John W. Cherrie

Particulate air pollution and the blood

BACKGROUND Particulate air pollution has been associated with excess deaths from, and increases in hospital admissions for, cardiovascular disease among older people. A study was undertaken to determine whether this may be a consequence of alterations in the blood, secondary to pulmonary inflammation caused by the action of fine particles on alveolar cells, by repeatedly measuring haematological factors in older people and relating them to measurements of exposure to airborne particles. METHODS One hundred and twelve individuals aged 60+ years in two UK cities provided repeated blood samples over 18 months, 108 providing the maximum of 12 samples. Estimates of individual exposure to particles of less than 10u2009μm diameter (PM10), derived from a mathematical model based on activity diaries and comparative measurements of PM10 at multiple sites and during a variety of activities, were made for each three day period prior to blood sampling. The relationships between blood values and estimates of both personal exposure and city centre measurements of PM10 were investigated by analysis of covariance, adjusting for city, season, temperature, and repeated individual measurements. RESULTS Estimated personal exposure to PM10 over the previous three days showed negative correlations with haemoglobin concentration, packed cell volume (PCV), and red blood cell count (p<0.001), and with platelets and factor VII levels (p<0.05). The changes in red cell indices persisted after adjustment for plasma albumin in a sample of 60 of the subjects. City centre PM10 measurements over three days also showed negative correlations with haemoglobin and red cell count (p<0.001) and with PCV and fibrinogen (p<0.05), the relationship with haemoglobin persisting after adjustment for albumin. C reactive protein levels showed a positive association with city centre measurements of PM10 (p<0.01). Based on a linear relationship, the estimated change in haemoglobin associated with an alteration in particle concentration of 100u2009μg/m3 is estimated to have been 0.44u2009g/dl (95% CI 0.62 to 0.26) for personal PM10 and 0.73u2009g/dl (95% CI 1.11 to 0.36) for city centre PM10 measurements. CONCLUSIONS This investigation is the first to estimate personal exposures to PM10 and to demonstrate associations between haematological indices and air pollution. The changes in haemoglobin adjusted for albumin suggest that inhalation of some component of PM10may cause sequestration of red cells in the circulation. We propose that an action of such particles either on lung endothelial cells or on erythrocytes themselves may be responsible for changing red cell adhesiveness. Peripheral sequestration of red cells offers an explanation for the observed cardiovascular effects of particulate air pollution.

Ultrafine particles and nitrogen oxides generated by gas and electric cooking

OBJECTIVES To measure the concentrations of particles less than 100 nm diameter and of oxides of nitrogen generated by cooking with gas and electricity, to comment on possible hazards to health in poorly ventilated kitchens. METHODS Experiments with gas and electric rings, grills, and ovens were used to compare different cooking procedures. Nitrogen oxides (NOx) were measured by a chemiluminescent ML9841A NOx analyser. A TSI 3934 scanning mobility particle sizer was used to measure average number concentration and size distribution of aerosols in the size range 10–500 nm. RESULTS High concentrations of particles are generated by gas combustion, by frying, and by cooking of fatty foods. Electric rings and grills may also generate particles from their surfaces. In experiments where gas burning was the most important source of particles, most particles were in the size range 15–40 nm. When bacon was fried on the gas or electric rings the particles were of larger diameter, in the size range 50–100 nm. The smaller particles generated during experiments grew in size with time because of coagulation. Substantial concentrations of NOX were generated during cooking on gas; four rings for 15 minutes produced 5 minute peaks of about 1000 ppb nitrogen dioxide and about 2000 ppb nitric oxide. CONCLUSIONS Cooking in a poorly ventilated kitchen may give rise to potentially toxic concentrations of numbers of particles. Very high concentrations of oxides of nitrogen may also be generated by gas cooking, and with no extraction and poor ventilation, may reach concentrations at which adverse health effects may be expected. Although respiratory effects of exposure to NOx might be anticipated, recent epidemiology suggests that cardiac effects cannot be excluded, and further investigation of this is desirable.

The London Underground: dust and hazards to health

Aims: To assess hazards associated with exposure to dust in the London Underground railway and to provide an informed opinion on the risks to workers and the travelling public of exposure to tunnel dust. Methods: Concentrations of dust, as mass (PM2.5) and particle number, were measured at different underground stations and in train cabs; its size and composition were analysed; likely maximal exposures of staff and passengers were estimated; and in vitro toxicological testing of sample dusts in comparison with other dusts was performed. Results: Concentrations on station platforms were 270–480 μg/m3 PM2.5 and 14 000–29 000 particles/cm3. Cab concentrations over a shift averaged 130–200 μg/m3 and 17 000–23 000 particles/cm3. The dust comprised by mass approximately 67% iron oxide, 1–2% quartz, and traces of other metals, the residue being volatile matter. The finest particles are drawn underground from the surface while the coarser dust is generated by interaction of brakes, wheels, and rails. Taking account of durations of exposure, drivers and station staff would have maximum exposures of about 200 μg/m3 over eight hours; the occupational exposure standard for welding fume, as iron oxide, is 5 mg/m3 over an eight hour shift. Toxicology showed the dust to have cytotoxic and inflammatory potential at high doses, consistent with its composition largely of iron oxide. Discussion: It is unjustifiable to compare PM2.5 exposure underground with that on the surface, since the adverse effects of iron oxide and combustion generated particles differ. Concentrations of ultrafine particles are lower and of coarser (PM2.5) particles higher underground than on the surface. The concentrations underground are well below allowable workplace concentrations for iron oxide and unlikely to represent a significant cumulative risk to the health of workers or commuters.

