Biomass Fuels and Lung Cancer

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INVITED REVIEW SERIES: AIR POLLUTION AND LUNG HEALTHSERIES EDITORS: IAN YANG AND STEPHEN HOLGATE

Biomass fuels and lung cancerresp_2088 20..31

WEI-YEN LIM AND ADELINE SEOW

Saw Swee Hock School of Public Health, National University of Singapore, Singapore

ABSTRACT

It is estimated that about 2.4 billion people around theworld, or about 40% of the worlds population, depend

on biomass fuels (wood, charcoal, dung, crop residue)to meet their energy needs for cooking and heating.The burden is especially high in Asia. Studies suggestthat levels of pollutants including particulate matter


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cancer in humans, and highlight several issues rel-evant to the design and conduct of epidemiologicstudies aiming to examine this association.

CURRENT EXTENT OF USE OFBIOMASS FUELS

TheWorld Health Organization estimates that about 3billion people today, or about 50% of the worldspopulation, use solid fuel for their household energyneeds. Of these, 600 million use coal, whereas 2.4billion use wood, charcoal, animal dung and cropwastes.5 The largest numbers of biomass fuel userscome from China and India: 27% of the population inChina depend on wood for energy, and in India, about58% depend on wood and 11% on dung for energy.5

More than 90% of the population in countries classi-fied as Least Developed Countries (including Asiancountries such as Myanmar, Bangladesh and Cambo-dia) depend on solid fuels (primarily biomass fuels)for their energy needs.5

Countries generally move up the energy ladder2

with economic development, as people shift fromusing biomass fuels to more modern fuels such askerosene, LPG and electricity as their economic situ-ation improves. In developed parts of the world, useof biomass fuels is uncommon, at less than 5% of thepopulation. Within each country, biomass fuel use islinked to poverty, with poorer communities reportinghigher use levels.6 Biomass fuel use is also morecommon in rural areas. Rural areas may not have theinfrastructure to allow access to modern fuels. Costsof biomass fuels are also typically very low, and inmany rural areas, free, as users harvest the necessaryfuels themselves. Because exposure to biomass fuels

is so prevalent, the population impact (i.e. populationattributable risk) of any adverse health effects associ-ated with biomass fuel use is likely to be very largeeven where the relative risks associated with use issmall.

BIOMASS FUEL SMOKE EMISSIONAND ITS COMPOSITION

Combustion of any fuel produces emission ofcomplex mixtures containing particles, semi-volatilematter and gases. Modern fuels burn more effi-ciently, resulting in a greater proportion of theintended end products of carbon dioxide and water(as steam). Biomass fuels are much less efficientlyburned, because of the greater difficulty in mixingthe fuel with air during burning.7 Consequently, alarger fraction of the carbon contained in the fuel isnot fully combusted to carbon dioxide, and insteadforms both particulate matter as well as a variety oforganic compounds. Impurities in the fuels alsoresult in the formation of inorganic compoundsincluding carbon monoxide, sulphur dioxide, nitricoxide and ammonia.4 Hundreds of individual com-pounds have been detected in wood smoke samplesto date, attesting to the complexity of these emis-

sions. Most of these constituents are organic carboncompounds. Alkanes with 17 carbons, alkenes with27 carbons, aromatic compounds such as benzene,xylene, toluene and styrene, a variety of polycyclicaromatic hydrocarbons (PAHs) and substitutedPAHs, alkanols, carboxylic acids, aldehydes andketones, alkyl esters and phenolic compounds haveall been identified in wood smoke emissions.4,8 A

wide variety of metals including nickel and arsenichave also been identified in wood smoke emissions,reflecting uptake of these elements by trees.9 Table 1summarizes constituents that have been identifiedin biomass fuel emission.

