na 3.04


1.13 3.68 5.61 3.473

1.50 1.45 1.09 1.347


2.25 1.19 na 1.72

2.42 0.90 na 1.66

Average S1, Metal stove

Average S2, Fired clay, 1-pot stove


Average S. typhimurium TA100 S3, traditional U-shaped mud stove

Average S1, Metal stove



Average Notes: Calculated from this table, Mukherji et al. [107]. na, not available. Averages for TA98, S9: wood, 1.085; dung, 2.145; briquettes, 2.225. Averages for TA98, +S9: wood, 1.30; dung, 2.23; briquettes, 3.45. Averages for TA100, S9: wood, 1.73; dung, 3.10; briquettes, 4.73. Averages for TA100, +S9: wood, 2.24; dung, 2.78; briquettes, 0.97.


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are of special interest due to their carcinogenicity, ubiquity in the environment, and vary with the fuel used, Singh et al. [110] examined the PAHs emitted from biomass fuels (dung cake, fuel wood, and crop residue) from rural households of six states in India. The PAH emissions were simultaneously determined from various biomass fuels. The average emission factors of total PAHs (from both the gas phase and particulate phase) were 59.5 19.9 mg/kg for dung cakes, 52.5 mg/kg for wood, and 40.9 mg/kg for crop residues. The emission factor of particulate phase PAHs was higher when compared to gas phase PAHs. Anthracene, fluoranthene, pyrene, benzo[a]anthracene and chrysene were predominant PAHs for all biomass fuels. One approach to reduce a nation’s dependence on fossil fuels is for electrical utility companies to use biomass to help alleviate this dependence. Biomass could have a significant impact both environmentally and economically. When compared to other types of biomass, animal waste has the greatest potential for methane production (0.3–0.4 m3 methane/kg volatile solids) [111]. Therefore, the amount of wastes produced by the animals and the corresponding energy that can be derived from the waste can be quite significant. Klasson and Nghiem [112] examined a source of fuel that has not received much attention, namely, zoo animal waste by using elephant and rhinoceros dung to investigate the feasibility of generating methane from the dung. The methane yield was approximately 0.020 L CH4/g dung. In another effort, Zadeh [113] reported on a full-scale project to address manure management issues, improve water quality, produce needed energy, and improve the quality of life for residents. Cayuga County, New York, is home to 280 dairy farms and 31,500 dairy milking cows that produce 855 million gallons of milk per year and 5.7 million gallons of manure daily (2080.5 million gallons per year). Digesters are expensive pieces of equipment, require attention and care, and the on-farm digester systems have fairly long payback periods (>10 years). In 2005, the county’s Soil and Water Conservation District decided to embark on a centralized community digester project. The digester facility consists of the following major components: (1) Transfer Station: This is an indoor truck bay, where 35,000 gallons of manure, 8500 gallons of liquid organic food-processor waste, and 1200 gallons of brown grease are unloaded from tanker trucks, (2) Anaerobic Digester: The digester is designed to process the daily feedstock and produce biogas, (3) Biogas Conditioning System: The biological biogas conditioning system removes H2S and any unneeded water from the biogas, (4) Combined Heat and Power System: The heat recovery system captures the waste heat from the engine exhaust, the jacket cooling water, and the engine oil circuit, (5) Electrical Substation and Power Distribution Systems: This system supplies electrical service to county buildings and the local electric grid, and (6) Thermal Energy Distribution System: The heat recovery system distributes heat to the thermal circuits for the anaerobic digester facility. On a daily basis, the plant generally produces 200,000 ft3/d of biogas and 44,000 gallons of pathogen-free, nutrient-rich digested slurry for agricultural use by farms in the local area. The biogas produces 5,157,000 kWh of electricity and 19,506 dekatherms of

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thermal energy per year. Such systems will help to decrease unneeded manure, improve water quality, decrease indoor and outdoor pollution levels while supporting the local economy.

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6. Studies about comparisons of solid fuels

