KEROSENE: A REVIEW OF HOUSEHOLD USES AND THEIR HAZARDS IN LOW- AND MIDDLE-INCOME COUNTRIES (2024)

Household Uses

Cooking, lighting, and heating are the main household services provided by kerosene, although there are kerosene refrigerators and other appliances in some areas. Kerosene heating is not widespread in temperate or highland areas of developing countries, mainly because of cost. Where heating fuel is needed, biomass or coal is usually used because it is cheaper or more available.

Portable kerosene room heaters are used primarily in developed countries, and some developing countries (e.g., Chile), although many countries have either prohibited or discouraged their use, particularly because of the risk of carbon monoxide (CO) poisoning (Long 1997).

Kerosene cooking is widespread in many developing countries, especially in urban populations, where biomass needs to be purchased, and electricity and LPG are expensive or unreliable. There are many kerosene stove designs, but they can be broadly categorized into two broad types depending on how the fuel is burned—wick stoves, which rely on capillary transfer of fuel, and the more efficient and hotter burning pressure stoves with vapor-jet nozzles that aerosolize the fuel using manual pumping or heat. In low-income households, wick stoves are more commonly used, because they are cheaper, they easily provide simmer heat for some staple foods, and they have no nozzles that can get clogged by soot.

Use of kerosene as a lighting fuel—either in wick lamps or brighter burning (but less common) pressure lamps—is common in some developing countries, particularly in regions where electricity supply is unaffordable, unreliable, or unavailable. An estimated one-fifth of the global population (approximately1.3 billion) in 2009 lacked access to electricity, while an even greater but unknown number had only intermittent access (IEA 2011). Detailed data on the source or frequency of lighting in houses are not as commonly collected as cooking fuel data in household surveys; however, fuel-based lighting is widely used in India and much of Africa (DGDA 2010). In India, in 2004–2005, an estimated one in three households reported kerosene as their primary source of lighting—44.4% of rural and 7.1% of urban households (NSSO 2007). In the lowest four socioeconomic deciles of India, 60% of households use kerosene for lighting (Parikh 2010). In several of the most populated African countries, including Uganda, Ethiopia, and Kenya, more than 60% of the population relies on kerosene as the primary lighting fuel (Apple et al. 2010; IFC/WB 2008a; Uganda Bureau of Statistics 2010). Less is known of the quantity of kerosene used for lighting, since it is often difficult to differentiate kerosene used for lighting from that used for other purposes, particularly cooking. Based on existing surveys, reports, and local correspondence from 23 countries, monthly consumption has been reported to vary between 1 and 10 L per household (Mills 2005). These estimates may include the use of kerosene to illuminate businesses as well as residences, which would imply that the higher end of this scale is an overestimate. Recognition of the potential welfare benefits resulting from cleaner and more effective lighting technology has led to several large-scale government and private sector efforts to develop and disseminate solar lighting appliances in India and Africa (DGDA 2010; Palit and Singh 2011).

Fuel Characteristics

Kerosene is a middle distillate of the petroleum refining process, defined as the fraction of crude oil that boils between 145 and 300°C (U.S. Environmental Protection Agency [EPA] 2011). Kerosene can be produced from distillation of crude oil (straight-run kerosene) or from the cracking of heavier petroleum streams (cracked kerosene). Raw kerosene has properties that make it suitable for mixing with performance additives for use in a variety of commercial applications, including transportation fuel. Although this review focused on kerosene in the residential sector, which typically contains no performance additives, studies of kerosene-based aviation fuel are included where they are informative. Kerosene is a complex mixture of branched and straight-chain compounds, which can be generally categorized into three classes: paraffins (55.2% w/w), naphthenes (40.9%), and aromatics (3.9%) (U.S. EPA 2011). Relative proportions vary depending on source of the crude oil and the nature of the refining process. The American Society of Testing and Materials (ASTM) defines two kerosene grades, 1–K and 2–K, acceptable for household appliances. Grades are designated by impurity content, particularly sulfur and aromatics, which reduce combustion efficiency and increase noxious emissions during combustion. 1–K (“low-sulfur”) kerosene contains no more than 0.04% sulfur by weight; 2–K has no more than 0.30%. ASTM considers 1–K as suitable for use in flueless appliances (e.g., portable heaters), while 2–K is suitable for flued appliances. Both grades are designated for use in “illuminating lamps” (ASTM 2008). Cleaner burning lamp oils (Fan et al. 2001), which are often deodorized kerosene or hydrocarbon mixes (e.g., 142 Flash), are not commonly available in developing countries. Unlike biomass fuels, which present no toxic risk prior to combustion, liquid kerosene fuel contains numerous compounds that potentially pose health risks, including n-hexane, naphthalene, and benzene.

Selected Pollutants Emitted From Kerosene Appliances

Kerosene, when burned in appliances, emits many potentially health-damaging pollutants. An exhaustive list would include hundreds of compounds. As a frame of reference for interpretation of concentrations reported in the following sections, short summaries of the best-established adverse health effects associated with some of these pollutants are presented. As applicable, guideline levels established by the World Health Organization (WHO) (2006, 2010) are included. WHO also provides interim target levels for some pollutants, which are higher than guideline levels and intended to provide incremental transition steps for situations with high baseline conditions, from which it is difficult to rapidly achieve guideline levels.

Particulate Matter (PM)

There is a strong and consistent body of evidence indicating that exposure to fine particulate matter (PM) increases the risk of respiratory and cardiovascular disease, cancer, and mortality (Krewski et al. 2005; Samet and Krewski 2007; Tsai et al. 2012; Yang 2008). Fine PM originates from both natural and anthropogenic sources and is emitted as a product of incomplete combustion. The median aerodynamic diameter of particles emitted from combustion is typically well below 2.5 μm (PM_2.5), the particle size below which the majority of PM deposits in the deep lung. The WHO has established PM_2.5 guideline concentrations for all nonoccupational environments (indoors and outdoors) of 10 μg/m³ (annual) and 25 μg/m³ (24 h) (WHO 2006). However, acknowledging the difficulty of achieving the annual guideline concentration in low- and middle-income countries, 3 interim targets for achieving the guideline values were provided—5, 25, and 35 μg PM_2.5/m³. Combustion sources are known also to emit ultrafine particles (UFP), which have aerodynamic diameters <0.1 μm. There is some evidence from laboratory-based studies to suggest that UFP exhibit higher toxicity per unit mass than larger particles in the respirable size range (e.g., PM_2.5) (Peters et al. 1997). Due to their small diameters, ultrafine particles typically contribute little mass to traditional mass-based PM measurements but may constitute the predominant contributor to particle count and surface area. Surface chemistry and composition may be determinants of toxicity, but their importance is still uncertain (Stanek et al. 2011). Compared to larger respirable particles, UFP more easily evade lung-clearance mechanisms and enter the lung interstitium and vascular space. The toxicological mechanisms are not well characterized and epidemiological evidence that distinguishes the risk of UFP from other respirable particles is limited. No UFP guideline levels currently exist.

Carbon Monoxide

Carbon monoxide (CO) is a colorless and odorless gas generated by the incomplete combustion of hydrocarbon fuels. When inhaled, CO binds to hemoglobin in red blood cells to form carboxyhemoglobin, reducing oxygen-carrying capacity of the blood and increasing the risk of chronic and acute adverse health effects in adults, children, and fetuses. The effects of acute exposures include dizziness, muscle cramping, loss of consciousness, and, in extreme cases, death. Low-level chronic exposures have been associated with neurodevelopmental effects (Dix-Cooper et al. 2012; Garland and Pearce 1967; Hiramatsu et al. 1996; Long 1997) and cardiovascular diseases (Yang et al. 1998). WHO guideline levels reflect air concentrations at which a normal adult would not exceed 2% carboxy-hemoglobin. Several time-weighted average guideline levels were established to protect against both chronic and acute adverse effects of CO: 100 mg/m³ (averaging time, 15 min), 35 mg/m³ (1 h), 10 mg/m³ (8 h), and 7 mg/m³ (24 h) (WHO 2010).

