About 50% of the world’s population (about 3 billion people) have little or no access to modern forms of energy, and use biomass fuels for cooking, heating and lighting. These are frequently burned within the households in open fires or inefficient stoves. In the rural areas of Latin America, 30–75% of households use biomass fuels for cooking, which have a dramatically high production of PM and carbon monoxide (CO). Solid fuels are still the dominant source of energy in households in rural China. In China, indoor air pollution from biomass fuels is responsible for approximately 1 000 000 premature deaths annually, compared with the 1 200 000 estimated to be caused in the country each year by outdoor PM pollution. A recent quantification of the disease burden caused by different risk factors globally indicates that in 2010, over 3.5 million deaths were attributable to household air pollution from solid fuels, representing more than 50% of the total deaths attributable to air pollution from particulate matter and ozone.
Figure 3 shows the main respiratory effects associated with biomass fuel smoke exposure. There is strong evidence of increased risk of acute lower respiratory infections in childhood (at least 2 million deaths annually in children under 5 years of age). There is also evidence of an association with the risk of developing chronic obstructive pulmonary disease (COPD), mostly for women, and with the risk of tuberculosis and asthma.
The International Agency for Research on Cancer has classified emissions from the indoor combustion of coal as a Group 1 carcinogen, i.e. a known carcinogen for humans. Indeed, there is strong evidence that women exposed to smoke from coal fires in the home have an elevated risk of lung cancer (the evidence is moderate for men) (figure 3).
Meta-analyses in low-income countries have estimated increased risks from solid fuel combustion averaging 3.5-fold for acute respiratory infections in children, 2.5-fold for chronic bronchitis in women, and 2.8-fold and 2.3-fold for COPD and chronic bronchitis in all adults, respectively.
Indoor nitrogen dioxide (NO2) is generated mainly by gas-fuelled cooking and heating appliances. The results of longitudinal studies on the asthmatic population (mainly children), or those at risk of developing asthma, indicate positive associations between NO2 concentration and respiratory symptoms, including wheezing, breathing difficulty, chest tightness, shortness of breath and cough. Adverse health effects in the general population are less evident. A recent study indicated that exposure to outdoor, but not indoor, NO2 during the first year of life increases the risk of persistent cough. Conflicting results could in part be explained by the difficulty of determining the amount of exposure, as this can fluctuate depending mainly on the season or the use of specific NO2 sources (i.e. peak concentrations occur during cooking or heating activities).
Volatile organic compounds
Exposure to volatile organic compounds (VOCs) may be related to a spectrum of illnesses ranging from mild (irritations) to very severe (cancer). Even the levels of exposure commonly found at the general population level are relevant. In infants and children, exposure to VOCs increases the risk of respiratory and allergic conditions such as asthma, wheezing, chronic bronchitis, reduced lung function, atopy and severity of sensitisation, rhinitis and respiratory infections. A recent meta-analysis estimated an average increase of 17% in the risk of asthma in children for each 10 μg·m-3 increase in formaldehyde concentration. In a national representative cross-sectional survey in France, high concentrations of VOCs in homes were associated with an increasing prevalence of asthma and rhinitis in adults.
The highest estimated risks between VOCs and health effects are: an approximately 8-fold increase for formaldehyde exposure with chronic bronchitis; 11- and 8-fold increases, respectively, for aromatic and aliphatic chemicals with increased specific immunoglobulin (Ig)E to milk; a 3.4-fold increase for plastics/plasticisers with persistent wheezing; and a 5.6-fold increase for painting with respiratory infections. The estimated increased risk for a diagnosis of asthma ranges from 1.2 to 2.9. Many of the effects observed in children have also been shown in adults. Exposure to VOCs generated by cleaning is a risk factor for asthma and it has been suggested that VOCs produced by microorganisms such as moulds (mVOCs) may contribute to asthma. At the population level, positive associations have been found between the exposure to mVOCs and nocturnal breathlessness, asthma, and chronic bronchitis-like symptoms. However, the role played by mVOCs is still controversial, due to their low specificity in relation to fungi and their very low concentrations in indoor air.
Phthalates also merit specific mention. These are semi-volatile organic compounds derived from the organic chemical compound phthalic acid. The main indoor sources of phthalate esters are plasticised polyvinyl chloride (PVC) materials, used in floor and wall coverings, shower curtains, adhesives, synthetic leather, toys, cosmetics and many other consumer products. There has been considerable concern about phthalates in relation to reproduction and human development; some recent studies have identified associations between phthalates in indoor dust and allergic respiratory symptoms. There is a need for large-scale epidemiological studies in different populations and housing conditions to investigate the respiratory effects of exposure to phthalates in homes.