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Bell and Kamens [114] examined the mutagenicity (Salmonella strains TA98, S9 and TA100, S9) of extracts of combustion particles from cow dung, crop residues, coconut shells, and compared the results to peat, hard wood (red oak), and soft wood (pine) emissions done in earlier studies. Biomass fuels that are easily gathered (e.g., dried cow dung, coconut shell and husk, cereal straws, tobacco stalks, and jute sticks) are commonly burned in open fires or unvented cookstoves inside the home used in developing countries. Collection of fuels such as firewood, charcoal, dung, and the inedible portions of agricultural crops has become in some areas an important demand on the labor and cash resources of low-income groups as well as a threat to the soil resources on which agricultural development depends [115]. For the Bell and Kamens [114] efforts (Table 3), combustion-particle extracts from dried cow dung and crop residue exhibited mutagenic potencies similar to wood-smoke extracts (0.0– 1.0 revertant/mg extract). Extracts from coconut-shell-smoke particles showed relatively higher mutagenicity, especially direct-acting mutagenicity; however, the testing of coconut shells in nitroreductase- and acetylase-deficient strains (i.e., TA98NR and TA98/1,8-DNP6) revealed no contribution from nitroarene-like compounds. Emissions (both gas and particle phases) of the three domestic fuels were analyzed for 17 PAHs (HPLC-UV), acute toxicity (Microtox test), and mutagenicity (in Salmonella TA98 and TA100, with and without exogenesis activation) [95]. On average, the gas phase of smoke contributed 95% of the 17 PAHs, 96% of toxicity, and 60% of mutagenicity. The highest emission factor for the 17 PAHs was from sawdust briquettes, but the highest emission of 11 genotoxic PAHs was from the kerosene fuel. All of the 17 PAHs were detected in the wood fuel smoke and sawdust smoke, including the 11 known genotoxic compounds (7 carcinogens and 4 cocarcinogens). In kerosene smoke, 14 compounds were detected. The emission factors of the total 17 PAHs on both fuel weight basis (mg/kg) and energy basis (mg/MJ) were highest for the sawdust briquettes, the second highest for kerosene, and the lowest for the wood fuel. If only the 11 genotoxic PAHs are taken into account, the emission factor ranking order was from the kerosene fuel to sawdust briquettes and lowest for the wood fuel. Most of the PAHs were found in the gas phase, especially the lower molecular weight compounds. Data from the Salmonella assay showed that both the particulate and gas phase emissions of the kerosene cookstove were not mutagenic in TA98 or TA100 with and without S9. TA98 results indicated both direct and indirect mutagenic activities in PM samples of sawdust and wood fuel, but with TA98 only direct mutagenic activity occurred in the gas phase. TA100 detected only direct mutagenic activities in both particulate and gas-phase samples. The high efficiency of the kerosene stove resulted in the lowest PAH, toxicity, and mutagenicity emissions. The toxicity and mutagenicity correlated with the PAH content of

1111 1112 1113 1114 1115 1116 1117 1118 1119 1120 1121 1122 1123 1124 1125 1126 1127 1128 1129 1130 1131 1132 1133 1134 1135 1136 1137 1138 1139 1140 1141 1142 1143 1144 1145 1146 1147 1148 1149 1150 1151 1152 1153 1154 1155 1156 1157 1158

Table 3 Mutagenic ratios when comparing cow dung, crop residue, and coconut shell emissions to peat, hard wood, and soft wood.a Test: Salmonella

TA98, S9

TA100, S9

TA100, +S9

Fuel/compared to

Pine

Oak

Peat

Pine

Oak

Peat

Oak

Oak

Dung, EWC Dung, Indian Coconut shell, EWC Crop residue, Indian

0.08 0.58 3.25 0.08

0.44 3.11 17.3 0.44

0.16 1.12 6.24 0.16

0.53 0.83 3.32 2.33

0.78 1.23 1.95 0.35

1.66 2.63 4.16 0.74

0.95 3.00 12.4 0.57

0.48 2.94 2.68 1.35

a

TA98, +S9

Calculated from mutagenic values given in Table 1 of Bell and Kamens [113].


G Model


12

1159 1160 1161 1162 1163 1164 1165 1166 1167 1168 1169 1170 1171 1172 1173 1174 1175 1176 1177 1178 1179 1180 1181

samples [95]. For a comparison, refer to the work of Kinouchi et al. [116] in which they examined kerosene emissions with four tester strains of Salmonella. Adonis and Gil [117] examined the indoor air pollution associated with several cooking and heating fuels used in areas of extreme poverty in La Pintana, Santiago, Chile. For economic reasons, the impoverished peoples of this area use solid fuels for cooking and heating fuels; and because of incomplete combustion, high levels of toxic pollutants are generated. They investigated the levels of carbon monoxide (CO), sulfur dioxide (SO2), respirable particulate matter (PM10), PAHs, and mutagenicity in the interior of 24 houses. The authors reported that higher levels of pollutants were seen during heating hours, in houses that used coal (mean values: PM10, 250 mg/m3; CO, 42 ppm; SO2, 192 ppb) or firewood (mean values: PM10, 489 mg/m3; CO, 57 ppm; SO2, 295 ppb). They concluded that the PAHs, detected in all the houses, came from inside the house and not from outdoor infiltration with coal, firewood, and cigarette smoke the important sources of mutagenic and carcinogenic PAHs. Table 4 gives the PM10 and mutagenicity levels seen in the homes. The indoor pollutant levels were much higher than those found outdoors in the highly polluted city of Santiago. Because so few houses were sampled, additional studies should be done.