Formaldehyde

Formaldehyde (HCHO) is produced by combustion sources as both a gas and adsorbed to particles. Being water soluble, over 90% of gas-phase formaldehyde is absorbed in the upper respiratory tract, unless it is bound to fine particles, which allow for deeper penetration into the lungs. Formaldehyde is classified as a Class 1 carcinogen (IARC 2006), because of sufficient epidemiologic evidence that it increases the risk of nasopharyngeal cancers and myeloid leukemia. Short-term effects include sensory irritation such as eye itching and frequent blinking at levels >0.38 mg/m³. A guideline concentration of 0.10 mg/m³ was established by WHO to protect against short- and long-term health effects (WHO 2010).

Polycyclic Aromatic Hydrocarbons (PAH)

Polycyclic aromatic hydrocarbons (PAH) are a class of multiringed compounds present in indoor environments in both the gas and particle phases, depending on molecular size and environmental conditions. PAH are present as constituents of some hydrocarbon fuels, including kerosene, and also generated as products of incomplete combustion. Benzo[a]pyrene (BaP) is commonly used as an indicator of the toxic potency of PAH mixtures and is the only PAH considered a Class 1 carcinogen (IARC 2010), although more than a dozen PAH compounds have been associated with cancer and other adverse health outcomes. There is emerging evidence in animal models that phenanthrene, which is present in many petroleum-based fuels, is a potent immunosuppressant in animals and possibly in humans (Nadeau et al. 2010). However, noncancer risks are not currently considered in WHO guidelines for these compounds. Specific PAH and their relative proportions vary by source. Using BaP as an indicator, WHO has established a unit risk for lung cancer as 8.7 × 10⁻⁵ per ng BaP/m³. WHO also provides a separate guideline for naphthalene (C₁₀H₈), a two-ring compound and the simplest PAH, which partitions almost entirely in the gas phase. Naphthalene is considered by IARC to be a Class 2 carcinogen (possibly carcinogenic to humans), with sufficient evidence of carcinogenicity from animal studies but lacking evidence from human populations (IARC 2002). A guideline level of 0.01 mg/m³ was established (WHO 2010). This is approximately one order of magnitude above background levels (0.001 mg/m³) in the absence of emission sources.

Sulfur Dioxide

Sulfur dioxide (SO₂) is generated from the sulfur content of fuels during combustion. The majority of sulfur emitted indoors exists as SO_2, but is later converted to secondary sulfur-containing compounds in the atmosphere (e.g., sulfate). Acute effects attributed to SO₂ exposure include changes in pulmonary function and respiratory symptoms, while chronic exposures at levels <20 μg/m³ have been associated with increases in all-age mortality and childhood respiratory disease. WHO established a precautionary 24-h indoor guideline level of 20 μg/m³, with interim target levels at 50 and 125 μg/m³ (WHO 2010). To protect against acute adverse effects, a 10-min guideline level was set at 500 μg/m³.

Nitrogen Oxides (NO_x)

Nitrogen oxide (NO) and nitrogen dioxide (NO₂) are formed in reactions between atmospheric nitrogen and oxygen during the combustion process, particularly at higher combustion temperatures. There is strong evidence linking NO₂ with adverse respiratory health effects in adults and children. These effects include inflammation, asthma, and reduced immune defenses that lead to exacerbation of, or susceptibility to, existing or new respiratory infections. WHO 1-h and annual guideline levels for NO₂ are 200 μg/m³ and 40 μg/m³, respectively (WHO 2006).

Heating

In response to rising electricity prices, portable household kerosene heaters became popular in developed countries in the early 1980s. They could be moved from room to room as needed and were less expensive than central heating. To reduce heat losses, these heaters were often used under low-ventilation conditions, raising concerns about indoor air quality (Leaderer 1982; Leaderer et al. 1986). Despite improvements in design and public education, exposure risk from kerosene heating is still a current topic in several countries, including Japan and Chile (Ruiz et al. 2010). Knowledge of emissions is dominated by results from laboratory-based chamber tests, while the majority of field-based measurements are from monitoring of a single microenvironment to infer exposure to all household inhabitants. Only one study of household exposures that used personal sampling devices was found (Adgate et al. 1992).

Two primary kerosene heater types are evaluated in the literature: convective and radiant heaters. Relatively cleaner burning “dual-stage” heaters are mentioned briefly, but only limited information regarding their emissions was found (Apte et al. 1989; Lionel et al. 1986). Both convective and radiant heater designs use wick capillary action to transfer kerosene to the burner unit. Radiant heaters generate infrared heat, reflected by a polished metal shield; convective heaters warm room air with a fan to force air through a steel tube containing the burner and typically generate more heat and consume more fuel.

Table 1 presents pollutant emission factors and Table 2 microenvironmental and personal monitoring results for criteria health pollutants measured in studies of kerosene heating. All studies were performed in developed countries using local kerosene (typically 1–K grade).

Laboratory chamber studies of kerosene heater emissions began in the early 1980s (Leaderer 1982; Traynor et al. 1983; Yamanaka 1984). Emission factors for fine particulate matter (PM), CO, SO₂, and NO_x (NO₂ and NO), were estimated using a well-mixed-room mass balance model (single-box model). The estimates of EF_NO2 and EF_SO2 suggested indoor concentrations of NO₂ and SO₂ could exceed ambient U.S. air quality standards, while emitted CO could pose health risks under conditions of low ventilation and small room volume (Leaderer 1982). The average CO level in mobile homes using kerosene heaters, for example, was 8.5 ± 1.6 mg/m³—approximately 7 times greater than in homes without kerosene heaters and sometimes exceeding the WHO guideline level. Field measurements confirmed that kerosene heaters increased indoor concentrations of NO₂, SO₂, PM_2.5, and PM₁₀ above ambient levels (Adgate et al. 1992; Leaderer et al. 1999; Mumford et al. 1991), and personal exposures to NO₂ in households using kerosene heaters were five to six times greater than in homes without these heaters (Adgate et al. 1992). Within apartment buildings in Santiago, Chile, a city known for high ambient air pollution levels, kerosene heaters were shown to increase average 24-h PM_2.5 concentrations by 44 μg/m³ above background (Ruiz et al. 2010). UFP, SO₂, and NO₂ were also elevated relative to outdoor levels and levels in houses using compressed natural gas (CNG) or liquid petroleum gas (LPG) for heating (Ruiz et al. 2010). Aggregated UFP concentrations were 163,800 particles/cm³, approximately 10-fold higher than levels measured in houses with electric heaters and 3-fold higher than in houses with CNG or LPG heating.

Elevated levels of carcinogenic polycyclic aromatic hydrocarbons (PAH) and nitro-PAH have been measured in mobile homes and apartments with kerosene heating devices (Mumford et al. 1991; Ruiz et al. 2010), and identified species were consistent with results from controlled chamber experiments (Girman et al. 1982; Traynor et al. 1990). Using chamber experiments, formaldehyde (HCHO) emission factors ranged from 2 to 36 μg/g kerosene, depending on heater type (Girman et al. 1982; Traynor et al. 1983). An indoor mass-balance model that accounts for loss by surface reactions suggests that these emission rates are unlikely to lead to indoor HCHO concentrations exceeding 0.10 ppm, or 0.12 mg/m³ at standard conditions, slightly above the WHO guideline level of 0.10 mg/m³ (Girman et al. 1982).

