Exposure to Air Pollution in Rural Malawi: Impact of Cooking Methods on Blood Pressure and Peak Expiratory Flow.

We made static and personal PM2.5 measurements with a miniature monitor (RTI MicroPEM) to characterise the exposure of women cooking with wood and charcoal in indoor and outdoor locations in rural Malawi, together with measurements of blood pressure and peak expiratory flow rate (PEFR). Mean PM2.5 concentrations of 1338 and 31 µg/m3 were observed 1 m from cookstove locations during cooking with wood and charcoal, respectively. Similarly, mean personal PM2.5 exposures of 706 and 94 µg/m3 were observed during cooking with wood and charcoal, respectively. Personal exposures to PM2.5 in indoor locations were 3.3 and 1.7 times greater than exposures observed in equivalent outdoor locations for wood and charcoal, respectively. Prior to the measured exposure, six out of eight participants had PEFR observations below 80% of their expected (age and height) standardised PEFR. We observed reductions in PEFR for participants cooking with wood in indoor locations. Five out of eight participants reported breathing difficulties, coughing, and eye irritation when cooking with wood but reported that symptoms were less severe when cooking with charcoal. In conclusion, we observed that exposure to PM2.5 was substantially reduced by cooking outdoor with charcoal. As both wood and charcoal fuels are associated with negative environmental and health impacts, the adoption of high-efficiency cookstoves and less polluting sources of energy will be highly beneficial. Cooking outside whenever possible, and minimising the time spent in close proximity to stoves, may be simple interventions that could reduce the risks of exacerbation and progression of respiratory and cardiovascular diseases in Malawi.

A chronology of ratios between black smoke and PM10 and PM2.5 in the context of comparison of air pollution epidemiology concentration-response functions.

BACKGROUND: For many air pollution epidemiological studies in Europe, 'black smoke' (BS) was the only measurement available to quantify ambient particulate matter (PM), particularly for exposures prior to the mid-1990s when quantification via the PM10 and/or PM2.5 metrics was introduced. The aim of this work was to review historic BS and PM measurements to allow comparison of health concentration-response functions (CRF) derived using BS as the measure of exposure with CRFs derived using PM10 or PM2.5. METHODS: The literature was searched for quantitative information on measured ratios of BS:PM10, BS:PM2.5, and chemical composition of PM; with specific focus on the United Kingdom (UK) between 1970 and the early 2000s when BS measurements were discontinued. RESULTS: The average BS:PM10 ratio in urban background air was just below unity at the start of the 1970s, decreased rapidly to ≈ 0.7 in the mid-1970s and to ≈ 0.5 at the end of the 1970s, with continued smaller declines in the 1980s, and was within the range 0.2-0.4 by the end of the 1990s. The limited data for the BS:PM2.5 ratio suggest it equalled or exceeded unity at the start of the 1970s, declined to ≈ 0.7 by the end of the 1970s, with slower decline thereafter to a range 0.4-0.65 by the end of the 1990s. For an epidemiological study that presents a CRF BS value, the corresponding CRF PM10 value can be estimated as R BS:PM10 × CRF BS where R BS:PM10 is the BS:PM10 concentration ratio, if the toxicity of PM10 is assumed due only to the component quantified by a BS measurement. In the general case of some (but unknown) contribution of toxicity from non-BS components of PM10 then CRF PM10 > R BS:PM10 × CRF BS, with CRF PM10 exceeding CRFBS if the toxicity of the other components in PM10 is greater than the toxicity of the component to which the BS metric is sensitive. Similar analyses were applied to relationships between CRF PM2.5 and CRF BS. CONCLUSIONS: Application of this analysis to example published CRF BS values for short and long-term health effects of PM suggest health effects from other components in the PM mixture in addition to the fine black particles characterised by BS.

Development, Evaluation, and Comparison of Land Use Regression Modeling Methods to Estimate Residential Exposure to Nitrogen Dioxide in a Cohort Study.