PAHs are present in both the gas phase as well asthe particle phase of emissions, with lower molecular-weight compounds (24 aromatic rings) found pre-dominantly in the gaseous phase of emissions, andhigher molecular weight PAHs adhered to smoke par-ticles.10 PAHs can also be found on surfaces of roomswhere biomass fuel-powered stoves are used.11 Inaddition to the respiratory route, PAHs can thereforealso enter the human body through ingestion and via

dermal absorption.12

CARCINOGENICITY OF BIOMASSFUEL SMOKE EMISSION ANDITS CONSTITUENTS

The key compounds of interest with regard to carci-nogenicity in biomass fuel emissions are particulatematter and PAHs. Small particulate matter (particu-late matter


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inhaled concentrations of particles are very high,lung overloading with impairment of particle clear-ance has been observed.15 Lung overloading causessustained neutrophilic inflammation. The subse-quent release of reactive oxygen species (ROS) directlydamages DNA. Cell damage (as well as the pro-cell growth signals from ROS) then promotes cellproliferation and turnover. These chronic pro-

inflammatory changes finally result in fibrosis withinthe lung parenchyma and development of lungtumours.16 Rat models have clearly shown thissequence of events,17 although corresponding evi-dence in humans is poor.

The International Agency for Research on Cancerhas classified PAH as a Group 1 carcinogen.18

Benzo(a)pyrene and larger molecular weight PAHs(47 rings) are clearly carcinogenic in both in vitroand in vivo studies, with a strong doseeffect rela-tionship.12,18 Activated PAH metabolites can formadducts with DNA, and error-prone repair or afailure to repair these adducts subsequently resultsin mutations.4,12 Gene hotspots for adduct forma-

tion by activated PAHs include oncogenes such asp53, the K-ras and the H-ras genes.19,20 PAH-DNAadducts are associated with cancer risk and recur-rence of breast and prostate cancers in epidemio-logic studies,21,22 and detectable adducts inleukocytes were also associated with a twofoldincreased risk of lung cancer.23

In addition, active PAH metabolites such as cat-echols can undergo repeated redox cycles, generat-ing ROS as a by-product.24 PAH metabolites alsoincrease cell proliferation through interaction withthe insulin-like growth factor signalling pathway,25

and through disruptions in calcium ion movementbetween intra and extracellular spaces, with the con-

sequent activation of the protein kinase C pathway.

26

Interactions with other important cell signallingpathways have been described including the epider-mal growth factor receptor pathway and the serine-threonine kinase Akt pathway.27 The epidermalgrowth factor receptor signalling pathway in particu-lar is known to be important in the carcinogenesis oflung adenocarcinomas.28

In vitro studies indicate that wood smoke emis-sion extracts cause DNA damage2932 and aremutagenic33,34 in Salmonella reverse-mutationassays. A substantial portion of the metabolicallyactivated mutagenic activity can be attributed toPAHs, although there are other compounds such asaromatic ketones, phenols, aromatic amines andnitroarenes33,34 that exhibit mutagenic activity. Inanimal model studies, dermal applications of woodsmoke extracts have shown increased papilloma butnot carcinoma formation,35 whereas inhalation expo-sure to wood smoke increased lung adenocarcino-mas in mice but not rats.36 A study in 1993 reportedhigher levels of DNA adducts in Xuan Wei womenwho used wood for cooking, compared with Beijingwomen who used natural gas.37 Further, higher levelsof P53 and MDM2 proteins have been reported inlung cancer patients who reported exposure to woodsmoke, compared with smokers with chronicobstructive pulmonary disorders and healthy

persons who did not report exposure.38 This isconsistent with in vitro data showing that PAH-DNAadduct formation occurs preferentially on promoterregions of the p53 gene.