1182 7. Role of environmental transformation 1183 1184 1185 1186 1187 1188 1189 1190 1191 1192 1193 1194 1195 1196 1197 1198 1199 1200 1201 1202 1203 1204 1205 1206 1207 1208 1209 1210 1211 1212

In 1986, Kleindienst et al. [118] irradiated dilute mixtures of wood combustion emissions in a smog chamber in order to examine the mutagenic activities of both the gas and particulate phase photooxidation products of wood smoke in the presence and absence of nitrogen oxides. Mutagenic activity was measured using S. typhimurium strains TA98 and TA100. The standard plate incorporation test was used for mutagenic assays of extracts of the particulate phase; whereas, the mutagenic activity of the gas phase was measured by exposure of uncovered test plates to the filtered gas phase. Neither the gas nor the particulate phase components of wood combustion demonstrated significant amounts of direct acting (S9) mutagenic activity alone. However, mutagenic activities increased significantly upon irradiation in the presence of nitrogen oxides. Measured in terms of revertants per microgram, the gas phase products were 3–30 times more mutagenic than the particulate phase products as measured with strain TA100, but the mutagenic activities were comparable for the two phases with TA98. The gas phase products were far more mutagenic than either the starting materials or the particulate products when compared on a per cubic meter basis. Such studies of woodsmoke show that gas phase emissions contribute a significant portion of the mutagenic activity that can be detected, especially after atmospheric transformation [118]. In 2004, Jain et al. [119] examined the vermicomposting (composting with worms) of flyash by examining the cytogenetic effects of pre- and post-vermicomposted flyash samples evaluated on the root meristem cells of Vicia faba. V. faba seedlings were directly planted in flyash-cow dung-soil (FCS) mixtures, and the roots were sampled at 5 days using cytogenetic analysis. A negative control (cow dung-soil (CS) mixture alone) was used. A vermicomposted FCS

(VFCS) mixture was made by introducing earthworms (Eisenia foetida) for 30 days. Chemical analysis done prior to vermicomposting revealed high concentrations of heavy metals such as Cr, Cu, Pb, Zn, and Ni in FCS samples. CS samples also showed the presence of these metals. Cytogenetic examinations of FCS mixtures showed significant inhibition of mitotic index (MI), induction of chromosome aberrations (CA), and a significantly increased frequency of mitotic aberrations (MA) with the increase of the aberrations being dependent on flyash concentrations. Cytogenetic analysis of VFCS revealed a 15–45% decline in the aberration frequencies whereas chemical analysis showed a10–50% decline in metal concentrations. These changes indicated, to the authors, that E. foetida is a potential accumulator of heavy metals. In addition, the decline of metal concentrations in the VFCS may be the cause of the decrease in aberration frequencies. The present study indicated two major conclusions, the testing of genotoxicity potential of flyash is useful, and the vermicomposting of metal-contaminated soil mitigates the genotoxicity of the soil.

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8. Summary

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Before the first use of petroleum, solid fuels like wood, animal dung, and coal were used for heat and cooking. Today, households that cannot meet the expense of fuels like kerosene, liquefied petroleum gas, and electricity resort to collecting wood, agricultural residue, and animal dung to use as household fuels. Globally, 50% of all households and 90% of all rural households use solid fuels for cooking or heating. Typically, these fuels are burnt in simple stoves with very incomplete combustion and exposed populations often see evidence of low birth weight, increased infant and perinatal mortality, head and neck cancer, and lung cancer. Therefore, most indoor air pollution worldwide is from the use of solid fuels. In the more developed countries, solid fuels are often used for electric power generation providing more than half of the electricity generated in the United States. The world’s coal reserves equal approximately one exagram (1 1015 kg). Today’s coal energy content equals 290 zettajoules (2.9 1023 J) equals 1 trillion barrels of crude oil (comparable to all the world’s known oil reserves) and could last for 600 years. Studies show that PAHs react with NO2 to form direct-acting mutagens, and such emission products would appear in extracted fly ash samples due to reactions of PAHs with NOX in the combustion gases. Although coal is recognized as a giving rise to a variety of compounds that contain mutagenic and carcinogenic PAHs, exposure to coal is also considered as an important source of reactive oxygen species that induces DNA damage. Many of the measured PAHs are found in both the indoor and electricity-generating combustors are the same, and genotoxic emissions are seen in both types of emissions. Therefore, the severity of the health effects will vary with both the intensity and the duration of exposure and also with the health status of the exposed population.