We used a network of 135 NO2 passive diffusion tube sites to develop land use regression (LUR) models in a UK conurbation. Network sites were divided into four groups (32-35 sites per group) and models developed using combinations of 1-3 groups of "training" sites to evaluate how the number of training sites influenced model performance and residential NO2 exposure estimates for a cohort of 13 679 participants. All models explained moderate to high variance in training and independent "hold-out" data (Training adj. R2: 62-89%; Hold-out R2: 44-85%). Average hold-out R2 increased by 9.5%, while average training adj. R2 decreased by 7.2% when the number of training groups was increased from 1 to 3. Exposure estimate precision improved with increasing number of training sites (median intralocation relative standard deviations of 19.2, 10.3, and 7.7% for 1-group, 2-group and 3-group models respectively). Independent 1-group models gave highly variable exposure estimates suggesting that variations in LUR sampling networks with relatively low numbers of sites (≤35) may substantially alter exposure estimates. Collectively, our analyses suggest that use of more than 60 training sites has quantifiable benefits in epidemiological application of LUR models.

Association between long-term exposure to air pollution and specific causes of mortality in Scotland.

OBJECTIVE: This study investigated the association between long-term exposure to black smoke (BS) air pollution and mortality in two related Scottish cohorts with 25 years of follow-up. METHODS: Risk factors were collected during 1970-1976 for 15331 and 6680 participants in the Renfrew/Paisley and Collaborative cohorts respectively. Exposure to BS during 1970-1979 was estimated by inverse-distance weighted averages of observed concentrations at monitoring sites and by two alternative spatial modelling approaches which included local air quality predictors (LAQP). RESULTS: Consistent BS-mortality associations (per 10 µg m(-3) increment in 10-year average BS) were observed in the Renfrew/Paisley cohort using LAQP-based exposure models (all-cause mortality HR 1.10 (95% CI 1.04 to 1.17); cardiovascular HR 1.11 (1.01 to 1.22); ischaemic heart disease HR 1.13 (1.02 to 1.25); respiratory HR 1.26 (1.02 to 1.28)). The associations were largely unaffected by additional adjustment for area-level deprivation category. A less consistent and generally implausible pattern of cause-specific BS-mortality associations was found for inverse-distance averaging of BS concentrations at nearby monitoring sites. BS-mortality associations in the Collaborative cohort were weaker and not statistically significant. CONCLUSIONS: The association between mortality and long-term exposure to BS observed in the Renfrew/Paisley cohort is consistent with hypotheses of how air pollution may affect human health. The dissimilarity in pollution-mortality associations for different exposure models highlights the critical importance of reliable estimation of exposures on intraurban spatial scales to avoid potential misclassification bias.

A comparison of short-term and long-term air pollution exposure associations with mortality in two cohorts in Scotland.

BACKGROUND: Air pollution-mortality risk estimates are generally larger at longer-term, compared with short-term, exposure time scales. OBJECTIVE: We compared associations between short-term exposure to black smoke (BS) and mortality with long-term exposure-mortality associations in cohort participants and with short-term exposure-mortality associations in the general population from which the cohorts were selected. METHODS: We assessed short-to-medium-term exposure-mortality associations in the Renfrew-Paisley and Collaborative cohorts (using nested case-control data sets), and compared them with long-term exposure-mortality associations (using a multilevel spatiotemporal exposure model and survival analyses) and short-to-medium-term exposure-mortality associations in the general population (using time-series analyses). RESULTS: For the Renfrew-Paisley cohort (15,331 participants), BS exposure-mortality associations were observed in nested case-control analyses that accounted for spatial variations in pollution exposure and individual-level risk factors. These cohort-based associations were consistently greater than associations estimated in time-series analyses using a single monitoring site to represent general population exposure {e.g., 1.8% [95% confidence interval (CI): 0.1, 3.4%] vs. 0.2% (95% CI: 0.0, 0.4%) increases in mortality associated with 10-µg/m³ increases in 3-day lag BS, respectively}. Exposure-mortality associations were of larger magnitude for longer exposure periods [e.g., 3.4% (95% CI: -0.7, 7.7%) and 0.9% (95% CI: 0.3, 1.5%) increases in all-cause mortality associated with 10-µg/m³ increases in 31-day BS in case-control and time-series analyses, respectively; and 10% (95% CI: 4, 17%) increase in all-cause mortality associated with a 10-µg/m³ increase in geometic mean BS for 1970-1979, in survival analysis]. CONCLUSIONS: After adjusting for individual-level exposure and potential confounders, short-term exposure-mortality associations in cohort participants were of greater magnitude than in comparable general population time-series study analyses. However, short-term exposure-mortality associations were substantially lower than equivalent long-term associations, which is consistent with the possibility of larger, more persistent cumulative effects from long-term exposures.