There are other studies that indirectly support arelationship between biomass fuel emissions andlung cancer, by showing evidence of in vivo changessuch as urinary metabolite excretion, DNA damage

and cytogenetic abnormalities in humans associatedwith wood smoke exposure. An Indian study com-paring women who reported using biomass fuels forcooking compared with women who used LPGshowed that women exposed to biomass fuels hadhigher levels of cytogenetic changes such as chro-mosomal aberrations and micronucleus formationin peripheral lymphocytes.39 Data from an occupa-tional study in Brazil reported higher levels of excre-tion of organic carbon metabolites in the urine (e.g.2-napthol, 1-pyrenol) in kiln-tenders exposed toeucalyptus wood smoke compared with tree cuttersin a charcoal production facility.40 The InternationalAgency for Research on Cancer classifies biomass

(primarily wood) fuel emissions as probable humancarcinogens (group 2A).4

HUMAN EXPOSURE TO BIOMASS FUELSMOKE EMISSIONS

The amount of smoke emission produced depends onthe nature of the fuel and the type of stove used. 4 Inaddition, house characteristics such as the size of theroom, the quality and extent of ventilation, and theuse of room partitions (for example separation ofcooking areas from living or sleeping areas) affect the

intensity and concentration of emissions encoun-tered.4 Over time, concentrations of emissionsequilibrate between indoor and outdoor air, and socommunity factors such as the number of neigh-bours, the extent to which biomass fuels are used bythe neighbours and the closeness of houses also areimportant.

Studies have generally focused on a limitednumber of pollutantstotal suspended particles,PM10 (particles of size 10 mm or smaller), PM4 (par-ticles of size 4 mm or smaller), benzo(a)pyrene andtotal PAHs. In general, reported ranges of exposureof 24-h indoor levels of PM10 and PM4 are in thehundreds of mg/m3 range, significantly above thelevel considered healthy in most guidelines forindoor air standards.4,41,42 Studies that have moni-tored benzo(a)pyrene have reported widely varyingestimates, over four orders of magnitude. Neverthe-less, use of traditional wood stoves in China resultedin emissions of benzo(a)pyrene that were higherthan households where coal was used in improvedstoves,43 and South Asian households using biomassfuels (dung, wood and charcoal) had exposure tobenzo(a)pyrene in the high hundreds or thousandsof nanograms per cubic metre.44 As comparison, theWorld Health Organization guidelines for indoor airpollution note that a lifetime exposure equivalent to1.2 ng/m3 results in an excess lifetime cancer risk of

W-Y Lim and A Seow22

2011 The AuthorsRespirology 2011 Asian Pacific Society of Respirology

Respirology(2012) 17, 2031


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1 in 10000, and report that induction of DNAdamage was observed with as low an exposure as1 ng/m3 of benzo(a)pyrene.12

EPIDEMIOLOGIC STUDIES OFBIOMASS FUEL USE AND

LUNG CANCER

We have been able to identify twenty studies that havereported on the association between solid fuels orbiomass fuels and lung cancer.4564 In addition, thereis 1 pooled analysis using data from seven studies inthe International Lung Cancer Consortium.65 Table 2summarizes results of these 21 studies, all of whichwere casecontrol studies, using either interviews ormedical records to obtain self-reported biomass fueluse as the exposure variable.

In understanding the current evidence regardingthe effect of biomass fuel use on lung cancer, somelimitations affect our interpretation of the findings

from the full list of studies cited in Table 2. Chiefamong these is the inability to separate the effect ofbiomass fuel use from coal use in many of the studies,because exposure was measured in terms of solid fuel(often stated as wood or coal) use,4552which in manycases would be mixed and predominantly coal ratherthan biomass. The reference group was also not uni-formly non-usersfor example, one study com-pared the effect of wood use with a reference group ofcoal users.54

Of the 12 studies that specifically examinedbiomass use (most commonly wood, charcoal, grassor straw), several early reports originated fromChinese populations in Asia. Studies in the 1980s5355

in Hong Kong and China did not find an elevated riskwith wood use in these populations, However, a posi-tive association was reported with wood or charcoaluse at a young age among women inTaiwan56,57 and innever-smoker women in Japan.58Two European mul-ticentre studies reported significantly elevated riskswith wood use.59,62 One of these was a large study thatused a common standardized questionnaire in allcentres, and collected detailed information of fuel useas well as other covariates, and achieved very highresponse rates. This study62 reported odds ratios forwood fuel use for cooking of 1.23 (95% confidenceinterval (CI): 1.001.52) and for heating of 1.31 (95%CI: 1.061.61).

