Smoky Coal Research Articles

Expanded PAH analysis of household air pollution in a rural region of China with high lung cancer incidence

The domestic combustion of locally sourced smoky (bituminous) coal in Xuanwei and Fuyuan counties, China, is responsible for some of the highest lung cancer rates in the world. Recent research has pointed to methylated PAHs (mPAHs), particularly 5-methylchrysene (5MC), within coal combustion products as a driving factor. Here we describe measurements of mPAHs in Xuanwei and Fuyuan derived from controlled burnings (i.e., water boiling tests, WBT, n = 27) representing exposures during stove use, and an exposure assessment (EA) study (n = 116) representing 24 h weighted exposures. Using smoky coal has led to significantly higher concentrations of known and likely human carcinogens than using smokeless coal, including 5MC (3.7 ng/m3 vs. 1.0 ng/m3 for EA samples and 100.8 ng/m3 vs. 2.2 ng/m3 for WBT samples), benzo[a]pyrene (38.0 ng/m3 vs. 7.9 ng/m3 for EA samples and 455.3 ng/m3 vs. 12.0 ng/m3 for WBT samples) and 7,12-dimethylbenz[a]anthracene (1.9 ng/m3 vs. 0.2 ng/m3 for EA samples and 47.7 ng/m3 vs. 0.6 ng/m3 for WBT samples). Mixed effect models for both EA samples and WBT samples revealed clear variation in mPAHs concentrations depending on smoky coal source while stove ventilation was consistently found to reduce measured concentrations (by up to nine fold and 65 fold for EA and WBT samples respectively when using smoky coal). Fuel type had a larger influence on mPAHs concentrations than stove type. These findings indicate that users of smoky coal experience exposure to many PAHs, including known and suspected human carcinogens (especially during cooking activities), many of which are not routinely tested for. Collectively, this provides insights into the potential etiologies of lung cancer in the region and further highlights the importance of targeting clean fuel transitions and stove refinements as the final goal for reducing household air pollution and its associated health risks.

The effect of “smoky” coal bans on chronic lung disease among older people in Ireland

Globally, coal is still widely used for heating. However, there are concerns about its effect on ambient air quality and health. We estimated the effect of bans prohibiting the sale and use of so-called “smoky coal” on the prevalence of chronic lung disease in older people. Our identification strategy relied on the phased extension of smoky coal bans to Irish towns after 2010. We examined five waves of The Irish Longitudinal Study on Ageing (TILDA), a large nationally representative survey containing detailed information on health, housing, and socio-economic status. Controlling for relevant factors, smoky coal bans reduced the probability that an older person reports being diagnosed with chronic lung disease by between three and five percentage points. In models where we estimated the effect of the ban on the incidence of new cases of chronic lung disease, rather than existing cases, we found the effect was between -0.96 and -2.5 percentage points. Our findings were robust to estimating the model using different sub-samples and control variables. Furthermore, to address potential endogeneity of the ban, we examined subsamples defined by whether participants lived in towns within a range of the population threshold at which the ban was imposed. Estimating our model using these subsamples showed a consistently negative effect of the ban. We also showed parallel trends in health outcomes before the treatment, and that the treatment did not affect attrition from the sample.

Household air pollution and epigenetic aging in Xuanwei, China

BackgroundHousehold air pollution (HAP) from indoor combustion of solid fuel is a global health burden linked to lung cancer. In Xuanwei, China, lung cancer rate for nonsmoking women is among the highest in the world and largely attributed to high levels of polycyclic aromatic hydrocarbons (PAHs) that are produced from combustion of smoky (bituminous) coal used for cooking and heating. Epigenetic age acceleration (EAA), a DNA methylation-based biomarker of aging, has been shown to be highly correlated with biological processes underlying the susceptibility of age-related diseases. We aim to assess the association between HAP exposure and EAA. MethodsWe analyzed data from 106 never-smoking women from Xuanwei, China. Information on fuel type was collected using a questionnaire, and validated exposure models were used to predict levels of 43 HAP constituents. Exposure clusters were identified using hierarchical clustering. EAA was derived for five epigenetic clocks defined as the residuals resulting from regressing each clock on chronological age. We used generalized estimating equations to test associations between exposure clusters derived from predicted levels of HAP exposure, ambient 5-methylchrysene (5-MC), a PAH previously found to be associated with risk of lung cancer, and EAA, while accounting for repeated-measurements and confounders. ResultsWe observed an increase in GrimAge EAA for clusters with 31 and 33 PAHs reflecting current (β = 0.77 y per standard deviation (SD) increase, 95 % CI:0.36,1.19) and childhood (β = 0.92 y per SD, 95 % CI:0.40,1.45) exposure, respectively. 5-MC (ng/m3-year) was found to be associated with GrimAge EAA for current (β = 0.15 y, 95 % CI:0.05,0.25) and childhood (β = 0.30 y, 95 % CI:0.13,0.47) exposure. ConclusionsOur findings suggest that exposure to PAHs from indoor smoky coal combustion, particularly 5-MC, is associated with GrimAge EAA, a biomarker of mortality.