Mortality among workers employed in the titanium dioxide production industry in Europe

AbstractObjectives: To assess the risk of lung cancer mortality related to occupational exposure to titanium dioxide (TiO2).nMethods: A mortality follow-up study of 15,017 workers (14,331 men) employed in 11 factories producing TiO2 in Europe. Exposure to TiO2 dust was reconstructed for each occupational title; exposure estimates were linked with the occupational history. Observed mortality was compared with national rates, and internal comparisons were based on multivariate Cox regression analysis.nResults: The cohort contributed 371,067 person-years of observation (3.3% were lost to follow-up and 0.7% emigrated). 2652 cohort members died during the follow-up, yielding standardized mortality ratios (SMRs) of 0.87 (95% confidence interval [CI] 0.83–0.90) among men and 0.58 (95% CI 0.40–0.82) among women. Among men, the SMR of lung cancer was significantly increased (1.23, 95% CI 1.10–1.38); however, mortality from lung cancer did not increase with duration of employment or estimated cumulative exposure to TiO2 dust. Data on smoking were available for over one third of cohort members. In three countries, the prevalence of smokers was higher among cohort members compared to the national populations.nConclusions: The results of the study do not suggest a carcinogenic effect of TiO2 dust on the human lung.

Cancer mortality among man-made vitreous fiber production workers.

We have updated the follow‐up of cancer mortality for a cohort study of man‐made vitreous fiber production workers from Denmark, Finland, Norway, Sweden, United Kingdom, Germany, and Italy, from 1982 to 1990. In the mortality analysis, 22,002 production workers contributed 489,551 person‐years, during which there were 4,521 deaths. Workers with less than 1 year of employment had an increased mortality [standardized mortality ratio (SMR) = 1.45; 95% confidence interval (CI) = 1.37–1.53]. Workers with 1 year or more of employment, contributing 65% of person‐years, had an SMR of 1.05 (95% CI = 1.02–1.09). The SMR for lung cancer was 1.34 (95% CI = 1.08–1.63, 97 deaths) among rock/slag wool workers and 1.27 (95% CI = 1.07–1.50, 140 deaths) among glass wool workers. In the latter group, no increase was present when local mortality rates were used. Among rock/slag wool workers, the risk of lung cancer increased with time‐since‐first‐employment and duration of employment. The trend in lung cancer mortality according to technologic phase at first employment was less marked than in the previous follow‐up. We obtained similar results from a Poisson regression analysis limited to rock/slag wool workers. Five deaths from pleural mesothelioma were reported, which may not represent an excess. There was no apparent excess for other categories of neoplasm. Tobacco smoking and other factors linked to social class, as well as exposures in other industries, appear unlikely to explain the whole increase in lung cancer mortality among rock/slag wool workers. Limited data on other agents do not indicate an important role of asbestos, slag, or bitumen. These results are not sufficient to conclude that the increased lung cancer risk is the result of exposure to rock/slag wool; however, insofar as respirable fibers were an important component of the ambient pollution of the working environment, they may have contributed to the increased risk.

Comparison between a personal PM10 sampling head and the tapered element oscillating microbalance (TEOM) system

Abstract A new personal PM10 sampling head has been developed by the Institute of Occupational Medicine (IOM), Edinburgh. The purpose of this study was to compare its performance in the field with the accepted fixed-location PM10 sampler, the tapered element oscillating microbalance (TEOM). The comparisons were carried out on three separate occasions during 1997 at each of two city centre locations in the UK. On each occasion two personal IOM PM10 sampling heads were located adjacent to a TEOM monitor and four successive sets of 24-h filter samples were collected. The data was compared with 24-h average TEOM concentrations, calculated as the arithmetic mean of the recorded hourly averages. There was a statistically significant linear relationship between the two types of monitor, although the concentrations from the IOM PM10 samplers were consistently higher than the TEOM data. It is therefore possible to use the regression equations presented in this paper to correct ambient PM10 concentrations measured by either method to equivalent values. Further research is needed to properly understand the reason for the difference between the TEOM and filter samplers.