1232 1233 1234 1235 1236 1237 1238 1239 1240 1241 1242 1243 1244 1245 1246 1247 1248 1249 1250 1251 1252 1253 1254 1255 1256 1257 1258 1259 1260 1261

9. Conclusion

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Solid fuels (like wood, animal dung, and coal) were used for heating and cooking for hundreds of years before other fuels

1263 1264

Table 4 Comparison of solid fuels used indoors from Adonis and Gil [116].a Type of home heating

PM10 (mg/m3)

Firewood Coal Kerosine Gas Smoking without heating

500 250 280 250 125

a

(2) (5) (7) (4) (2)

Mutagenicity Salmonella TA98, S9 (rev/m3) 1500 2000 250 250 1500

(1) (2) (4) (3) (2)

Mutagenicity Salmonella TA98, +S9 (rev/m3) 1300 3000 350 300 1300

(1) (2) (4) (3) (2)

Taken from Figs. 1 and 3 of Adonis and Gil [116]. The numbers in parentheses are the number of homes sampled.


G Model


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became available. Today, about 50% of the people in developing countries rely on solid fuels for domestic energy. The combustion of such fuels involved elevated temperatures and altered pressures. Under these conditions, genotoxicants (e.g., PAHs) were likely to form. Some of these compounds have carcinogenic activity for a variety of organ sites in experimental animals. Epidemiological studies implicate these fuels and their emissions as carcinogens in man. As expected, many liquid fractions from solid fuel emissions are carcinogenic when subjected to bioassay. While even small amounts of BaP exhibit carcinogenic activity in the bioassay of a fraction from solid fuels, it does not follow that a non-BaP-containing fractions will be noncarcinogenic. Although solid fuels are generally used in modern combustors at higher temperatures, many genotoxicants are still produced. Additional research (chemical and bioassay) includes the need to examine for potential health effects associated with synfuels and waste products produced from solid fuels. For further information about coal emissions in indoor air see the IARC monograph [120]. The IARC evaluation for indoor use of coal is ‘‘There is sufficient evidence in experimental animals for the carcinogenicity of coal-derived soot extract. There is sufficient evidence in experimental animals for the carcinogenicity of emissions from combustion of coal. Indoor emissions from household combustion of coal are carcinogenic to humans (Group 1).’’ For other aspects of coal see IARC monographs volume 100F and volume 103 [121,122]. For further information about wood dusts see the IARC monograph [123]. The IARC evaluation for wood dust is ‘‘There is sufficient evidence in humans for the carcinogenicity of wood dust. Wood dust causes cancer of the nasal cavity and paranasal sinuses and of the nasopharynx. There is inadequate evidence in experimental animals for the carcinogenicity of wood dust. Wood dust is carcinogenic to humans (Group 1).’’

1297

Conflict of interest statement

1298

The author declares that there are no conflicts of interest.

1299

Acknowledgements

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Special thanks go to Mutation Research and to David DeMarini and Mike Waters for their encouragement and assistance. I want to think my former colleagues (there are too many to mention by name) at the USEPA who contributed to my understandings and efforts in examining environmental complex mixtures. Such efforts help to protect the public’s health through protecting the air breathed, the water ingested, and the soils contacted.

1307

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G Model

MUTREV 8087 1–15 14

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The history, genotoxicity and carcinogenicity of carbon-based fuels and their emissions: part 4 - alternative fuels.

The history, genotoxicity, and carcinogenicity of carbon-based fuels and their emissions: 1. Principles and background.

The history, genotoxicity, and carcinogenicity of carbon-based fuels and their emissions. Part 3: diesel and gasoline.

Comparative Study of the Thermal Conductivity of Solid Biomass Fuels.

Fluidized bed gasification of industrial solid recovered fuels.

Dangerous properties of petroleum-refining products: carcinogenicity of motor fuels (gasoline).

Hedgehog fuels gut regeneration.

Temperature effects on particulate emissions from DPF-equipped diesel trucks operating on conventional and biodiesel fuels.

Fossil fuels' future.

Inflammation fuels tumor progress and metastasis.

Metabolic fuels and reproduction in female mammals.

Solar energy for electricity and fuels.

Gas fermentation for commodity chemicals and fuels.

Epigenetic noise fuels cancer evolution.

Intermediate pyrolysis of biomass energy pellets for producing sustainable liquid, gaseous and solid fuels.

The future of oil: unconventional fossil fuels.

Well-to-Wheels Greenhouse Gas Emissions of Canadian Oil Sands Products: Implications for U.S. Petroleum Fuels.

PETA fuels animal lab improvements.

Monolithic cells for solar fuels.

Cytoplasmic methylation fuels leukocyte invasion.

Estimating the number of low-income americans exposed to household air pollution from burning solid fuels.

Outdoor, indoor, and personal black carbon exposure from cookstoves burning solid fuels.

Design, quality, and quality assurance of solid recovered fuels for the substitution of fossil feedstock in the cement industry.

Review of the genotoxicity and carcinogenicity of 4,4'-methylene-dianiline and 4,4'-methylene-bis-2-chloroaniline.