EDITORIAL

Gas cooking appliances and indoor pollution

The contribution of the home environment and other life-style factors in the pathogenesis of allergic disease hasattracted much attention, particularly the role of indoorpollution from gas cooking appliances and its associationwith asthma-like symptoms. Recognizing that the preva-lence of gas cookers in developed countries is high at 50–70%, any evidence of a deleterious effect on health repre-sents a major public health issue.

The predominant sources of indoor pollutants are gascooking (and heating) appliances and tobacco smoke, whichproduce complex mixtures of volatile organic compounds,sulphur dioxide, water vapour, particulates, carbon dioxideand oxides of nitrogen. The most extensively studied indoorpollutant is nitrogen dioxide, the concentrations of whichare determined partly from outdoor concentrations, but arehighest in kitchens with gas cookers, often at levels higherthan the World Health Organization’s guideline value foroutdoorair of 150mg/m3 in 24 h [1].

Despite such concerns, the strength of the epidemiologi-cal evidence linking the effects of gas cooking (and nitrogendioxide exposure) to respiratory health has been inconsis-tent. Many of the epidemiological studies focused onchildren. Some studies have shown a small but significanteffect of NO2 exposure on respiratory symptoms and lungfunction [2–4], while others have failed to confirm theassociation [5–7]. Samet and Utell [8] reviewed the incon-sistencies in the epidemiological literature and concludedthat methodological issues such as low statistical power,confounding or effect modification by other pollutants,misclassification of exposure and the use of insensitivemeasures of health outcome could explain the inability toderive definitive conclusions. In particular, many studiesused the presence or absence of gas cookers as a proxy forexposure to NO2, and some measured the levels of NO2 inhomes at fixed points. Monitoring analyses confirm thatneither fixed site monitoring or use of categorical variablessuch as gas or electric cooking accurately predict personalNO2 exposure [1] as this will be influenced by outdoorlevels, indoor sources, the rate of exchange between indoorand outdoor air, time spent in the microenvironment by theindividual and other characteristics of the dwelling and itsfurnishings that influence NO2 dispersal and removal. Therehave been recent studies which have included direct mea-sures of NO2 exposure, and have reported increased sorethroats and colds in children with high hourly peak NO2

exposures [9], a small reduction in FVC with personal NO2

exposure [10], and increased respiratory symptoms inchildren with gas stove exposure even after adjusting for

NO2 levels (OR 2.2 [1.0–4.8]) [11]. However, two otherstudies conducted in infants and children revealed noassociation between measured NO2 exposure and respira-tory illness [12,13].

In a landmark meta-analysis by Hasselbladet al. [14], theresults of 11 studies were combined including those where asurrogate estimate of NO2 exposure, such as a presence ofgas cooker was used, or NO2 levels were directly measuredin relation to long-term exposure to a 30-mg/m3 increase inNO2 (comparable with the increase resulting from exposureto a gas stove). The conclusions after using four differentstatistical methods were all in agreement; the relative risk oflower respiratory illness in studies using gas stoves as asurrogate for NO2 exposure was 1.18, but when four studiesincluding measured NO2 levels were combined, the riskincreased to 1.27 with an overall combined risk of 1.20, i.e.exposure to a 30-mg/m3 increase in NO2 exposure wouldresult in a 20% increase in respiratory illness. A furtheranalysis of the evidence allowing for heterogeneity in studydesign was in agreement and concluded that according toage, the estimated risk is higher (1.29–1.60) in childrenaged 5–6 years and 6–12 years compared with infantsparticularly for health end-points that did not includeasthma [15].

If children, the elderly and women tending to youngfamilies spend more time at home, it follows that thesegroups are likely to be exposed to the highest levels of NO2.There is little data specifically on the elderly population,while evidence in adults is equally fraught with inconsis-tency as in children, largely because of the same methodo-logical limitations. Jarviset al. described two cross-sectional studies; women using gas for cooking had anincreased risk of current asthma-like symptoms (duringthe past 12 months) and reduced lung function (FEV1),and these associations were not observed in men [16].Similarly using a meta-analysis approach as part of theEuropean Community Respiratory Health Survey [17], datafrom 5561 males and 6029 females from 11 countries (23centres) were analysed, and although there was no associa-tion between respiratory symptoms and gas cooking inmales, the association varied between centres in femaleswith an overall positive association with current wheeze andbreathlessness. Gender differences in the effects of gascooking have also been described in children [2,4,18,19].Few studies have directly compared measured personal NO2

exposure between children and adults who cook, but thedata does not support the notion that children have consis-tently higher personal NO2 exposures than their mothers

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[20–22]. While the pattern of exposures in cooking womenmay be different, children may equally be exposed to asimilar 1-hr peak and weekly mean NO2 exposures [21].The majority of epidemiological studies have focused onchildren largely because their period of exposure to pollu-tion is recent, exposure to active smoking and occupationalexposures are absent, and the frequency of respiratory virusinfections is high, rather than any convincing evidence ofincreased biological susceptibility.