Exposure to smoky coal combustion emissions and leukocyte Alu retroelement copy number.

Household air pollution (HAP) from indoor combustion of solid fuel is a global health burden that has been linked to multiple diseases including lung cancer. In Xuanwei, China, lung cancer rate for non-smoking women is among the highest in the world and largely attributed to high levels of polycyclic aromatic hydrocarbons (PAHs) that are produced from combustion of smoky (bituminous) coal. Alu retroelements, repetitive mobile DNA sequences that can somatically multiply and promote genomic instability have been associated with risk of lung cancer and diesel engine exhaust exposure. We conducted analyses for 160 non-smoking women in an exposure assessment study in Xuanwei, China with a repeat sample from 49 subjects. Quantitative PCR was used to measure Alu repeat copy number relative to albumin gene copy number (Alu/ALB ratio). Associations between clusters derived from predicted levels of 43 HAP constituents, 5-methylchrysene (5-MC), a PAH previously associated with lung cancer in Xuanwei and was selected a priori for analysis, and Alu repeats were analyzed using generalized estimating equations. A cluster of 31 PAHs reflecting current exposure was associated with increased Alu copy number (β:0.03 per standard deviation change; 95% confidence interval (CI):0.01,0.04; P-value = 2E-04). One compound within this cluster, 5-MC, was also associated with increased Alu copy number (P-value = 0.02). Our findings suggest that exposure to PAHs due to indoor smoky coal combustion may contribute to genomic instability. Additionally, our study provides further support for 5-MC as a prominent carcinogenic component of smoky coal emissions. Further studies are needed to replicate our findings.

Abstract 4219: Smoky coal exposure is associated with epigenetic accelerated aging

Abstract Household air pollution (HAP) from indoor combustion of solid fuel is a global health burden that has been linked to lung cancer. A striking example occurs in Xuanwei, China where the lung cancer rate for never smoking women is among the highest in the world and largely attributed to high levels of various toxic constituents, including polycyclic aromatic hydrocarbons (PAHs), a combustion product of smoky (bituminous) coal used for cooking and heating. Several air pollution constituents have been associated with epigenetic accelerated aging (EAA) derived from DNA methylation (DNAm)-based biomarkers that are highly correlated with biological processes underlying aging-related diseases. We aim to assess the association between HAP exposure and EAA in Xuanwei, China. We analyzed 106 never smoking women in an exposure assessment study in Xuanwei, China with a repeat DNA sample from 23 subjects. Household fuel type used for cooking and heating (smoky vs. smokeless coal) was collected using a questionnaire, and exposure models were used to predict levels of 43 individual HAP constituents for current and childhood exposure. Leukocyte DNAm was measured using Illumina EPIC array. EAA was derived for five clocks using the Horvath calculator and defined as the residuals resulting from regressing each clock on chronological age. We used generalized estimating equations to assess the associations between fuel type, clusters derived from predicted levels of HAP exposure, and ambient 5-methylchrysene (5-MC), a carcinogenic PAH previously associated with lung cancer in Xuanwei and selected a priori for analyses, as independent variables and EAA clocks as dependent variables, while accounting for repeated-measurements. We observed a significant increase in GrimAge EAA among smoky coal users compared to smokeless coal users for current (β=1.84 years (y), 95% confidence interval (CI): 0.59, 3.09, P-value=0.004) and childhood (β=4.14 y, 95% CI: 1.63, 6.64, P-value=0.001) exposures. We also observed a monotonic increase in GrimAge EAA for a cluster of 31 PAHs reflecting current exposure (β=0.77 y, 95% CI: 0.36, 1.19, P-value=3 × 10−4) and for a cluster of 33 PAHs reflecting childhood exposure (β=0.92 y, 95% CI: 0.40, 1.45, P-value=0.001). Ambient 5-MC, one of the constituents within the PAH clusters, was found to have an increasing monotonic relationship with GrimAge EAA for current (β=0.15 y, 95% CI: 0.05, 0.25, P-value=0.003) and childhood (β=0.30 y, 95% CI: 0.13, 0.47, P-value=4.7 × 10−4) exposures. Our findings suggest that exposure to PAH from indoor smoky coal combustion is associated with EAA, particularly for the GrimAge clock, a strong biomarker of mortality. This finding is consistent with our recent observation linking accelerated GrimAge to increased risk of lung cancer in a prospective study of never smoking women in China. Additionally, our study provides further support for 5-MC as a prominent carcinogenic component of smoky coal emissions. Citation Format: Batel Blechter, Andres Cardenas, Seraphina (Junming) Shi, Mohammad L. Rahman, Jason Y.Y. Wong, Wei Hu, George S. Downward, Lutzen Portengen, Richard Cawthon, H. Dean Hosgood, Jihua Li, Debra T. Silverman, Yunchao Huang, Roel Vermeulen, Nathaniel Rothman, Qing Lan. Smoky coal exposure is associated with epigenetic accelerated aging. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4219.