Notably, recent results from a pooled analysis of4181 cases and 5125 controls65 found an increasedrisk with wood smoke exposure odds ratio (OR) 1.21,95% CI: 1.061.38 among individuals from Europeand North America who reported predominant useof wood fuels in the house. No effect of wood usewas seen in never-smokers (OR 1.01, 95% CI: 0.741.37), although wood use was risk-conferring in ever-smokers (OR 1.22, 95% CI: 1.051.42). No estimatescould be made for the effect of wood use in Asiabecause of the small number of exposed cases fromthe studies representedin contrast, coal use wasassociated with an almost fivefold increased risk inthese populations.

Evaluating the evidence

Methodologic issues

Overall, the epidemiologic evidence is suggestive butnot strong. All the studies to date have been casecontrol in design, and methodological limitations ofcasecontrol studies are well known.66 The risk of

selection bias is higher in hospital- or clinic-basedstudies, especially when controls are picked fromlimited patient groups,45,47,50,61 such as patients attend-ing respiratory clinics.50,61 Because some respiratoryconditions may be exacerbated or caused by biomassfuel emissions, the risk of biomass fuel use on lungcancer might be under-estimated in these studies.

Most studies have elicited information on historicalexposure type of fuel and the type of stove most com-monly used in the household as a proxy for exposureto fumes emitted from these fuels. This is reasonablegiven that environmental sampling and individualmonitoring or biomarker measurement would nothave been feasible. Liu et al.54 showed that household

characteristics such as having a separate kitchen, self-reported quality of ventilation, and size of ventilationopenings in living areas and kitchens were associatedwith lung cancer risk, and this data may be importantin providing a more accurate measurement oftrue exposure. The use of historical reporting alsoacknowledges that the relevant period of exposurecould have been 2030 years prior to diagnosis.However, it is particularly susceptible to recall biasthat may lead to both differential and non-differentialmisclassification. Almost all studies have necessarilydichomotized exposure into use/no use or into verybroad categories. All these factors may contribute tothe fact that none of the studies to date have demon-

strated a convincing doseresponse relationship,which would have strengthened the evidenceconsiderably.

Most of the studies were able to control for con-founding to a reasonable extent. However, while allstudies took into account smoking status, either byrestricting the study population to non-smokers,or through adjustment,48,54,60,64 fewer considered thepotential confounding effect of socioeconomic statusand adjusted for this.49,56,57,61,64 A strong inverseassociation between socioeconomic factors such asincome and wealth and lung cancer has beendetected.67Although it is not yet clear what drives thisassociation, it is possible that income and wealth mayaffect downstream factors such as nutrition thatfinally result in differences in risk. Fuel use similarlyexhibits a strong socioeconomic gradient, withbiomass fuel use usually confined to people in thelowest socioeconomic groups of that community.

Effect of smoking history

Relative to smoking, solid fuel emissions are low-riskagents for lung carcinogenesis and their effects maybe masked when studied in populations with a highprevalence of active smokers; adjustment for smokingwill also not allow detection of the true effects. This

Biomass fuels and lung cancer 23




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Table2

Continued

Authors

Typeandlocatio

n

ofstudy

Yearof

study

Exposureclassifica

tion

Numberof

subjects

Keyfindings

Oddsratios(ORs)(95%

confidenceinterval(CI))

Remarks

13

Leeetal.57

Hospitalcase

control,

Kaohsiung,

Taiwan

19931999

Nocookingorgasascoo

kingfuel;

Coaloranthracite;

Woodorcharcoal

Datacollectedduringparticipants

mainperiodinlifewhe

nshe

cooked(2040yearsof

age)

527cases805

controlswithout

tobaccorelated

illness.