Numerous studies demonstrated that heater design (radiant or convective) is influential on emissions of pollutants (Apte et al. 1989; Cheng et al. 2001; Leaderer 1982; Lionel et al. 1986; Traynor et al. 1983; 1987; 1990; Yamanaka et al. 1979; Yamanaka 1984; Zhou et al. 2000). EF_co were, on average, four- to fivefold higher for radiant heaters than for convective heaters; conversely, EF_NOx from convective heaters were two- to fourfold higher than from radiant heaters (Table 1), indicative of the hotter combustion temperatures of convective heaters. SO₂ was not influenced greatly by device type, as emissions are primarily dependent on fuel sulfur content.

The grade of kerosene was also shown to affect pollutant emissions from heaters. In two studies investigating the exposure of soldiers to pollutants generated from kerosene heaters in tents, three grades of kerosene—one commonly available (1–K) and two kerosene-based jet fuels—were tested in both convective and radiant heaters. Indoor concentrations of PM₁₀ and PM_2.5 varied up to eightfold, depending on fuel grade (Zhou et al. 2000). A follow-up study reported that emissions of elemental carbon (EC), organic carbon (OC), SO₄²⁻, NH⁴⁺, CO, SO₂, and NO were also influenced (Cheng et al. 2001).

Most of the investigations into the exposure risk of kerosene heaters were performed more than 20 years ago, when use of such heaters was more widespread. This makes current interpretation difficult, since the extent to which those heaters were replaced by improved designs is not known. However, more recent studies (Cheng et al. 2001; Ruiz et al. 2010; Zhou et al. 2000) suggest that improvements in emissions have not been significant. There is strong laboratory- and field-based evidence suggesting that fine PM, NO₂, and SO₂ are generated at rates that could exceed WHO guideline concentrations in households. Given the high combustion temperatures, UFP and PAH formation would also be expected to be high. However this has been confirmed by only a handful of field measurements (Mumford et al. 1991; Ruiz et al. 2010).

Lighting

The few published studies that document pollutant emissions and resulting air quality impacts of kerosene lighting are summarized in Tables 3 and ​and4.4. All studies were performed under controlled conditions intended to simulate real-world applications. To date, no study has reported personal exposure or environmental concentrations from field-based measurements, partly because it is difficult to distinguish the contribution of lighting from that of other common and coemitting household sources, such as cooking or smoking.

Household kerosene lighting devices are of three types: “simple wick” lamps, hurricane lamps, and pressure lamps. The “simple wick” (synonyms include kerosene candles, taboodas, tuki) is the cheapest, most basic design, typically constructed locally from recycled metal or glass containers. Fuel is burned via capillary action of a wick, usually made of cloth or rope. The hurricane lantern also uses capillary action to transport fuel, but with a standard rope wick that can be adjusted for height. The flame is shrouded within a glass enclosure and more luminescent than a simple wick lantern, but typically consumes more fuel (simple wick = 14.9 ± 6.6 g fuel/h; small hurricane = 14.4 ± 2.6 g fuel/h; large hurricane = 20.5 ± 6 g fuel/h, as calculated by Apple et al. [2010]). In pressure lamps (primus, mantle lamps), fuel is transferred via pressurization with a manual pump or heat, aerosolized in a “jet” of fuel, and burned, heating a metal (e.g., thorium) oxide-coated mantle that generates a bright white light. Pressure lamps produce substantial amounts of light, but also have the highest fuel consumption rate (74.1 ± 15.6 g/h) and capital cost, limiting their use in households without electricity.

In a chamber study, total suspended particles (PM₁₀), CO, methane, and total hydrocarbons (THC) emissions from a hurricane lantern were calculated using a mass-balance model. Emission factors of 3.2 and 9 mg PM₁₀/g kerosene under “normal” and “tall” wick settings (Fan et al. 2001), respectively, were similar to those measured previously by Schare et al. (1995) from a similar lantern design (Table 3). EF_PM from a simple wick lamp was significantly higher than from a hurricane lamp measured in the same study, generating an average of 8 mg PM_TSP/g kerosene under “normal” conditions and 32 mg PM_TSP/g with a “high” wick height (Schare et al. 1995). However, since mass concentrations were obtained from an uncalibrated light-scattering monitor, absolute values should be interpreted with caution. Measurements of size-resolved particle count indicated that almost all emitted particles from the hurricane lamp were <0.4 μm and no particles were observed above 1.0 μm in diameter (Fan et al. 2001). Increased wick height was associated with a higher PM count, mostly in particles <0.5 μm. The EF_CO was low at 0.52 ± 0.19 mg CO/g kerosene.

Fan and Zhang (2001) then modeled indoor concentrations using emission measurements and the assumption of well-mixed room conditions. Model results indicated that hurricane lamps operated indoors could easily lead to exceedances of U.S. National Air Quality Standards for PM_2.5. It could be inferred that simple wick lamps may also lead to exceedances, since their emission rates appear to be higher (Schare et al. 1995). From model results, it appears that either lamp design might also elevate indoor PM_2.5 concentrations above WHO guideline and interim targets. Using lamp oil, often a deodorized kerosene or lighter hydrocarbon blend (e.g., Flash 142 solvent), the hurricane lamp EF_PM10 decreased by approximately one order of magnitude (0.35 ± 0.06 mg_PM10/g) when operated normally, but less so when operated with a high wick (7.3 ± 1.2 mg_PM10/g), suggesting that more refined fuel grades (e.g., with fewer aromatics) may significantly decrease emissions from lighting appliances. No measurements for pressure lamps were found in the literature.

Two studies quantified the effects of lighting on indoor air quality, both using mock setups to represent real-world conditions. Simple and hurricane lamps operated at “normal” wick height resulted in steady-state indoor PM concentrations of 2500 ± 900 and 6700 ± 1800 μg/m³, respectively (Schare et al. 1995). Operated at high wick settings, these levels rose to 5000 and 21,800 μg/m³, respectively. Size-resolved PM concentrations varying from 0.02 to 1 μm were measured during lamp operation inside a mock roadside kiosk, similar to those used in many African countries. Results indicated that the majority of the particles counted were in the inhalable size range (0.3–10 μm), leading to calculated PM_2.5 and PM₁₀ mass concentrations of 10 to 400 μg/m³ and 20 to 10,000 μg/m³, respectively (Apple et al. 2010). PM_2.5 and PM₁₀ mass concentrations were increased with breathing zone elevation, but a marked effect horizontally from the source (same elevation) was not reported. The increase in concentration with elevation may be due to the thermal plume generated by some lamps. Wick height and device type (e.g., simple wick or hurricane) were found to be important determinants of indoor PM concentrations in both studies. To our knowledge, no study has measured SO₂ from lighting appliances. Kerosene fuel is known to contain low levels of sulfur, usually <0.10%, or <0.04% for 1–K grade. These levels of sulfur would be expected to generate low indoor SO₂ emission rates and would not be likely to exceed WHO guideline concentrations. Higher kerosene sulfur content is possible in developing-country settings, however, and fuel mixing (e.g., with diesel) might also increase exposure risk.