Methylated polycyclic aromatic hydrocarbons from household coal use across the life course and risk of lung cancer in a large cohort of 42,420 subjects in Xuanwei, China

BackgroundWe previously showed that exposure to 5-methylchrysene (5MC) and other methylated polycyclic aromatic hydrocarbons (PAHs) best explains lung cancer risks in a case-control study among non-smoking women using smoky coal in China. Time-related factors (e.g., age at exposure) and non-linear relations were not explored. ObjectiveWe investigated the relation between coal-derived air pollutants and lung cancer mortality using data from a large retrospective cohort. MethodsParticipants were smoky (bituminous) or smokeless (anthracite) coal users from a cohort of 42,420 subjects from four communes in XuanWei. Follow-up was from 1976 to 2011, during which 4,827 deaths from lung-cancer occurred. Exposures were predicted for 43 different pollutants. Exposure clusters were identified using hierarchical clustering. Cox regression was used to estimate exposure–response relations for 5MC, while effect modification by age at exposure was investigated for cluster prototypes. A Bayesian penalized multi-pollutant model was fitted on a nested case-control sample, with more restricted models fitted to investigate non-linear exposure–response relations. ResultsWe confirmed the strong exposure–response relation for 5MC (Hazard Ratio [95% Confidence Interval] = 2.5 [2.4, 2.6] per standard-deviation (SD)). We identified four pollutant clusters, with all but two PAHs in a single cluster. Exposure to PAHs in the large cluster was associated with a higher lung cancer mortality rate (HR [95%CI] = 2.4 [2.2, 2.6] per SD), while exposure accrued before 18 years of age appeared more important than adulthood exposures. Results from the multi-pollutant model identified anthanthrene (ANT) and benzo(a)chrysene (BaC) as risk factors. 5MC remained strongly associated with lung cancer in models that included ANT and BaC and also benzo(a)pyrene (BaP). ConclusionWe confirmed the link between PAH exposures and lung cancer in smoky coal users and found exposures before age 18 to be especially important. We found some evidence for the carcinogen 5MC and non-carcinogens ANT and BaC.

Overall and cause-specific mortality rates among men and women with high exposure to indoor air pollution from the use of smoky and smokeless coal: a cohort study in Xuanwei, China

ObjectivesNever-smoking women in Xuanwei (XW), China, have some of the highest lung cancer rates in the country. This has been attributed to the combustion of smoky coal used for indoor...

Smoky coal exposure is associated with increased white blood cell DNA Alu retroelement copy number

Smoky coal exposure is associated with increased white blood cell DNA Alu retroelement copy number

On the use of reference mass spectra for reducing uncertainty in source apportionment of solid-fuel burning in ambient organic aerosol