Impairment of colour vision in workers exposed to organic solvents

OBJECTIVES To investigate loss of colour vision related to exposure to solvents and the role of three enzyme polymorphisms in modifying the risk in exposed workers. METHODS A sample was studied of 68 male dockyard workers and 42 male community controls with and without neuropsychological symptoms from a previous cross sectional study. Indices of cumulative and intensity based exposure to solvents were calculated for all subjects. Alcohol, drug, and smoking histories were obtained. Colour vision was tested by Lanthony D15d colour vision test. Genotype of glutathione S-transferase M1 and T1 and N-acetyltransferase 2 polymorphisms were determined. RESULTS The relation between impairment of colour vision and exposure to solvents was investigated with multiple regression techniques. Increasing annual exposure to solvents was significantly associated with reduced colour vision (p=0.029). Impairment of colour vision was not associated with neuropsychological symptoms as measured by the Q16 solvent symptom questionnaire. No significant association was found between acquired impairment of colour vision and genetic polymorphisms when GSTM1, GSTT1 or NAT2 phenotypes were included in the analyses. CONCLUSIONS Exposure to mixed solvents is associated with impairment in colour vision, the risk increases with increasing exposure. The risk of impairment of colour vision was not altered in this study by the presence of different GSTM1, GSTT1 or NAT2 polymorphisms.

A Dermal Model for Spray Painters. Part I: Subjective Exposure Modelling of Spray Paint Deposition

The discriminative power of existing dermal exposure models is limited. Most models only allow occupational hygienists to rank workers between and within workplaces according to broad bands of dermal exposure. No allowance is made for the work practices of different individuals. In this study a process-based, structured approach has been used to estimate dermal exposure from overspray generated by a spray painting process. Factors for spray technique, object shape and workers individual work practices involved in the processes of droplet formation and deposition were incorporated into the model. The model was applied to predict dermal exposure of airless spray painters and the results were compared with exposure data. The predicted levels of exposure showed reasonable rank correlation with the measured exposure, although the model tended to over-predict the actual level of exposure. It was concluded that a structured, process-based approach has the potential to produce reliable estimates of dermal exposure. The reliability of exposure models of this type should be explored further and the relationship between the determinants of exposure should be validated by additional field studies.

Lung cancer among rock and slag wool production workers.

Background. Previous cohort studies have found an elevated risk of lung cancer among rock and slag wool (RSW) production workers. The aim of the present study was to investigate the risk of lung cancer associated with exposure to RSW while controlling for other occupational exposures and tobacco smoking. Methods. Since 1971, a total of 196 lung cancer cases occurred among men who worked in seven plants in Denmark, Norway, Sweden, and Germany, with start of production between 1937 and 1950. We obtained information on occupational history and extra-occupational factors from either the subject or the next of kin for 133 cases and 513 matched controls. We assessed occupational exposure on the basis of interview data combined with information from expert panels set up in each factory. Results. For cumulative exposure to RSW assessed with a 15-year lag, the smoking-adjusted odds ratios in the second, third, and fourth quartiles of exposure were 1.3 (95% confidence interval [CI] = 0.7–2.3), 1.0 (CI = 0.5–1.9), and 0.7 (CI = 0.3–1.3). Similar results were obtained when we included only those workers employed for more than 1 year, when we included other indicators of RSW exposure, and after control for co-exposures. Conclusions. This study provides no evidence of a carcinogenic effect on the lung of rock and slag wool under exposure circumstances in the production industry during the last four to five decades.

Assessment of dermal exposure during airless spray painting using a quantitative visualisation technique

The range of dermal exposure to non-volatile compounds during spray painting was studied in a semi-experimental study involving three enterprises and 12 painters. A fluorescent tracer was added to the paint and deposition of the tracer on clothing and uncovered parts of the skin was assessed using video imaging and processing techniques. A container (volume 36 m(3)) was sprayed with a colourless laquer (varnish) containing 66.7 mg/l fluorescent whitening agent. All painters sprayed the outside of the container. Nine painters repeated the painting a second time and five also sprayed the inside of the container. The painters wore white Tyvek coveralls, but no gloves. Duration of spraying the outside ranged from 4 to 21 min with a mean of 10 min and the amount of paint sprayed ranged from 3.0 to 12.8 l (mean 6.6 l). The mass of tracer deposited on the coverall ranged from 2.2 to 471 microg (90th percentile 256 microg), whereas, mass deposited on skin (i.e. the hands, wrists, and face) ranged from 0.01 to 52 microg tracer (90th percentile 20 microg). The quantity of tracer on the coverall was three times higher after spraying the inside of the container compared to spraying the outside, whereas the quantity on the skin was similar in both cases. On average 10% of the surface area of the coverall and skin was exposed during spraying the outside. Exposures, expressed in units of mass per area exposed were slightly higher for skin compared to coverall. In this study, deposited mass of tracer was correlated with an alternative exposure metric, i.e. surface area exposed multiplied by the duration of exposure, which has been proposed as a surrogate for uptake. Using a quantitative fluorescent tracer technique, it could be demonstrated that body parts which showed the lowest mass of tracer had the highest exposure as mass per surface area. Compared to other techniques which only determine mass, the ability to identify and quantify the actual surface area exposed is a clear advantage of the quantitative fluorescent tracer technique.