Kerosene lighting devices were used in laboratory settings to generate particles (referred commonly in the literature as “soot”) for various analytical purposes. In some cases, particles were analyzed to determine composition, including elemental (EC) and organic carbon (OC). Elemental carbon is sometimes treated as if it were black carbon (BC), despite recognized limitations resulting from differences in the way each are measured (Bond et al. 2005). Both EC and BC have served as indicators for PM originating from diesel sources in cities; however, there are presently few data that distinguish health effects attributed to EC or BC from those of traditional mass-based PM measures (Smith et al. 2009). Using a thermal optical measurement method, EC was found to compose the majority (approximately 80%) of aerosol carbon (Chen et al. 2007) taken from an unspecified type of lamp burning kerosene. In another study, light absorbance by particles from a poorly trimmed kerosene lamp, similar to a hurricane design, was measured using a photoacoustic instrument. Results indicated that emitted particles were highly light-absorbing (single scattering albedo = 0.20 at 532 nm), suggesting a high proportion of black carbon (Arnott et al. 2000). Optical properties of kerosene particles from the lamp were similar to those of diesel soot. These studies provide some insight into the potential characteristics of particles emitted in kerosene-using houses.

One study provided a qualitative indicator of exposure using measurements of particulate loading of alveolar macrophages. Samples from 57 Malawian male and female subjects who reported using various forms of lighting and cooking devices were analyzed with digital image analysis software to quantify the particles within the alveolar macrophages (AM) (Fullerton et al. 2009). Higher loading was associated with reported use of kerosene wick lamps, compared to use of electric lighting. Due to the method used to quantify PM loading, it is likely that investigators were able to count only darker colored particles on the film, making this more of a quantification of black carbon loading. Analysis of variance showed a significant difference across lighting device types—simple-wick lamps were associated with the highest median levels, followed by candles, hurricane lamps, and electricity. Caution is needed in interpreting these results, as no adjustment was made for solid fuel cooking, which was also associated with greater AM particulate loading.

The significant quantities of PM generated by some lighting appliances, coupled with the user–device interaction characteristics (e.g., studying, room illumination), suggest that kerosene lighting could be a significant source of household exposure. Unfortunately, few studies investigated this issue in depth, and only a few pollutants have been characterized. No studies to date have quantified exposure or microenvironmental pollutant concentrations in real-world settings. Proximity is likely to be an important exposure component not captured in area-based measurements. There appear to be large differences in emission and exposure potentials across lamp designs (e.g., wick or pressure) and operator settings, which are likely associated with usage purpose (e.g., room lighting versus close proximity reading). This information could be captured easily with a simple questionnaire accompanying household monitoring sessions. Assessing fuel quality inexpensively would be more challenging, but potentially important.

Cooking

The literature on household cooking in developing countries has focused on solid fuels (e.g., wood, dung, charcoal), as they are the most prevalent primary household fuels. Furthermore, kerosene is often regarded as a “step up the energy ladder” from solid cooking fuels (Smith et al. 1994), and often becomes more prominent as a primary or secondary cooking fuel as countries develop and urbanize. This has been observed, for example, in India, where, kerosene was reported as the primary cooking fuel in 8% of urban households and in <1% of rural households in 2005 (NSSO 2007). However, it is often used as a backup fuel in urban areas for when LPG is unavailable and in rural areas for when biomass fuel is unavailable (Rao 2012). Nationally representative cooking fuel assessments conducted by Demographic and Health Surveys (http://www.measuredhs.com) show a similar urban/rural usage pattern for other countries: Kenya (2008), 26.9%/1.5%; Nigeria (2008), 51.6/11.3%; Indonesia (2007), 54.6/18.7%; Nepal (2006), 15.8%/1%; Peru (2000), 25.7%/4%; and Honduras (2005), 10.4%/1%.

Unlike studies on heating and lighting, several studies on cooking-related exposure to household air pollution have attempted to account for user behavior and time–activity patterns. With the exception of one study in Mozambique, Africa (Ellegard 1996), all field studies reported here took place in India, although kerosene is used for cooking in many developing countries. There are two main categories of kerosene cooking stoves described in the literature: “wick” stoves, with 6–10 wicks (but as many as 20–30), and “pressure” stoves, which pressurize the kerosene manually or using heat, and burn the aerosolized fuel.

Pollutant emission factors for PM, CO, NO₂, and SO₂ from kerosene cooking appliances are presented in Table 5. Few measurements of kerosene cookstove emissions exist, especially in comparison to solid fuel stoves, and all are from laboratory test cycles, rather than emissions during actual household use (Habib et al. 2008; Smith et al. 2000; Zhang et al. 2000). Table 6 presents measured microenvironmental and personal exposure concentrations of the same pollutants over various exposure sampling durations. PM concentrations in kitchens ranged from 300 to 750 μg/m³. This variation may be due to variability in room sizes, ventilation, and contributions of outdoor sources, which were substantial in some studies (Raiyani et al. 1993; Saksena et al. 2003). Studies reported in Table 6 employed a variety of particle size cut-points, which adds some complexity when comparing across studies. Size-resolved measures of PM from one study showed that 88% of the PM mass in emissions from kerosene stoves was attributable to particles with aerodynamic diameter <9 μm (Raiyani et al. 1993).

With the exception of one study (Raiyani et al. 1993), average kitchen CO concentrations were consistently below 5–6 mg/m³. Since exposure-averaging times are on the order of hours (e.g., cooking events) for all studies reported, it is possible that short-term guideline exposure limits could be exceeded during cooking periods.

Only two studies reported SO₂ concentrations in houses. Although average levels during cooking reported by Raiyani et al. (1993) are high (121 μg/m³), they were only twice the levels found in LPG-using households (65 μg/m³) and lower than those in households using solid fuels (wood, dung, coal), suggesting a strong contribution of outdoor sources. This trend was seen for other pollutants, including CO, reported in the study. Kandpal et al. (1995) reported kitchen SO₂ concentrations of 48 and 74 μg/m³ at squatting and standing heights, respectively, during kerosene stove use. To our knowledge, there are no reported measurements of the sulfur content in kerosene fuels used in houses. However, for kerosene with sulfur levels similar to those found in 1–K grade kerosene (<0.04% sulfur by weight), it seems unlikely that kerosene stoves alone may generate concentrations of SO₂ in exceedance of WHO guidelines in most indoor environments.

Simultaneous measurement of personal exposure and microenvironmental pollutant concentrations is uncommon in the literature, but can provide insights into cooking habits and exposure characteristics. In a study by Saksena et al. (2003), average personal exposure to RSP (respirable suspended particles) in Indian households using kerosene was 800–900 μg/m³, depending on kitchen design and background concentration (Saksena et al. 2003). From the methods, it is clear that RSP is PM₅ in this study. These concentrations were higher than those measured in the kitchen during the same sampling period (750–800 μg/m³). Furthermore, although wood users experienced twice the average kitchen concentration of PM₅ as kerosene users, average personal exposure concentrations were similar in the two groups. An earlier study in India found the average personal exposure concentration of PM₁₀ to be approximately 10% higher than corresponding kitchen concentrations, while the trend was reversed (30–60% lower for personal exposure) with solid fuels (agricultural residues, wood, and biomass) (Smith et al. 1994).

Saksena et al. (2003) suggested three distinguishing characteristics of kerosene users to explain why personal/microenvironment concentration ratios differed from solid fuel users in their study: Kerosene users: (1) cook for longer durations, (2) spend more time in close proximity to the stove, and (3) are more likely to cook indoors.