Abstract. Reference mass spectra are routinely used to facilitate source apportionment of ambient organic aerosol (OA) measured by aerosol mass spectrometers. However, source apportionment of solid-fuel-burning emissions can be complicated by the use of different fuels, stoves, and burning conditions. In this study, the organic aerosol mass spectra produced from burning a range of solid fuels in several heating stoves have been compared using an aerosol chemical speciation monitor (ACSM). The same samples of biomass briquettes and smokeless coal were burnt in a conventional stove and Ecodesign stove (Ecodesign refers to a stove conforming to EU Directive 2009/125/EC), while different batches of wood, peat, and smoky coal were also burnt in the conventional stove, and the OA mass spectra were compared to those previously obtained using a boiler stove. The results show that although certain ions (e.g., m/z 60) remain important markers for solid-fuel burning, the peak intensities obtained at specific m/z values in the normalized mass spectra were not constant with variations ranging from < 5 % to > 100 %. Using the OA mass spectra of peat, wood, and coal as anchoring profiles and the variation of individual m/z values for the upper/lower limits (the limits approach) in the positive matrix factorization (PMF) analysis with the Multilinear Engine algorithm (ME-2), the respective contributions of these fuels to ambient submicron aerosols during a winter period in Dublin, Ireland, were evaluated and compared with the conventional a-value approach. The ME-2 solution was stable for the limits approach with uncertainties in the range of 2 %–7 %, while relatively large uncertainties (8 %–29 %) were found for the a-value approach. Nevertheless, both approaches showed good agreement overall, with the burning of peat (39 % vs. 41 %) and wood (14 % vs. 11 %) accounting for the majority of ambient organic aerosol during polluted evenings, despite their small uses compared to electricity and gas. This study, thus, accounts for the source variability in ME-2 modelling and provides better constraints on the primary factor contributions to the ambient organic aerosol estimations. The finding from this study has significant implications for public health and policymakers considering that it is often the case that different batches of solid fuels are often burnt in different stoves in real-world applications.

Elevated urinary mutagenicity among those exposed to bituminous coal combustion emissions or diesel engine exhaust.

Urinary mutagenicity reflects systemic exposure to complex mixtures of genotoxic/carcinogenic agents and is linked to tumor development. Coal combustion emissions (CCE) and diesel engine exhaust (DEE) are associated with cancers of the lung and other sites, but their influence on urinary mutagenicity is unclear. We investigated associations between exposure to CCE or DEE and urinary mutagenicity. In two separate cross-sectional studies of nonsmokers, organic extracts of urine were evaluated for mutagenicity levels using strain YG1041 in the Salmonella (Ames) mutagenicity assay. First, we compared levels among 10 female bituminous (smoky) coal users from Laibin, Xuanwei, China, and 10 female anthracite (smokeless) coal users. We estimated exposure-response relationships using indoor air concentrations of two carcinogens in CCE relevant to lung cancer, 5-methylchrysene (5MC), and benzo[a]pyrene (B[a]P). Second, we compared levels among 20 highly exposed male diesel factory workers and 15 unexposed male controls; we evaluated exposure-response relationships using elemental carbon (EC) as a DEE-surrogate. Age-adjusted linear regression was used to estimate associations. Laibin smoky coal users had significantly higher average urinary mutagenicity levels compared to smokeless coal users (28.4 ± 14.0 SD vs. 0.9 ± 2.8 SD rev/ml-eq, p=2 × 10-5 ) and a significant exposure-response relationship with 5MC (p=7 × 10-4 ). DEE-exposed workers had significantly higher urinary mutagenicity levels compared to unexposed controls (13.0 ± 10.1 SD vs. 5.6 ± 4.4 SD rev/ml-eq, p=.02) and a significant exposure-response relationship with EC (p-trend=2 × 10-3 ). Exposure to CCE and DEE is associated with urinary mutagenicity, suggesting systemic exposure to mutagens, potentially contributing to cancer risk and development at various sites.

Household air pollution from, and fuel efficiency of, different coal types following local cooking practices in Xuanwei, China

The domestic combustion of smoky (bituminous) coal in the Chinese counties of Xuanwei and Fuyuan, are responsible for some of the highest rates of lung cancer in the world. Cancer rates vary between coal producing regions (deposits) in the area, with coals from Laibin exhibiting particularly high risks and smokeless (anthracite) coal exhibiting lower risks. However, little information is available on the specific burning characteristics of coals from throughout the area. We conducted an extensive controlled burning experiment using coal from multiple deposits in either a traditional firepit or ventilated stove, accompanied by a detailed examination of time-weighted and real-time size-aggregated particle concentrations. Smoky coal caused higher particle concentrations of all sizes than smokeless coal, with variations observed by geological source. Virtually all particle emissions were in the PM2.5 fraction (98% - mass based), and 75% and 46% were in the PM1 and PM0.3 fraction respectively. Real-time concentrations of PM1 and PM0.1 peaked after coal was added and declined afterwards. Ventilation reduced particle concentrations by up to 15-fold and increased the coal burning rate by 1.9-fold. These findings may provide valuable insight for reducing exposure and adverse health effects associated with domestic coal combustion.