Age-gender

matched

Women:Woodorcharcoaluseforcookingversus

gasorno

ne

Small-cellc

arcinoma3.1

(1.09.2

)

Adenocarcinoma3.0

(1.46.4

)

Adjustedforsmoking,residential

area

,socioeconomicstatusand

education.

Only7

%ofmenreportedcooking

14

Sobueetal.58

Hospital

casecontrol,

OsakaJapan

19861998

Useofwoodorstrawas

cooking

fuelatage15,age30a

ndat

timeofinterview

144never-smoker

women.

731

unmatched

neversmokers

Straworwoodforcookingatage30

1.7

7(1.08

2.9

1)

Adjustedforage,

ETSexposure,

maternalsmokinginchildhood

15

Malatsetal.59

Casecontrolin8

countries:Brazil,

France,

Germany.Italy.

Poland,

Romania.

Russia,

Sweden

Notmentioned

Useofwoodorcoalforc

ooking

orheating,anddurationof

exposure

122never-smoker

cases

121never-smoker

hospitalcontrols

or,inSweden

andGermany,

population

controls

Indoorpollutionfromwoodfuel>20yearsversus

nouse

2.5

(1.06

.2)

Adjustedforage,gender,centre

16

Guptaetal.60

Hospitalcase

control,

Chandigarh,

India

19951997

Woodfueluse,anddurat

ionof

exposure

265cases525

controls

matchedbyage

andgender

Woodfuelforcooking

Men1

45years0.9

4(0.5

81.5

4)

>45years

0.8

7(0.5

81.3

0)

Females

145years0.7

4(0.2

02.6

5)

>45years

1.1

1(0.3

43.6

0)

Woodfuelforheating

Men1

45years2.6

2(0.4

714.5

)

>45years

0.9

7(0.6

51.4

3)

Women

145yearsnotcalculatedasnocasesexposed

>45years

2.7

8(0.9

77.9

8)

Adjustedforage,education,

smo

king,gender

17

Hernandez-

Garduoetal.61

Hospital

casecontrol,

MexicoCity,

Mexico

19861994

Evercookedusingwood

fuel,and

durationofexposurein

years

113never-smoker

femalecases

(adenocarcinomas),

273never-smoker

femalecontrols

fromNational

Instituteof

Respiratory

Disease

Yearsofcookingwithwoodversusnouseof

woodfue

l

120years0.6

(0.31.2

)

2150years0.6

(0.31.3

)

>50years

1.9

(1.13.5

)

Adjustedforage,

ETSexposure,

socioeconomicstatusand

education





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18

Lissowskaetal.62

Hospitaland

population

casecontrol,

CzechRepublic,

Hungary,

Poland,

Romania,

Russia,

Slovenia,

United

Kingdom

19982002

Principalfuelsusedineach

residenceofmorethan

1year

forcookingandforhea

ting

Multicentrestudy

fromseven

European

countries,2861

casesfrom15

hospitals,

3118

hospitaland

population

controls

matchedbyage,

genderandarea

Everusedwoodforcookingcomparedwithno

solidfueluse:

1.2

3(1.00

1.5

2)

Everusedwoodforheatingcomparedwithno

solidfueluse:

1.3

1(1.06

1.6

1)

Adjustedforage,gender,

education,smokingandcentre

19

Tangetal.63

Hospitalbased

casecontrol,

Singapore

19961998,

20052008

Frequencyofwood-stove

useat

period25yearspriorto

diagnosis

703femalecases,

1578controls

Never-smokers:0.8

1(0.5

61.1

7)

Smokers:1

.25(0.7

42.1

2)

(refgroupinbothcases:030years:0.4

9(0.2

90.8

3)

>3050years:1.2

7(0.8

71.8

5)

>50years

:0.9

5(0.6

51.3

7)