Measurements in Indian kitchens showed that households using kerosene stoves had higher particle surface area concentrations relative to coal-, LPG-, and biogas-using households; results for wood were not reported (Sahu et al. 2011). These high surface area concentrations were attributed to the majority of particles being in the ultrafine size region, which also resulted in low mass concentrations for kerosene relative to other fuels. Sahu et al. (2011) suggested that this may be a particular characteristic of kerosene stove combustion, with important health implications. These results also provide evidence that most particles emitted by kerosene stoves are less than 2.5 μm. The implication is that the particle size cutoff (e.g., TSP, PM_2.5, PM₁₀) used in sample collection should exert little effect on the resulting mass concentrations (Table 5).

Several studies measured noncriteria air pollutants from kerosene stoves, PAH and volatile organic compounds (VOC). Laboratory emissions from Thai kerosene stoves identified 17 PAH, of which 11 induced genotoxicity by the Ames test (Oanh et al. 2002). Total PAH emission factors were 67 mg/kg for all 17 measured compounds and 28 mg/kg for genotoxic PAH. The aggregated emission factor for the 17 PAH was similar to that from a wood-stove (66 mg/kg) but less than from sawdust briquettes (260 mg/kg) assessed in the same study. The genotoxic PAH emission factor was greater than for both wood (22 mg/kg) and sawdust briquettes (22 mg/kg). Kerosene has a higher energy density than wood and generally burns more efficiently, requiring less fuel mass to complete the same cooking task and therefore producing a lower mass of total PAH emissions. Simultaneous indoor and outdoor concentration measurements of kerosene-using houses in India showed indoor/outdoor (I/O) ratios for 12 measured PAH as high as 10.5 (naphthalene) (Pandit et al. 2001; Raiyani et al. 1993).

Molar emission ratios for 59 nonmethane hydrocarbons (NMHC) from three laboratory-tested kerosene stove designs (wick, pressure, and gravity) were several fold higher than those from wood or charcoal for several NMHC, including cyclohexane (~10×), heptane (~80×), toluene (~2×), 1,3,5-trimethylbenzene (~91×), and n- and p-xylene (~6×). The kerosene wick stove generated the highest molar emission ratios for nearly all 59 measured compounds (Zhang et al. 1996). Elevated levels of benzene were measured in a sample of five households with kerosene stoves in Mumbai, India (103.4 μg/m³; I/O ratio = 3.3) (Pandit et al. 2001; Srivastava et al. 2000). Six other VOC measured in the same studies, including hexane and toluene, had average I/O ratios >1.

Available measurements of kitchen and personal exposure concentrations suggest that kerosene-fueled stoves elevate indoor respirable PM concentrations above WHO guideline and interim targets, while CO may pose risks under some conditions. Substantial quantities of hydrocarbon species, possibly from uncombusted fuel, may be a differentiating exposure characteristic for kerosene among household fuels (Zhang et al. 1996), but this requires field-based measurement confirmation. The generation of particles with a relatively small size distribution, resulting in a greater surface area for chemical adsorption, may also be a distinguishing characteristic (Sahu et al. 2011). There is also an indication that the shift from solid to liquid fuels may influence cooking behaviors, such that reductions in exposure due to lower emissions are negated by the behavioral changes that increase the exposure concentrations (e.g., proximity, time cooking, indoors with less ventilation) (Saksena et al. 2003; Smith et al. 1994). That there are a wide variety of kerosene stove types in use, but few available pollutant emissions data for kerosene stoves in general, underlines the need for more detailed assessments that cover the range of kerosene stove models used in developing-country households.

Kerosene Fuel Vapor and Aerosols

There is an extensive body of literature on the toxicity of liquid kerosene (uncombusted) and its derivatives due to its use as a motive fuel. Excluding poisonings, the extent to which kerosene aerosol or vapor contributes to daily exposures in households is unclear but contribution could reasonably be assumed to occur at least at a low level. For example, in addition to exposure to vapors released to the room from the fuel appliance or the fuel storage container, it is likely that uncombusted fuel components are present in the pollutant plume or adsorbed to the surface of emitted particles. Kerosene fuel is a mixture of hundreds of chemical compounds, several with known adverse health risks. Although present in varying quantities, depending on fuel source and quality, naphthalene, benzene, n-hexane, toluene, BaP, and xylene are among several such chemicals present in residential kerosene fuels. The adverse health effects of individual chemical constituents as vapors were reviewed comprehensively by Ritchie et al. (2003). The majority of available literature on kerosene toxicity focuses on the dermal exposure route, and usually in the occupational context (e.g., aviation industry). Several animal studies investigated the toxicity of inhaled aerosolized kerosene, although this route is often regarded as secondary in occupational settings. Therefore, it has received less attention.

Using results provided by the American Petroleum Institute, the U.S. Environmental Protection Agency (EPA) performed a screening-level hazard characterization for kerosene/jet fuel (U.S. EPA 2011). Sponsored chemicals for the assessment included kerosene and hydrosulfurized kerosene, while aviation kerosene blends were considered as “supporting chemicals” due to their compositional similarities to the sponsored chemicals. The assessment concluded that the acute oral and dermal toxicity of kerosene was low, while acute inhalation toxicity posed moderate risks. The assessment cites several studies in support of their conclusions. Repeated dermal exposure to kerosene for 4 wk resulted in a decreased red blood cell count in male rabbits and increased spleen weights in females, at dosages of 200 mg/kg body weight (bw)/d (lowest dose tested). A no-observed-adverse-effect level (NOAEL) for repeated dermal exposure was determined to be 330 mg/kg-bw/d. For inhalation, no observed effects were seen in rats exposed for 4 wk to 0.024 mg/L, the highest concentration tested. Repeated dermal exposure to hydrosulfurized kerosene in rats lasting from 14 d premating through d 20 of gestation resulted in a NOAEL for reproductive toxicity of 494 mg/kg/d (highest dose tested) in both males and females, although body weight was decreased in males at this exposure level. No indication of maternal or developmental toxicity was observed at 494 mg/kg/d. Inhalation studies on rats found no signs of maternal or developmental toxicity at 364 ppm/d, regarded as the no-observed-adverse-effect concentration (NOAEC).

A review by Ritchie et al. (2003) considered a wider range of toxicological effects resulting from exposure to kerosene-based jet fuels and kerosene (Ritchie et al. 2003). As with the U.S. EPA report, the review was occupationally focused, drawing largely from studies of kerosene-based jet fuels. Repeated occupational inhalation exposures to jet fuel and kerosene were determined to result in changes to brainstem/cerebellar systems and complex neurobehavioral performance capacity. Repeated exposures in humans and animals were associated with hematological changes, including reductions in red and white blood cell counts. Acute or long-term exposure to aerosolized kerosene-based jet fuel was associated with persisting damage to the pulmonary system.

Other studies, not included in the review, provide evidence of acute airway activity effects. Inhalation of aerosolized kerosene (20–35 mg/L air) for 4–20 min was associated with bronchoconstriction, hyperirritability, and indicators of inflammatory response (Casacó et al. 1985a; 1985b; Mesa et al. 1988a; 1988b; Rodriguez de la Vega et al. 1990). Human and animal studies indicated that acute or chronic dermal exposure resulted in damage to the dermal barrier, irritation, and tumorigenesis. Hepatic damage was also found in both animal and human studies, ranging from changes in hepatic metabolism to persisting liver histopathology following repeated kerosene exposures. Based on numerous animal studies, there is evidence that exposure to kerosene-based jet fuels or unmodified kerosene results in immunosuppression. Polycyclic aromatic hydrocarbons are present in all kerosene fuels and were also shown to mediate immunosuppression (Nadeau et al. 2010).