Study of Emissions from Domestic Solid-Fuel Stove Combustion in Ireland.

Solid-fuel stoves are at the heart of many homes not only in developing nations, but also in developed regions where there is significant deployment of such heating appliances. They are often operated inefficiently and in association with high emission fuels like wood. This leads to disproportionate air pollution contributions. Despite the proliferation of these appliances, an understanding of particulate matter (PM) emissions from these sources remains relatively low. Emissions from five solid fuels are quantified using a “conventional” and an Ecodesign stove. PM measurements are obtained using both “hot filter” sampling of the raw flue gas, and sampling of cooled, diluted flue gas using an Aerosol Chemical Speciation Monitor and AE33 aethalometer. PM emissions factors (EF) derived from diluted flue gas incorporate light condensable organic compounds; hence they are generally higher than those obtained with “hot filter” sampling, which do not. Overall, the PM EFs ranged from 0.2 to 108.2 g GJ–1 for solid fuels. The PM EF determined for a solid fuel depends strongly on the measurement method employed and on user behavior, and less strongly on secondary air supply and stove type. Kerosene-based firelighters were found to make a disproportionately high contribution to PM emissions. Organic aerosol dominated PM composition for all fuels, constituting 50–65% of PM from bituminous and low-smoke ovoids, and 85–95% from torrefied olive stone (TOS) briquettes, sod peat, and wood logs. Torrefied biomass and low-smoke ovoids were found to yield the lowest PM emissions. Substituting these fuels for smoky coal, peat, and wood could reduce PM2.5 emissions by approximately 63%.

Characterization of outdoor air pollution from solid fuel combustion in Xuanwei and Fuyuan, a rural region of China

Outdoor air pollution is a growing public health concern, particularly in urban settings. However, there are limited epidemiological data on outdoor air pollution in rural areas with substantial levels of air pollution attributed to solid fuel burning for household cooking and heating. Xuanwei and Fuyuan are rural counties in China where the domestic combustion of locally sourced bituminous (“smoky”) coal has been associated with the highest lung cancer rates in China. We previously assessed indoor and personal air pollution exposures in this area; however, the influence of indoor coal combustion and household ventilation on outdoor air pollution has not been assessed. Therefore, we measured outdoor fine particulate matter (PM2.5), species of polycyclic aromatic hydrocarbons (PAHs) including naphthalene (NAP) and the known carcinogen benzo(a)pyrene (BaP), sulfur dioxide (SO2), and nitrogen dioxide (NO2) over two consecutive 24-h sampling periods in 29 villages. Just over half of the villages were revisited two to nine months after the initial sampling period to repeat all measurements. The overall geometric mean (GM) of outdoor PM2.5, BaP, NAP, and NO2 were 45.3 µg/m3, 9.7 ng/m3, 707.7 ng/m3, and 91.5 µg/m3, respectively. Using linear mixed effects models, we found that burning smoky coal was associated with higher outdoor BaP concentrations [GM ratio (GMR) = 2.79] and lower outdoor SO2 detection rates (GMR = 0.43), compared to areas burning smokeless coal. Areas with predominantly ventilated stoves (> 50% of stoves) had higher outdoor BaP (GMR = 1.49) compared to areas with fewer ventilated stoves. These results show that outdoor air pollution in a rural region of China was associated with the type of coal used for cooking and heating indoors and the presence of stove ventilation. Our findings suggest that efforts of household stove improvement to reduce indoor air pollution have resulted in higher outdoor air pollution levels. Further reducing adverse health effects in rural villages from household coal combustion will require the use of cleaner fuel types.