Another important facet of gas cooking and allergicdisease is whether exposure to gas stoves in childhoodalters the prognosis of asthma. Given that recent controlledexposure studies suggest that NO2 exposure either alone orin combination with other pollutants may alter the early andlate asthmatic response and potentiate specific bronchialhyperresponsiveness to inhaled allergen [23,24], childhoodexposure to gas stoves and effects on asthma incidence andprognosis have been postulated, but until recently not testeddirectly in an epidemiological study. Two studies specifi-cally designed to address the question of gas cooking inchildhood and prognosis of asthma later in life have beendescribed, one of which is so far published only in abstractform [25]. The other is described in this issue of the Journal;Moranet al. [26] report the results of a cross-sectional studydrawn from the British 1958 birth cohort that addresses thequestion of gas cooking in childhood and adulthood and therisk of asthma symptoms, allergic sensitization and lungfunction in early adulthood. From 5470 individuals whocontributed data at birth and all five follow-ups rangingfrom ages 7–33 years, 1989 index cases with a history ofasthma, wheezy bronchitis or pneumonia and 626 controls(a random 20% of the remainder) were selected, of which afinal number of 1119 cases and 330 controls were inter-viewed (at ages 34–35 years). Assessment was made of thepresence and severity of respiratory symptoms, measures ofspirometric indices of lung function and atopic status byskin prick testing to common indoor and outdoor inhaledaeroallergens. Exposure to gas cooking in childhood at age11 years (but not at 7 years) was assessed retrospectively atthe interview, as cooking fuel use was not ascertaineddirectly during childhood, while the prognosis of asthmawas determined prospectively by the presence or absence oftypical symptoms/wheeze at each cohort follow-up visit.Among those interviewed, the reported exposure to gas andelectric cooking fuel alone at age 11 was high at 58 and36%, respectively, while current exposure was lower at 45and 35%, respectively. Furthermore, of those reportingcurrent exposure to gas and electric cooking fuel, 34 and51% were not exposed to the respective cooking fuel at age11 years. The authors found no significant associationbetween the use of gas cooking in childhood or adulthoodand the incidence or prognosis of asthma/wheeze, currentseverity of symptoms or allergic sensitization. The results,

however, indicated that individuals who developed asthmain childhood and were exposed to gas cooking currently orin childhood had a non-significant increased risk of persis-tent asthma at age 35 years. Of particular interest was theobservation that subjects who were currently exposed to gasfor cooking had a significantly reduced FEV1 (– 0.07 L,95% CI 0.056) and FEV1/FVC ratio (– 1.0%, 0.8) com-pared with those who currently used electricity for cooking.These observed effects are small and of uncertain clinicalsignificance. The authors also noted that the reduction inlung function was concentrated amongst males and thosewith current asthma/wheeze (but not those with past asthma/wheeze).

Despite the methodological limitations, particularly inclassification of exposure that are acknowledged by theinvestigators, the conclusions drawn are important. Firstly,the discrepancy in gender effects between this study andthose described by Jarviset al. [16,17] are not new, and arein keeping with the observations of Viegiet al. [27] whonoted increased cough and phlegm in males with use ofbottled (but not natural) gas for cooking, and wheeze andshortness of breath in females with the use of a gas stove orforced-air circulation. Comstocket al. [28] also reported anincreased frequency of respiratory symptoms and impairedventilatory function only among men, particularly amongthose who never smoked. Overall the data suggest somedifferences in health risk between genders in both childrenand adults, but the evidence is not consistent in the groupsexpected to be at highest risk. One cannot conclude these aresolely due to chance or variances in study design; furtherinformation is required to accurately reflect relevant expo-sures determined by factors such as length and intensity ofcooking, personal exposures of individuals directly exposedto cooking irrespective of gender, kitchen ventilation char-acteristics and effective use and availability of extractorfans. In stratified analyses of women from East Anglia,Jarviset al. [16] noted that among women who used gascookers, they did not find a lower risk (as one might expect)in employed women or students compared with housewivesor unemployed women, or in women who had extractor fanscompared with those who did not. These latter observationslikely reflect limitations in accurate pollutant exposure asone cannot ascertain whether employed women use gascookers less often than housewives, or that the presence ofextractor fans reflect their effective use. There is also littleevidence that adult women are more susceptible than men tothe effects of exposure to NO2 in controlled exposurestudies [29], and very little data comparing measured NO2

exposures between genders. Dockeryet al. [20] documentedthat the difference in weekly mean personal NO2 exposurebetween spouses was only 4 and 3mg/m3 from homes withgas and electric cookers, respectively.

A second important point from the study by Moranet al.