Combustion Products

Both kerosene stoves and lamps can emit substantial quantities of fine PM even during normal operation. Both size and composition play a role in determining the toxicological risk of inhaled particles. In general, the median diameter of particles emitted from combustion is well below 2.5 μm, ensuring the majority will deposit in the deep lung (Apple et al. 2010; Sahu et al. 2011). The influence of combustion source, which may alter the extent to which chemicals are adsorbed to the surface of particles, and hence their toxicity, has been less studied. The toxicity of soot generated from residential kerosene combustion sources has been investigated. Arif et al. (1991; 1993) exposed rats intratracheally to kerosene soot. Single exposures of 5 mg resulted in effects on the respiratory tract, including increased levels of AM and hydrogen peroxide generation (Arif et al. 1993). Similar effects were also observed in rats given a single 0.05-ml dose of kerosene fuel intratracheally. Dogs exposed in a room to kerosene emissions, generated by a stove for 15 min/d for 21 d, showed mild to moderate edema, compensatory emphysema, focal areas of collapse, and pneumonitis. Many of these effects were attributed to oxidative stress and tissue inflammation resulting from the effects of PAH, reactive oxygenated species, and sulfur compounds in kerosene smoke. In addition to pulmonary effects, Rai et al. (1980) also reported a thickening of aortic walls. A similar thickening of aortic walls, as well as development of aortic plaques and valvular changes, was later observed in guinea pigs exposed to kerosene cookstove emissions after exposure durations similar to those in the study by Rai et al. noted by (Noa et al. 1987). On histopathologic examination, both exposed groups showed changes characteristic of early atherosclerotic lesions, not observed in the control animals. Exposed groups also showed significant elevation in total serum cholesterol and decreases in HDL cholesterol relative to control animals. Unfortunately, neither study reported measurements of pollutant concentrations, but exposure levels were intended to be representative of levels found in household kitchens during cooking events.

Kerosene Coexposures

In animal studies, coexposure to kerosene soot or fuel and asbestos resulted in apparently synergistic alterations of the normal metabolic processes of the lung. Arif et al. (1994) reported that rats given a single intratracheal dose of kerosene soot (5 mg) and chrysotile asbestos (5 mg) showed inhibition of drug-metabolizing enzymes critical in the clearance mechanism of the lung. The joint effect was greater than that measured for exposures to soot or asbestos alone. A follow-up study found that rats given intratracheal doses of either kerosene fuel (5 ml) or soot (5 mg) with asbestos exhibited alterations to biochemical parameters indicative of tissue inflammation and injury to alveolar macrophages (Arif et al. 1997). Both kerosene soot and chrysotile asbestos were found to be genotoxic on an approximately additive scale when hamster embryo fibroblasts were exposed (Lohani et al. 2000). Coexposure effects were also demonstrated with dermal exposures. LaDow et al. (2011) recently found that coexposure to kerosene and BaP for mouse skin increased the uptake of BaP by skin and internal organs. These findings suggest that kerosene aerosol/vapor, and perhaps soot, may modify the risk of other health-damaging pollutants that are coemitted or present from other sources.

Accidental Poisonings

Poisonings from ingestion of kerosene, particularly in children, are unfortunately common in developing countries. The problem is exacerbated by the common practice of insecure storage of small amounts of kerosene in soft-drink bottles without safety closures, often because purchasers of kerosene can only afford to buy a small amount at a time and provide their own containers for suppliers to fill. Kerosene poisoning has been well summarized previously (Tshiamo 2009), and only key points are briefly highlighted here. In addition to inadequate storage and packaging of kerosene, risk factors for kerosene ingestion include age, season, poverty, and living in rural areas. Young children have relatively undeveloped senses of taste and smell and may mistake kerosene for familiar drinks, such as water and some sodas. The summer heat increases consumption of fluids, and kerosene lamps are more common in rural and poor households.

The low viscosity and surface tension of kerosene allow it to be aspirated into the lungs of people who have ingested it, provoking a chemical pneumonitis, which can be fatal if untreated. Fortunately, most kerosene ingestions are nonfatal. Nevertheless, kerosene poisonings make up a significant portion of total poisoning incidents each year, particularly in developing countries. For example, a study of 120 unintentional childhood poisoning cases in Pakistan produced a population-attributable risk of 40% (95% confidence interval [CI] 38–42%) for storage of kerosene and petroleum in soft-drink bottles (Ahmed et al. 2011). Studies emphasize the preventability of such poisonings by a few measures: child-proof caps, avoiding decanting into drink bottles, colorizing the liquid, storage out of reach of children, and education programs (Tshiamo 2009).

TABLE 7

Summary of Results for Epidemiologic Studies Investigating Kerosene Use as a Possible Risk Factor for Health Effects

Cancer

A few studies examined kerosene use as a possible cancer risk factor. The International Agency for Research on Cancer (IARC) concluded that there was inadequate evidence for kerosene as a human carcinogen, and limited evidence for its carcinogenicity in experimental animals (IARC 1989). It was generally not possible to distinguish between any direct effects of kerosene and those of its combustion products. The following is a brief review of the available epidemiologic studies.

Respiratory Cancer

In a survey of 314 Hong Kong families, 36% used kerosene stoves “habitually” (daily use for more than 2 yr) (Leung 1977). Of 44 female lung cancer cases, 40 (91%) were “habitual” kerosene stove users. From the published data, an unadjusted odds ratio (OR) of 17.8 (95% CI 6.2–70) for having a kerosene stove can be calculated. Leung (1977) concluded that female lung cancer was associated with kerosene stove use.

In a case-control study of bronchial cancer in Hong Kong, Chan et al. (1979) examined the relationship of kerosene used for cooking in 189 female cancer cases and 189 female controls from orthopedic wards. The authors reported “no significant difference” between nonsmoking cases and controls for an unadjusted analysis. We calculated unadjusted OR from data presented in Table IX of the paper. For nonsmokers the OR for ever cooking with kerosene was 1.79 (95% CI: 0.96–3.36) and for all women, the OR was 1.51 (95% CI: 0.97–2.35).

Koo et al. (1984) conducted a case-control study in Hong Kong of 200 female lung cancer patients and 200 controls matched by age, housing type, and district. Of the cases, 91.5% had ever used kerosene for cooking, compared with 93.5% of controls. However, cases had cooked with kerosene 2–4 yr longer than controls. OR were elevated only for more than 30 yr of kerosene use. Evidence indicated that data provided minimal evidence for a role of kerosene in lung cancer.

Salivary-Gland Cancer

To identify possible risk factors for salivary-gland cancer, Zheng et al. (1996) conducted a population-based case-control study of 41 cancer cases and 414 controls, in Shanghai, China. Risk factors identified included use of kerosene cooking fuel (OR = 3, 95% CI: 1.4–6.8). This lone study is difficult to interpret. It had few cases and many exposures were examined.

Nonmalignant Effects

Studies are divided into those that examined (1) respiratory symptoms and spirometry values, (2) asthma, (3) respiratory infections, and (4) effects on the eye.

Respiratory Symptoms and/or Spirometry

Azizi and Henry (1990) studied 1600 school children aged 7–12 yr in Kuala Lumpur, Malaysia. In multivariate regression, after adjusting for a number of covariates, including asthma, both wood-burning and kerosene-burning stoves, as well as sharing a bedroom with an adult smoker, were associated with decrements in spirometric parameters. For household kerosene stove use, mean percent predicted values, all statistically significant, were forced vital capacity (FVC), 95.8%; forced expiratory volume in 1 s (FEV₁), 95.7%; forced expiratory flow between 25% and 75% of forced vital capacity (FEF_25–75), 96.8%; and peak expiratory flow rate (PEFR), 97.2%. The authors concluded that exposure to wood- or kerosene-burning stoves affected lung function adversely. However, inclusion of asthma in the same model may have led to underestimates of the effects, as asthma is on the causal pathway for spirometric results. In a subsequent publication, intended to define normal spirometric parameters for ethnic groups in Malaysia and restricted to 1098 of these children without respiratory symptoms, decrements of 3–8% in lung function parameters were reported for children whose families cooked with kerosene (Azizi et al. 1994). The exclusion of children with respiratory symptoms potentially led to an underestimate of any kerosene-related effect on lung function. Azizi et al. (1991) also reported on respiratory symptoms in these Kuala Lumpur children and found no association between having either wood stoves or kerosene stoves and any of chronic cough or phlegm, persistent wheeze, asthma, or chest illness.