Analysis of the associations of indoor air pollution and tobacco use with morbidity of lung cancer in Xuanwei, China

BackgroundIndoor air pollution emitted by smoky coal combustion in unventilated fire pits used to cause high lung cancer mortality in Xuanwei. Stove improvements were implemented from the 1970s to the 1980s. However, the present lung cancer mortality rate in Xuanwei shows almost no significant declining trend. Tobacco use is another established risk factor for lung cancer. Smoking prevalence and secondhand smoke (SHS) exposure rate are both high in Xuanwei. Therefore, in this study we evaluated the relationship among indoor air pollution over 30 years ago, tobacco use, and lung cancer risk, to further explore the competitive effects of these two risk factors. MethodsA case-control study design was used. We constructed an unconditional logistic regression model to evaluate the relationship among indoor air pollution, tobacco use, and lung cancer risk, adjusting the covariates and with an interactive term between the two key variables. We further quantitatively assessed the maximum decrease in the indoor air pollution effect when facing competition from tobacco use via a sensitivity analysis. First, the effect of indoor air pollution on lung cancer without considering tobacco use was estimated. Then, we calculated a “bias factor” and divided the effect estimation by this factor. ResultsWe found a strong delayed effect of indoor air pollution over 30 years ago in each subgroup with different tobacco use history. The effects of tobacco use were relatively small, but in areas without smoky coal combustion and indoor air pollution over 30 years prior, the lung cancer risk caused by tobacco use became much stronger and statistically significant. Moreover, we assessed that the effects of tobacco use on lung cancer could reduce a maximum of 18%-30% of the effects of indoor air pollution, but did not influence their statistical significance; the competitive effect from ever smoking was stronger than that from SHS exposure. ConclusionsAt present in Xuanwei, delayed effect of the indoor air pollution over 30 years ago remains the major risk factor for lung cancer. Concomitantly, the adverse effect of tobacco use on lung cancer is becoming more apparent; local governments should start considering public health activities for smoking cessation promotion and SHS exposure prevention.

Increased risk of carotid atherosclerosis for long-term exposure to indoor coal-burning pollution in rural area, Hebei Province, China

Smoky coal burning is a predominant manner for heating and cooking in most rural areas, China. Air pollution is associated with the risk of atherosclerosis, however, the link between indoor air pollution induced by smoky coal burning and atherosclerosis is not very clear. Therefore, we designed a cross-sectional study to evaluate the association of long-term exposure to smoky coal burning pollutants with the risk of atherosclerosis. 426 and 326 participants were recruited from Nangong, China and assigned as the coal exposure and control group according to their heating and cooking way, respectively. The indoor air quality (PM2.5, CO, SO2) was monitored. The association between coal burning exposure and the prevalence of atherosclerosis was evaluated by unconditional logistic regression analysis, adjusted for confounding factors. The inflammatory cytokines mRNAs (IL-8, SAA1, TNF-α, CRP) expression in whole blood were examined by qPCR. People in the coal exposure group had a higher risk of carotid atherosclerosis compared with the control (risk ratio [RR], 1.434; 95% confidence interval [95%CI], 1.063 to 1.934; P = 0.018). The association was stronger in smokers, drinkers and younger (<45 years old) individuals. The elevation of IL-8 (0.24, 95%CI, 0.06–0.58; P < 0.05), CRP (0.37, 95%CI, 0.05–0.70; P < 0.05), TNF-α (0.41, 95%CI, 0.14–0.67; P < 0.01) mRNAs expression in whole blood were positively related to coal exposure. Our results suggested long-term exposure to smoky coal burning emissions could increase the risk of carotid atherosclerosis. The potential mechanism might relate that coal burning emissions exposure induced inflammatory cytokines elevation which had adverse effects on atherosclerotic plaque, and then promoted the development of atherosclerosis.

Constituents of Household Air Pollution and Risk of Lung Cancer among Never-Smoking Women in Xuanwei and Fuyuan, China.

Background:Lung cancer rates among never-smoking women in Xuanwei and Fuyuan in China are among the highest in the world and have been attributed to the domestic use of smoky (bituminous) coal for heating and cooking. However, the key components of coal that drive lung cancer risk have not been identified.Objectives:We aimed to investigate the relationship between lifelong exposure to the constituents of smoky coal (and other fuel types) and lung cancer.Methods:Using a population-based case–control study of lung cancer among 1,015 never-smoking female cases and 485 controls, we examined the association between exposure to 43 household air pollutants and lung cancer. Pollutant predictions were derived from a comprehensive exposure assessment study, which included methylated polycyclic aromatic hydrocarbons (PAHs), which have never been directly evaluated in an epidemiological study of any cancer. Hierarchical clustering and penalized regression were applied in order to address high colinearity in exposure variables.Results:The strongest association with lung cancer was for a cluster of 25 PAHs [odds ratio (OR): 2.21; 95% confidence interval (CI): 1.67, 2.87 per 1 standard deviation (SD) change], within which 5-methylchrysene (5-MC), a mutagenic and carcinogenic PAH, had the highest individual observed OR (5.42; 95% CI: 0.94, 27.5). A positive association with nitrogen dioxide () was also observed (OR: 2.06; 95% CI: 1.19, 3.49). By contrast, neither benzo(a)pyrene (BaP) nor fine particulate matter with aerodynamic diameter () were associated with lung cancer in the multipollutant models.Conclusions:To our knowledge, this is the first study to comprehensively evaluate the association between lung cancer and household air pollution (HAP) constituents estimated over the entire life course. Given the global ubiquity of coal use domestically for indoor cooking and heating and commercially for electric power generation, our study suggests that more extensive monitoring of coal combustion products, including methylated PAHs, may be warranted to more accurately assess health risks and develop prevention strategies from this exposure. https://doi.org/10.1289/EHP4913