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[26] is that exposure to gas cooking in childhood or adult-hood was not associated with the prognosis of asthma. Amore pertinent observation was that the prevalence ofindividuals exposed to either gas or electric cooking fuelhad fallen by 13 and 1%, respectively. Although this issubject to recall bias, it is supported by the observation thatof the total domestic energy consumption by cooking in theUK in 1995, 68 and 30% was accounted for by gas andelectricity, respectively, and that there has been a gradualfall in total energy consumption by gas cooking from 2.8Million tonnes of oil equivalent (Mtoe) in 1970 to 2.1 Mtoein 1995 paralleled by an increase in electrical energyconsumption by electrical cooking appliances (includingovens and hobs) from 11.2 to 13.8 TWh between 1970 and1994 [30]. A decrease in use of electrical ovens has not beenenough to offset the rapid proliferation in electrical energyconsumption due to microwave ovens since the early 1980s.The consumption of residential energy due to gas andelectrical cooking fuels show a similar trend in the US[31]. Given that the prevalence of individuals using gascookers and energy consumption by gas cooking has fallenin real terms, the findings on the prognosis of asthma byMoranet al. (and the overall prevalence of allergic disease)are not surprising.

The observation that current (but not childhood) gasexposure was associated with a small reduction in lungfunction in current asthmatics in the study by Moranet al.argues against any long-term effect of gas cooking on lungfunction. The decrement in FEV1 was small (0.070 L), andis supported by evidence from controlled exposure andepidemiological studies of NO2 [32]. Although there issome, but not consistent, evidence for a small increase inairway resistance with higher concentrations of NO2, themajority of studies have found no change in resting lungfunction in either normal or asthmatic subjects exposed toconcentrations of NO2 of 1000 p.p.b. (< 1880mg/m3) orless [33]. Bronchial responsiveness has been shown toincrease slightly in normal subjects exposed to greaterthan 1880mg/m3 NO2, and in only about a third of studiesspecifically in asthmatic subjects. Given that the major siteof NO2-induced injury is the transitional zone (the areabetween the terminal bronchioles and alveoli), conventionalpulmonary function tests most sensitive to changes in largeairway function may be a relatively insensitive means ofdetecting the earliest responses in small peripheral airways,which may account for the relatively small changes inpulmonary function responses in both controlled exposureand epidemiological studies. Despite the methodologicalshort comings, the evidence for significant effects on lungfunction in adult asthmatics from controlled exposure stu-dies is limited, while the evidence on lung function andexposure to gas cooking in children and young women fromepidemiological studies is inconsistent with some studies

showing a reduction [3,16,28,34–36] while others haveshown no effect [37–40].

So does gas cooking and exposure to NO2 cause asthma?If criteria of causality such as magnitude, consistency,specificity, coherence, temporal relationship and biologicalplausibility for the association are applied, then the evidenceis absent. The wealth of literature on gas cooking andrespiratory health does offer moderate evidence that somesusceptible groups, particularly children and cookingwomen are at risk, and it is current exposure with acutebut reversible respiratory effects that are likely to beimportant, particularly as there is little evidence of effectson long-term outcome [25,26]. The challenge lies in identi-fying why some groups are susceptible and to accuratelyclassify which aspects of gas cooking exposure are hazar-dous. Measurements of average NO2 levels by passivemonitors have offered an improvement over surrogateinformation such as presence of gas cookers, but animal[41] and more recently human studies [9] have suggestedthat peaks of exposure which more closely mimic ‘real life’domestic exposures to gas cooking may be more relevant tohealth effects. Some studies have suggested that averagedweekly NO2 exposures predict maximum 1-hr peak expo-sures [42] while others have argued for only a weakassociation at best [21], hence more effective and consistentcharacterization of these exposures are required. Accurateclassification of exposure relies on measuring the rightpollutant(s), and because gas cooking is associated withother indoor pollutants, of which nitric oxide (the predomi-nant oxide of nitrogen which is quickly oxidized to NO2

soon after combustion) and particulates are important, theeffects of these factors need to be accounted for in futurestudies. The epidemiological evidence for the effects ofoutdoorparticulate pollution on respiratory morbidity andmortality are powerful [43], and the possibility that nitricoxide is also related to adverse outcome cannot be dis-counted [44,45]. Garrettet al. [11] measured average indoorNO2 levels in the homes of 148 children and reported thatgas cooker exposure was a significant risk factor forrespiratory symptoms even after adjusting for NO2 levels(OR 2.2 [1.0–4.8]), suggesting an additional risk apart fromthe average NO2 exposure associated with gas cookers. Thepossibility that there are other confounders or interactions ofother pollutants during gas cooking in addition to NO2 [11]could also explain some of the discrepancies in the epide-miological evidence but requires confirmation.

Despite the inconsistencies, the current evidence wouldargue for a modest risk of gas cooking on health, with publichealth concerns due to the high prevalence of exposureresulting in a considerably increased attributable risk. Whatis missing from the evidence is knowing whether otherpollutants in addition to NO2 are involved, what patternsof exposure are important and plausible biological

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mechanisms such as the interaction with respiratory infec-tions [46].

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A. J. CHAUHAN

Mailpoint 810Southampton General Hospital

Tremona RoadSouthampton SO16 6YD

UK

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