To investigate the relationship between household fuel type and lung function, 3991 women were recruited from villages near Chandigarh, India (Behera et al. 1994). After excluding smokers and women with respiratory symptoms or other concomitant diseases, 3318 women remained. Women were categorized by cooking fuel used: biomass, LPG, kerosene, and “mixed.” For all 4 groups, mean FVC was in the range of 73–77% of expected, although the biomass group had the lowest (73.4%) and kerosene the highest (76.7%). Mean PEFR values were 74–76% of expected for all 4 groups and FEV₁ was in the range of 90–94%, with the biomass group again having the lowest values. It is difficult to draw conclusions from these results, for several reasons. First, there was no unexposed comparison group, as all the women cooked with a combusting fuel. Second, excluding women with respiratory symptoms may have introduced a selection bias, making the groups more similar. Third, data were not adjusted for possible confounding factors. Mitigating the latter concern, all the women came from the lower or lower-middle classes.

Behera et al. (1998) also carried out spirometry on 200 school children in Chandigarh. The children were divided into four categories, based on cooking fuel used at home: biomass, LPG, kerosene, and mixed fuels. Predicted (normal) values were available only for PEFR. For boys, PEFR values as percent predicted were lower for kerosene (67.6%) and biomass (67.3%) than for LPG (75.2%) and mixed fuels (72.6%). For girls, PEFR was highest for kerosene (72.3%), relative to biomass (67.4%), LPG (70.3%), and mixed fuels (68.3%). As children with respiratory illnesses were excluded from the participant group, this study is hard to interpret. No potential confounding factors were fully taken into account.

In Lucknow, India, Awasthi et al. (1996) carried out a cross-sectional survey involving 650 children less than 5 yr of age. The outcome measure was observation on the day of the interview of one or more of the following without the presence of exanthematous rash: runny nose, cough, sore throat, breathlessness, and stridor or wheeze. Cooking fuel exposures were the fuel(s) used by the family in the last week. In a logistic regression model the only fuel that was associated with symptoms was dung cakes (OR = 2.69, 95% CI: 1.37–5.31). Coal (OR = 0.61), wood (OR = 0.96), and kerosene (OR = 0.87) were not associated with symptoms.

A study of the association between winter respiratory symptoms and home heating sources was carried out in 890 infants, aged 3–5 mo, born in Connecticut and Virginia hospitals in 1993–1996 (Triche et al. 2002). Mothers recorded wheeze and cough in their children. Kerosene heater use was associated with about a 7% elevation in episodes of cough for each 8–h increase in use, but there was no rise in total days of cough. An increase in gas heater use by 8 h/d was associated with a 25% rise in days of wheeze and a 28% elevation in episodes of wheeze; increase in woodstove use of 8 h/d was associated with a 10% rise in days with cough. This study did not include air pollution measurements.

A later study of respiratory symptoms and heating focused on the mothers of these children (n = 888), and included indoor air pollution measurements (Triche et al. 2005). After controlling for various factors, each hour-per-day increase in kerosene heater use was associated with an elevation in wheezing (RR = 1.06; 95% CI: 1.01–1.11). Each 10-ppb rise in SO₂, produced only by the kerosene heaters, was associated with increased wheezing (RR = 1.57; 1.10–2.26) and chest tightness (RR = 1.32; 1.01–1.71). Median SO₂ concentrations associated with kerosene heater use and with no use were 6.4 ppb and 0.2 ppb, respectively. Elevated NO₂ was associated mainly with gas space heater use (median concentrations, 54.8 and 12.5 ppb for use and no use, respectively) and less strongly with kerosene heater use (17.7 and 11.5 ppb, respectively). When NO₂ concentration was dichotomized at 80 ppb, associations were found for chest tightness (RR = 1.94; 95% CI: 0.98–3.85) and wheezing (RR = 4.00; 95% CI: 1.45–11.0). This study provides some evidence that kerosene appliance use, and possibly gas appliance use, is associated with respiratory symptoms. However, a later study of these women (nonsmokers only) that examined variability of peak expiratory flow rates in relation to self-reported use of supplementary heating sources in winter found no marked association with any source, including kerosene heaters (Beckett et al. 2006).

Mallol et al. (2008) studied self-reported wheezing in children from a low-income population in Santiago, Chile. Two random samples (100 each) of children aged 13–14 yr were selected according to whether or not they reported wheezing in the past 12 mo. The unadjusted OR for kerosene used for heating or cooking at home was 1.3 (0.7–2.5). Wood and gas were combined in the reference group. No adjusted results were presented.

To identify risk factors for wheeze in children in the first year of life in low-resourced countries, Bueso et al. (2010) surveyed parents of 1827 children in 2 communities in Honduras and El Salvador. Results from the two countries combined showed some evidence of an association with kerosene for cooking, compared to electricity, for recurrent wheeze (three or more episodes) (OR = 2.78, 95% CI: 0.94–8.25).

In the Niger-Delta region of Nigeria, Mustapha et al. (2011) carried out a cross-sectional study of respiratory symptoms in relation to sources of outdoor and indoor air pollution sources in children aged 7–14 yr. Compared with gas cooking, nonsignificant positive associations with phlegm production were found for cooking with wood or coal (OR = 2.99, 95% CI: 0.88–10.18) and for kerosene cooking (OR = 2.83, 95% CI: 0.85–9.44). In general, the magnitudes of associations with night cough, asthma diagnosis (ever), and rhinitis (ever), although weaker than for phlegm production, were similar for kerosene and coal.

In summary, these studies are hard to interpret in a coherent way. Interpretation is complicated by the range of symptoms studied, the different ages of the populations, and the variations in reference fuel categories. However, there is some indication of an association of kerosene use with wheeze and cough, and reduction in spirometric values.

Asthma and Allergic Diseases

In a study in Richmond, VA, Cooper and Alberti (1984) showed that use of kerosene heaters in homes might lead to levels of SO₂ that would be expected to produce bronchospasm in some people with asthma. Further study of adverse health effects of kerosene heater emissions was recommended in asthmatics, as well as long-term effects in both sensitive and normal persons.

To investigate indoor air pollution effects on asthma, a case-control study was conducted with 158 children, aged 1–60 mo, hospitalized with asthma for the first time in Kuala Lumpur, Malaysia (Azizi et al. 1995). Controls were 201 children of the same age hospitalized in the same 24 h for nonrespiratory reasons. Although sharing a bedroom with a smoker and a mosquito coil used at least three nights per week were both associated with asthma, neither kerosene- nor wood-burning stoves in the household appeared to be risk factors. The unadjusted OR for kerosene stoves was 0.9 (95% CI: 0.5–1.6) and for woodstoves was 1.4 (0.6–3.6).

A case-control study involving 77 asthma cases and 77 controls was conducted among children aged 9–11 yr in Nairobi, Kenya (Mohamed et al. 1995). Cases and controls were drawn from a cross-sectional study. The use of kerosene as a cooking fuel was less frequent in the families of cases (26%) than in control families (29%), and indoor cooking fuels were not associated with asthma.

