A6.1.1. Carcinogenicity
Carcinogenicity of household use of coal was reviewed by the International Agency for Research on Cancer (IARC, (1), using standard assessment methodology involving review of exposure data, studies of cancer in humans, studies of cancer in experimental animals, and mechanistic and other relevant data. It was concluded that for household use of coal:
There is sufficient evidence in humans for the carcinogenicity of household combustion of coal. Household combustion of coal causes cancer of the lung.
There is sufficient evidence in experimental animals for the carcinogenicity of emissions from combustion of coal.
There is sufficient evidence in experimental animals for the carcinogenicity of extracts from coal-derived soot.
It is noted that the type of coal used by households in most, if not all, of the epidemiological studies in this assessment, was raw (unprocessed)1 coal. The overall evaluation concluded that indoor emissions from household combustion of coal are carcinogenic to humans (Group 1). This evidence was assessed as being of high quality. While this evidence confirms that emissions from household coal combustion are carcinogenic, this does not provide risk estimates for the use of coal compared to the use of an alternative clean fuel.
A6.1.2. Health risks from incomplete combustion of coal
The systematic reviews reported in Review 4 examined evidence for household air pollution (HAP) emitted by solid fuel use causing a range of disease outcomes, along with estimates of disease risk and intervention impacts. Most studies investigated biomass fuel use, however, or did not differentiate between solid fuels clearly. Risk estimates linked to coal use were only available for risk of lung cancer and COPD, although there were too few studies on chronic obstructive pulmonary disease (COPD) to permit grading of the evidence for this outcome. As per the IARC assessment, most (if not all) of the epidemiological evidence relates to household use of unprocessed coal. reports grading of evidence for public health interventions (GEPHI) assessment for coal use and lung cancer, which provided an intervention effect estimate of 0.46 (95% confidence interval (CI): 0.35, 0.62) and was assessed as being of moderate quality. The integrated exposure-response (IER) function for risk of lung cancer, although not specific to coal exposure, indicates that risk from exposure to fine particulate matter (PM2.5) remains elevated right down to the counterfactual level of 7.5 μg/m3 of PM2.5. This evidence was assessed as being of moderate quality.
Grading (GEPHI) assessment of evidence on risk of lung cancer with exposure to household coal use. For full details of the systematic reviews and GEPHI assessments (including scoring for importance of outcomes and grading in table), please refer to Review (more...)
A6.1.3. Toxic contaminants
Review 8 identified studies reporting on health effects of five toxic contaminants in coal, arsenic, fluorine, selenium, mercury and lead. These studies provide evidence on toxin content of coals, combustion and emissions chemistry, exposure routes (i.e. food, air, water), air pollution and exposure levels, and health impacts. Of the contaminants, the risks and effects of arsenic and fluorine are the two most comprehensively investigated and reported. Most of the evidence on the effects of contaminants derives from studies in China.
The assessment of evidence for health risks from toxic contaminants of coal was based on an overall evaluation of the available studies covering all of the aspects noted above. The data obtained on the content of toxic contaminants in coal, the fact that these are not destroyed on combustion, measurements of toxins in air and food (which are the main routes of exposure), and some dose measurements (e.g. in blood) strongly indicate that use of contaminated coals in the home puts members of the household at risk.
All the epidemiological studies examining toxin-specific health outcomes were observational. Most of these compared the prevalence of health outcomes caused by the contaminants (i.e. arsenicosis, dental and skeletal fluorosis, etc.) in areas or homes using contaminated coal with those in areas using fuel with lower levels of contamination. There were no studies directly investigating health effects of mercury or lead associated with household coal use. However, there was some indirect evidence available for lead. For example, a study performed after leaded gasoline was phased out in China, found that child blood lead levels strongly correlated with coal consumption but not gasoline consumption.
In summary, the available evidence shows that toxins are widely distributed in coal and present important health risks where coal is used in the home. While the evidence shows that use of coal with toxic contaminants leads to serious adverse health effects, most of this evidence has been derived from studies conducted in affected areas of China.
Experimental studies provide evidence that exposure can be reduced, but not eliminated, by processing the coal, using chimney stoves and behavioural interventions (for example to encourage drying of food outside the home, rather than indoors where it would be more heavily contaminated). These studies have demonstrated reductions in emissions and/or urinary levels of some of these toxins, but have not included evaluation of health impacts.
Summary
Taking all of this evidence together, including the specificity of effect linking coal containing toxins, emissions of the toxins, high measured levels in air, food etc. (routes of exposure) and disease outcomes specific to the toxins, this evidence was assessed as being of moderate quality. It is noted, however, that this assessment applies to evidence relating primarily to raw coal, except where the studies concerned state that the coal has been processed to reduce toxic effects.