The respiratory tract microbiome and its relationship to lung cancer and environmental exposures found in rural china.

We previously reported that bacterial diversity in sputum samples from never-smoking women in rural China varied by lung cancer status and household air pollution (HAP) exposure type. Here, we expand on our associations between environmental exposures and respiratory tract microbiota with an additional 90 never-smoking women from Xuanwei, China. DNA from sputum samples of cases (n = 45) and controls (n = 45) was extracted using a multistep enzymatic and physical lysis, followed by a standardized clean up. V1-V2 regions of 16S rRNA genes were Polymerase chain reaction (PCR) amplified. Purified amplicons were sequenced by 454 FLX Titanium pyrosequencing and high-quality sequences were evaluated for diversity and taxonomic membership. In our population of never-smokers, increased risk of lung cancer was associated with lower alpha diversity compared to higher alpha diversity (Shannon: ORhigh = 1.00 [reference], ORmedium = 3.84 [1.02-14.48], ORlow = 3.78 [1.03-13.82]; observed species: ORhigh = 1.00 [reference], ORmedium = 2.37 [0.67-8.48], ORlow = 2.01 [0.58-6.97]; Phylogenetic Diversity (PD) whole tree: ORhigh = 1.00 [reference], ORmedium = 3.04 [0.85-10.92], ORlow = 2.53 [0.72-8.96]), as well as a decreased relative abundance of Fusobacteria (ORhigh = 1.00 [reference], ORmedium = 1.24 [0.42-3.66], ORlow = 2.01 [0.63-6.44], ptrend = 0.03). Increasing alpha diversity was associated with smoky coal use compared to clean fuel use among all subjects (observed species, P = 0.001; PD whole tree, P = 0.006; Shannon, P = 0.0002), as well as cases (observed species, P = 0.02; PD whole tree, P = 0.03; Shannon, P = 0.03) and controls (observed species, P = 0.01; PD whole tree, P = 0.05; Shannon, P = 0.002). Increased diversity was also associated with presence of livestock (observed species, P = 0.02; PD whole tree, P = 0.02; Shannon, P = 0.03) in the home for cases. Our study is the first to report that decreased microbial diversity is associated with risk of lung cancer. Larger studies are necessary to elucidate the direct and indirect effects attributed to the disease-specific, HAP-specific, and animal-specific associations. Environ. Mol. Mutagen. 2019. © 2019 Wiley Periodicals, Inc.

Household coal combustion, indoor air pollutants, and circulating immunologic/inflammatory markers in rural China

ABSTRACTThe study aim was to investigate whether household bituminous (“smoky”) coal use and personal exposure to combustion emissions were associated with immunologic/inflammatory marker levels. A cross-sectional study of healthy never-smoking women from rural Xuanwei and Fuyuan, China was conducted, which included 80 smoky coal and 14 anthracite (“smokeless”) coal users. Personal exposure to fine particulate matter (PM2.5) and benzo[a]pyrene (BaP) was assessed using portable devices, while 67 circulating plasma immunologic/inflammatory markers were measured using multiplex bead-based assays. Multivariable linear regression models were employed to estimate associations between smoky coal versus smokeless coal use, indoor air pollutants, and immunologic/inflammatory markers. Six markers were altered among smoky coal users compared to smokeless coal, including significantly decreased interferon-inducible T-cell alpha chemoattractant (CXCL11/I-TAC), and increased serum amyloid P component (SAP). CXCL11/I-TAC was previously found to be reduced in workers exposed to high levels of diesel engine exhaust, which exhibits similar constituents as coal combustion emissions. Further, there was evidence that elevated PM2.5 and BaP exposure was associated with significantly diminished levels of the serum amyloid A (SAA); however, the false discovery rates (FDRs) were >0.2 after accounting for multiple comparisons. Inflammatory processes may thus mediate the carcinogenic effects attributed to smoky coal emissions.