A study of Kenyan schoolchildren investigated why higher rates of exercise-induced bronchospasm (EIB), a common feature of asthma, were reported for children living in urban areas compared to rural areas (Ng’ang’a et al. 1998). Children (N = 1071) aged <12 yr at schools in Nairobi (urban) and in Muranga district (rural) underwent an exercise challenge test. A questionnaire was administered to parents/guardians. Kerosene was used for cooking by 37% of rural households and 81% of urban households. The OR for kerosene use was 1.17 (95% CI: 0.74–1.84) when a broad range of covariates was included in the model. Unfortunately, household lighting type was not included in models. It is likely that many of the rural households used kerosene lamps, and electric lighting may have been more common in urban areas. If so, this may have attenuated any true relationship with asthma.

A cross-sectional study in Jimma district, Ethiopia, was prompted by evidence that switching from biomass to fossil fuels was potentially associated with increased allergic diseases, including asthma (Venn et al. 2001). The study recruited 9844 people, an estimated 95% of the eligible population. Data were collected by questionnaire. Allergen skin sensitization testing was conducted in a sub-sample of 2372 people. Biomass fuels were used for cooking by 99% of the study population. However, “modern fuels” (gas, electricity, and kerosene) were used concurrently by 10%, with only 34 (<1%) reporting exclusive use. The majority of kerosene stoves were the wick type. For kerosene, after controlling for age, gender, socioeconomic status, and identified confounders, the odds ratio for allergen skin sensitization was 1.95 (95% CI 1.02–3.73). Kerosene use was also associated with all allergic symptom outcomes (wheeze in past year: adjusted OR 1.55 [CI 1.01–2.38]; rhinitis, 2.57 [1.76–3.75]; eczema ever, 2.99 [1.78–5.04]; and eczema in past year, 2.22 [1.08–4.57]). For allergen skin sensitization, the adjusted OR for gas use was 3.20 (95% CI 1.62–6.32), but there were no associations between gas or electricity use and reported symptoms. Evidence The authors hypothesized that exposure to combustion pollutants from refined fossil fuels may have played a major role in the emergence of allergic diseases in the developing and developed world. Data on lighting were not reported.

As a follow-up to the Venn et al. (2001) study, 7155 children aged 1–4 yr living in Jimma and surrounding rural regions in Ethiopia were recruited (Dagoye et al. 2004). During the last year, the prevalence of wheeze in the urban area was 4.4% and 2% in the rural area. In the urban area, the OR for wheeze and daily household use of kerosene was 3.36 (95% CI: 1.77–6.36), with a rising trend in risk for increasing kerosene use. Few rural households reported use of kerosene for cooking, so it was not possible to examine this separately. Again, data on lighting were not reported.

In Isfahan, Iran, a study of respiratory illness in 561 females aged 1 mo to 81 yr (mean age 27.6 yr) was carried out to identify risk factors (Golshan et al. 2002). The adult women in the study were mostly housewives and there was extensive use of gas, kerosene, and wood fuels for cooking and heating. For current asthma, defined as a reported history of dyspnea attacks associated with wheezy breathing during the last 12 mo, the adjusted OR for kerosene was 62.4 (95% CI: 7.5–520). For asthma ever, the OR for kerosene use was 5.01 (95% CI: 1.45–17.32), with the corresponding result for wood fuel being 1.08 (1.01–1.27).

In summary, evidence for an association between kerosene and asthma is inconsistent, with the strongest evidence of an association coming from studies in Ethiopia and in Iran. The high OR for current asthma in the Iranian study is anomalous. A possible explanation is that the kerosene stoves used in that area are portable and are reportedly taken into living rooms for heating, especially when it is cold.

Respiratory Infections

Acute lower respiratory infections (ALRI) were investigated in 633 infants (<1 yr) in two slums in Delhi, India (Sharma et al. 1998). Approximately equal numbers of participants reported use of wood and kerosene for cooking, and all were monitored for 9 wk in winter. Expressed as ALRI cases per 100 wk of observation, the rates for Kusumpur Pahari were 6.3 and 5.9 for the wood and kerosene groups, respectively, while corresponding rates for Kathputly were 1.6 and 2.9. Families using kerosene were generally of a higher socioeconomic status than those using wood. The study shows little difference in ALRI rates between the wood and kerosene groups. However, if the results of other studies showing biomass use to be associated with increased ALRI risk (Torres-Duque et al. 2008) are applicable here, then cooking with kerosene may confer little advantage over cooking with biomass, at least for ALRI in infants. At least one study (Saksena et al. 2003) suggested that kerosene users tend to cook more frequently indoors, which may counteract the benefits of reduced emissions from kerosene, compared to biomass cooking. This result needs to be confirmed in other settings.

Savitha et al. (2007) carried out a case-control study of 104 ALRI cases and 104 controls among children aged 1 mo to 5 yr in Mysore, India. Controls were healthy siblings of the case children. Consistent with the established association with ALRI, 93% of cases and 30% of controls used firewood for cooking fuel. The results for kerosene were more discrepant: 5% of cases and 25% of controls used the fuel for cooking (unadjusted OR = 0.15, exact 95% CI: 0.04–0.43), whereas 37% of cases and 3% of controls used kerosene for lighting (unadjusted OR = 19.4, exact 95% CI: 5.7–101). Only three variables were retained in a logistic regression model—partial immunization, overcrowding, and malnutrition. This result is puzzling and raises questions about the modeling procedure, for which virtually no information was provided. Nonetheless, the unadjusted results for kerosene lighting are striking and would be difficult to explain purely by confounding.

In Pokhara, Nepal, associations between pulmonary tuberculosis (TB) and the use of biomass and kerosene fuels were investigated in a hospital-based case-control study (Pokhrel et al. 2010). Cases (n = 125) were women, ranging in age from 20 to 65 yr, with a confirmed TB diagnosis. Age-matched controls (n = 250) were female patients without TB. Compared with using a gas fuel stove, the adjusted OR for using a biomass-fuel stove was 1.21 (95% CI: 0.48–3.05), and 3.36 for use of a kerosene-fuel stove (95% CI: 1.01–11.22). The OR for use of biomass fuel for heating was 3.45 (95% CI: 1.44–8.27) and for use of kerosene lamps for lighting was 9.43 (95% CI: 1.45–61.32). Complicating interpretation of the Nepal study, a similar study in Chandigarh, India, obtained an OR of 3.14 (95% CI: 1.15–8.56) for biomass cooking and 0.49 (95% CI: 0.21–1.20) for cooking with kerosene, both relative to use of liquefied petroleum gas as the reference fuel (Lakshmi et al. 2010). However, an interaction term in the model for the combination of kerosene cooking and having a smoker in the family produced an OR of 2.58 (95% CI: 0.80–8.32). This study did not report data on lighting type.

The few studies on infection are insufficient for any conclusions to be confidently drawn. In particular, the inconsistent results of the Nepal and Chandigarh TB studies underline the need for further studies of this issue.

Effects on the Eye

Results from a case-control study in Nepal (206 cases, 203 controls), intended to investigate whether biomass cooking fuel use was associated with cataract, provided some suggestion of a possible association between kerosene lamp use and cataract (Pokhrel et al. 2005). The adjusted OR for kerosene lamp use was 1.37 (0.81–2.32). This appears to be the only study to have investigated this association, albeit secondarily to the main hypothesis. An association is plausible, as a number of studies found evidence of an association between cooking with solid fuel and cataract (Pokhrel et al. 2005). However, further investigation is needed.

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