Using mass reconstruction along a four-site transect as a method to interpret PM10 in west-central Scotland, United Kingdom.

Concurrent 24-hr samples of particulate matter of median aerodynamic diameter less than 10 microm (PM10) were collected over a 10-day period in August 2000 at four sites along a transect in west-central Scotland, UK (passing from the coast through the city of Glasgow) in line with the prevailing southwesterly wind. Each sample was analyzed for chloride (Cl(-)), nitrate (NO3(-)), sulfate (SO4(2-)), ammonium (NH4(+)), calcium (Ca(2+)), iron (Fe), and organic hydrocarbon material (OHM). The contribution from elemental carbon (EC) was estimated. Sampling days were categorized according to local wind direction, synoptic flow, and air mass back trajectories. Chemical mass balance (CMB) reconstruction of the following PM10 components was derived for each wind direction group and at each transect location: ammonium sulfate ((NH4)2SO4), ammonium nitrate (NH4NO3), sodium chloride (NaCl), gypsum (CaSO4), OHM, EC, soil/surface dusts, and particle-bound water. The results showed that PM10 at the coastal site was dominated by the marine background (NaCl) compared with the urban sites, which were dominated by local primary (EC and soil/resuspension) and secondary sources (NH4NO3, (NH4)2SO4, and OHM). There was evidence of Cl(-) depletion as NaCl aerosol passes over urban areas. There was also evidence of long-range transport of primary PM10 (EC and OHM); for example, at the coastal site from transport from Ireland. The work demonstrates how the general approach of combining mass reconstruction along a transect with other information such as wind/air-mass direction generates insight into the sources contributing to PM10 over a more extended spatial scale than at a single receptor.

Soluble transition metals cause the pro-inflammatory effects of welding fumes in vitro.

Epidemiological studies have consistently reported a higher incidence of respiratory illnesses such as bronchitis, metal fume fever (MFF), and chronic pneumonitis among welders exposed to high concentrations of metal-enriched welding fumes. Here, we studied the molecular toxicology of three different metal-rich welding fumes: NIMROD 182, NIMROD c276, and COBSTEL 6. Fume toxicity in vitro was determined by exposing human type II alveolar epithelial cell line (A549) to whole welding fume, a soluble extract of fume or the "washed" particulate. All whole fumes were significantly toxic to A549 cells at doses >63 microg ml(-1) (TD 50; 42, 25, and 12 microg ml(-1), respectively). NIMROD c276 and COBSTEL 6 fumes increased levels of IL-8 mRNA and protein at 6 h and protein at 24 h, as did the soluble fraction alone, whereas metal chelation of the soluble fraction using chelex beads attenuated the effect. The soluble fraction of all three fumes caused a rapid depletion in intracellular glutathione following 2-h exposure with a rebound increase by 24 h. In addition, both nickel based fumes, NIMROD 182 and NIMROD c276, induced significant reactive oxygen species (ROS) production in A549 cells after 2 h as determined by DCFH fluorescence. ICP analysis confirmed that transition metal concentrations were similar in the whole and soluble fractions of each fume (dominated by Cr), but significantly less in both the washed particles and chelated fractions. These results support the hypothesis that the enhanced pro-inflammatory responses of welding fume particulates are mediated by soluble transition metal components via an oxidative stress mechanism.