Five-year lung cancer mortality risk analysis and topography in Xuan Wei: a spatiotemporal correlation analysis

BackgroundIn Xuan Wei, China, the lung cancer mortality rate is rising significantly more than that of the nation overall. However, it remains unclear 1) if improved diagnosis can just partially explain this observation and how other local risk factors may be correlated with the lung cancer mortality rate and 2) how the lung cancer mortality rates differ within Xuan Wei and how these spatiotemporal patterns are linked with local risk factors. To increase etiological knowledge, this study evaluated the spatial and temporal distributions of the health effects (the lung cancer mortality rates) from 2011 to 2015.MethodsFour steps of spatial analysis were applied, as follows: 1) hotspot analysis to determine the geographical patterns of lung cancer mortality, 2) spatially-weighted sum to identify areas with higher health risks, 3) bivariate statistical analysis to assess the overall correlation between coal mines and lung cancer mortality, and 4) geographically-weighted regression to test for correlations among different towns within Xuan Wei.ResultsWomen had higher lung cancer mortality rates than those in men, with an increasing trend in both sexes over time. The incidence rates in Laibin Town were the highest in Xuan Wei every year. Over the 5-year study period, the lung cancer mortality was increasingly concentrated in Laibin, Shuanglong, and Longchang, where the smoky coal mines are most concentrated. The population-level health risks from the coal mine in Xuan Wei were mapped and divided into five types of risk areas (Type I – Type IV). Correlation analysis revealed that there was no significant correlation between lung cancer mortality as a whole and coal mine distribution during the 5-year study period. However, the geographically-weighted regression revealed a stronger correlation in medium (Type III) and second-lowest (Type IV) health risks.ConclusionsXuan Wei lung cancer mortality has increased continuously since the third national retrospective surveys on the causes of death by the Ministry of Health of the People’s Republic of China (2004–2005), especially for local women and residents over 35 years of age. Geographically, lung cancer in Xuan Wei showed unique spatiotemporal clustering. The local lung cancer mortality was significantly correlated with the smoky coal mine geographically. Some specific towns (Laibin, Shuanglong, and Longchang) within Xuan Wei manifested high correlations between lung cancer mortality and coal mines. The effects of coal mines on lung cancer mortality rates also spread geographically outward from these areas. Public health concern regarding lung cancer in Xuan Wei should prioritize higher-risk towns surrounded by smoking coal mines. Intervention strategies for particular toxic coal types require further studies on their chemical characteristics and mechanisms of carcinogenesis. Additional studies are also warranted to systematically examine the local environmental health risks related to coal industries and combustion air pollution and eventually to conduct early screening of lung cancer for local people who are more exposed to smoky coal in high-risk areas.

Lung cancer risk by geologic coal deposits: A case-control study of female never-smokers from Xuanwei and Fuyuan, China.

Coal types vary around the world because of geochemical differences in their source deposits; however, the influence of coal emissions from different deposits on human health remains unexplored. To address this issue, we conducted the first study of the relationship between coal use from various deposits and lung cancer risk in Xuanwei and Fuyuan, counties in China where lung cancer rates are among the highest in the world among female never-smokers due to use of bituminous ("smoky") coal for heating and cooking. We conducted a population-based case-control study of 1031 lung cancer cases and 493 controls among never-smoking women in Xuanwei and Fuyuan. Logistic regression models were used to estimate associations between coal use from various deposits across the lifecourse and lung cancer risk. There was substantial heterogeneity in risks by coal deposit (p = 7.8E-05). Compared to non-smoky coal users, risks by smoky coal deposit ranged from OR = 7.49 (95% CI: 3.43-16.38) to OR = 33.40 (95% CI: 13.07-85.34). Further, women born into homes that used smoky coal and subsequently changed to non-smoky coal had a higher risk (OR = 10.83 (95% CI: 4.61-25.46)) than women born into homes that used non-smoky coal and changed to smoky coal (OR = 4.74 (95% CI: 2.03-11.04, pdifference = 0.04)). Our study demonstrates that various sources of coal have considerably different impact on lung cancer in this population and suggests that early-life exposure to carcinogenic emissions may exert substantial influence on health risks later in life. These factors should be considered when evaluating the health risks posed by exposure to coal combustion emissions.