Pfortren

d0.8

6

(alwaysm

odernfuelsasreference)

Adjustedforcentre,agegender,

education,

familyincome,

crow

dednessandcumulative

toba

ccoconsumption

21

HosgoodIII

etal.65

Pooledstudyof

seven

casecontrol

studiesinthe

International

LungCancer

Consortium

(5105casesand

6535controls)

Rangeof

dates:

19852008

Predominantfuelsusedinone

study,fuelusedasana

dult

(threeotherstudies)

Participantscharacterized

as

predominantwoodfuelusers,

predominantcoalusers

,

predominantnon-solid

fuel

users

4184casesand

5125controls

fromNorth

Americanand

Europestudies

PooledOR

1.2

1(1.0

61.3

8)forpredominant

wood-users(Referencegroup:predominant

non-solid

fuelusers)

Adjforage,gender,education,

ethn

icity,studycentreand

smo

king,andproducttermsof

covariatesandstudies





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may explain why some of the studies reviewed heredid not demonstrate a positive association over-all.48,54,60 On the other hand, of the six studies thatrestricted or stratified their study populations tolow-risk individuals, either non-smokers56,64 or non-smoking women in particular,50,58,59,61,63 all but two63,64

reported positive associations with odds ratios in therange of 1.8 or higher. Unfortunately, most of these

studies did not include smokers, with whom a directcomparison could be made. One study that did wasconducted in India with 67 cases and 46 controls ofnon-cancer patients in a respiratory clinic50 andreported higher risks for non-smokers (OR 5.3 95% CI:1.716.7) than smokers (OR 3.0, 95% CI: 1.18.4).

Recent evidence suggests the possibility of a differ-ent pattern of risk in relation to smoking that of asynergistic effect between smoking and other indoorair pollutants.63 This scenario is not implausible, giventhat both tobacco smoke and biomass fuel smokeshare similar carcinogenic constituents such as PAH,and if it were to apply we would expect to see a stron-ger association among smokers than non-smokers.

In the pooled analysis by Hosgood et al.,65

a risk-conferring effect was observed for wood use in ever-smokers (OR 1.22, 95% CI: 1.051.42) and a null effectin never-smokers (OR 1.01, 95% CI: 0.741.37). In astudy conducted in Singapore,63 the risk associatedwith daily (vs


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However, for GSTT1, the association was only presentwith non-null genotypes and the small number ofsubjects in this study (122 cases and 121 controls) wasa limiting factor.

Evaluation of interventions

China and India have both implemented wood stoveimprovement programmes in which modified stovesthat result in more complete burning and lower levelsof emissions have been given or sold at subsidizedrates to poor communities.72,73 Programme evaluationof these initiatives has focused on the uptake and useof the improved stoves, and changes in indoor airpollution levels after programme implementation.Extending the evaluation to look at biomarkers ofexposure or DNA damage, as well as long-term out-comes such as development of lung cancer, in pro-grammes where good uptake and sustained use of thenew stoves have been documented, and using anappropriate control group will help establish if this

intervention has succeeded in mitigating exposure tothese putative environmental carcinogens.

CONCLUSIONS

The data thus far relating biomass fuel emissions tolung cancer is highly suggestive but not yet conclu-sive. There is good evidence that the constituents ofbiomass fuels are carcinogenic in in vitro models, andemission extracts are clearly mutagenic and cause celldamage in in vitro studies. However, the evidence inanimal models is not as convincing, and the epide-miologic evidence in humans, particularly that of a

doseresponse relationship is incomplete. Given thatmany households combine coal with biomass fuelsuse, establishing a causal association using epidemio-logic methods is challenging. Large well-designedstudies with comprehensive exposure ascertainment,careful control for confounders, conducted in studypopulations with sufficient variation in type of fuelused for energy needs, combined with a consider-ation of genetic factors that influence susceptibility,will be needed in order to place this on a more solidfooting.

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Biomass Fuels and Lung Cancer

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