In the early 1920s, in eastern Europe, miners working in mines with high levels of radon were found to have an elevated risk of lung cancer, suggesting a causal relationship. Subsequent studies on miners, including never-smokers, showed a strong association of radon exposure with lung cancer risk. The natural occurrence of radon in indoor environments, including homes, is therefore a public health concern. Numerous studies have shown that radon represents a risk at any level of exposure, irrespective of smoking. After cigarette smoking, radon is the second main cause of lung cancer in the general population with no occupational exposure, and it is a well-established cause of lung cancer in never-smokers. Indoor radon significantly increases the relative risk of lung cancer – probably in a linear dose–response relationship with no threshold – by 8–16% for every 100 Bq·m-3 increment in its concentration. In the USA, 2100–2900 cases of lung cancer in never-smokers each year are attributable to radon exposure, while in the UK, about 1100 deaths each year from lung cancer are related to radon. A pooled analysis of studies in North America showed that the risk of lung cancer increased by 10% for each concentration increment of 100 Bq·m-3 of residential radon; a similar result was found in a meta-analysis in Europe (a risk increase of 10.6% per 100 Bq·m-3).
The exposure–response relationship between indoor allergens and respiratory/allergic conditions is complex, depending on several factors, such as genetic susceptibility or gene–environment interaction. The reported results are conflicting, with several studies reporting respiratory effects of indoor allergen exposure, including allergic sensitisation and the development of asthma.
Endotoxins are derived from the cell wall of Gram-negative bacteria and are ubiquitous in the environment. High exposure to endotoxins is significantly associated with the risk of COPD and COPD-like symptoms, as well as with bronchial hyperresponsiveness and wheezing. However, other studies have found that early or high exposure to cat allergens or dampness-related allergens have a protective effect against asthma/wheeze/atopy. This protective effect has been discussed extensively, and further studies are needed to better understand possible interactions with the immune system.
A pooled analysis using a large database of European birth cohort studies (22 000 children) indicates that pet ownership in early life does not appear to either increase or reduce the risk of asthma or allergic rhinitis symptoms in children aged 6–10 years. However, a recent study found that asthmatic children sensitised and exposed to low levels of common household allergens, including mould, dust, cat and dog allergens, have an increased risk of illness.
Dampness is present in 10–50% of houses. Moulds are a source of allergens, mVOCs and mycotoxins. Meta-analyses show associations of dampness/mould with increases of approximately 30–50% in respiratory and asthma-related health outcomes, including current asthma, ever-diagnosed asthma, upper respiratory tract symptoms, cough, wheezing and the development of asthma. According to the World Health Organization (WHO), dampness-related factors are also associated with dyspnoea, respiratory infections, bronchitis and allergic rhinitis. Positive associations, although not always statistically significant, have been found in children/infants or young adults between fungal concentration (expressed by culture colony counts) and risk of allergic sensitisation and asthma. Significant associations have also been found between exposure to moulds and respiratory symptoms or doctor-diagnosed asthma, regardless of atopy.
Some studies have found increased risks of wheezing and allergic sensitisation in relation to high exposure to ergosterol (a mould marker), whereas others found no such association. Other epidemiological studies have evaluated mould exposure based on β-glucans (components of the bacterial cell wall) or mycotoxins (fungal products). Exposure to β-glucans did not affect respiratory/allergic disorders, whereas there is insufficient evidence to implicate mycotoxins in mould-related respiratory effects. Recently, a new method has been developed to measure fungal DNA as a mould marker in dust/air. The main advantage of using DNA is the possibility of also identifying dead or dormant organisms. Significant positive associations have been reported between the quantity of DNA of certain fungi and wheezing, nocturnal dry cough, persistent cough, daytime breathlessness or a diagnosis of asthma.
Many studies have focused on the respiratory risks of exposure to a single pollutant. However, combined exposure to two or more agents is common. Indeed, indoor environments always contain complex mixtures of substances from different sources, which may jointly contribute to the toxic effects. There is evidence, mostly from in vitro or animal studies, of an interaction between air pollutants and allergens in the development of respiratory allergic diseases. In one human study addressing such interactions, a significant association between respiratory symptoms – consistent with asthma exacerbation – and PM was noted only in asthmatic children who owned a dog. Another study found that in mild asthmatics, exposure to a typical home concentration of NO2 enhanced the decrease in airflow associated with inhaled allergen. In a recent study of children at high risk of asthma, co-exposure to dog allergen and NO2, or to dog allergen and environmental tobacco smoke, appeared to increase the risk of asthma.
In a large Indian study (about 100 000 women and 57 000 men, aged 20–49 years), living in a household using biomass for cooking and solid fuels showed a significantly higher risk of asthma in women, whereas tobacco smoking was associated with higher asthma prevalence in both sexes. The combined effects of biomass and solid-fuel use and tobacco smoke on the risk of asthma were higher in women. The combination of VOCs and allergens may also be of importance.