Martine Dennekamp

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.

Detection of estrogenic activity in sediment-associated compounds using in vitro reporter gene assays

Sediments may be the ultimate sink for persistent (xeno-)estrogenic compounds released into the aquatic environment. Sediment-associated estrogenic potency was measured with an estrogen receptor-mediated luciferase reporter gene (ER-CALUX) assay and compared with a recombinant yeast screen. The ER-CALUX assay was more sensitive to 17beta-estradiol (E2) than the recombinant yeast screen, with an EC50 of 6 pM E2 compared to 100 pM in the yeast screen. Yeast cells were unable to distinguish the anti-estrogens ICI 182,780 and (4-hydroxy)tamoxifen, which were agonistic in the yeast. Acetone-soluble fractions of hexane/acetone extracts of sediments showed higher estrogenic potency than hexane-soluble extracts in the ER-CALUX assay. Sediments obtained from industrialized areas such as the Port of Rotterdam showed the highest estrogenic potency of the 12 marine sediments tested (up to 40 pmol estradiol equivalents per gram sediment). The estrogenic activity of individual chemicals that can be found in sediments including: alkylphenol ethoxylates and carboxylates; phthalates; and pesticides, was tested. Increasing sidechain length of various nonylphenol ethoxylates resulted in decreased estrogenic activity. Of the phthalates tested, butylbenzylphthalate was the most estrogenic, though with a potency approximately 100,000 times less than E2. The organochlorine herbicides atrazine and simazine failed to induce reporter gene activity. As metabolic activation may be required to induce estrogenic activity, a metabolic transformation step was added to the ER-CALUX assay using incubation of compounds with liver microsomes obtained from PCB-treated rats. Results indicate that metabolites of E2, NP and bisphenol A were less active than the parent compounds, while metabolites of methoxychlor were more estrogenic following microsomal incubations.

The effects of bushfire smoke on respiratory health.

Bushfire smoke has the potential to affect millions of people and is therefore a major public health problem. The air pollutant that increases most significantly as a result of bushfire smoke is particulate matter (PM). During bushfire smoke episodes, PM concentrations are usually much higher than urban background concentrations, at which effects on respiratory health have been observed. The smoke can cover large areas including major cities and even small increases in the risk of respiratory health effects can cause large public health problems.

Hypothesis: Ill health associated with low concentrations of nitrogen dioxide: an effect of ultrafine particles?

The epidemiological associations between illness and nitrogen dioxide may be the consequence of confounding by particle numbers In 1996 the Expert Panel on Air Quality Standards (EPAQS) recommended an ambient air standard for nitrogen dioxide (NO2) in the UK of 150 ppb measured hourly.1 This recommendation, like those for carbon monoxide (CO) and sulphur dioxide (SO2) that had preceded it, was based on human toxicology rather than on epidemiology. The EPAQS was unable to find evidence that these gases were likely to be toxic to humans at the recommended concentrations. However, at the time of the NO2 recommendation there was already epidemiological evidence that effects on populations rather than individuals might be associated with much lower concentrations and the EPAQS recommended that steps be taken to reduce annual average concentrations, although without proposing a long term standard. The UK government has subsequently adopted, as targets to be achieved by 2005, World Health Organization NO2 guideline standards of 105 ppb (200 μg/m3) over 1 hour and 21 ppb (40 μg/m3) as an annual average, the latter having been based on possible relationships between exposure to the gas and respiratory illness in children.2 Achievement of a long term standard does, of course, have the desirable consequence of reducing peaks and therefore short term exccedences. However, compliance with a very low average concentration of NO2 implies a substantial reduction in the concentration of the primary pollutant released from vehicle exhausts—that is, nitric oxide (NO). Since NO reacts with ozone to form NO2, lower concentrations will result in raised urban ozone concentrations, a gas that also has known toxic effects on the lungs and that, until now, has been seen primarily as a rural pollutant in the UK. Progressive reductions in pollution are …

Outdoor air pollution as a trigger for out-of-hospital cardiac arrests.

Background: Epidemiologic studies have reported associations between fine particulate air pollution and cardiovascular mortality or hospitalization for cardiac events. However the evidence regarding the association between air pollution and acute cardiac events, such as out-of-hospital cardiac arrest, is inconsistent. Methods: We investigated the association between particulate matter (PM) air pollution and out-of-hospital cardiac arrest using a case-crossover study of adults (age, 35+ years) in Melbourne, Australia. We included 8434 cases identified through the Victorian Cardiac Arrest Registry from 2003 through 2006. We excluded arrests with an obvious preceding noncardiac event such as trauma, poisoning, or drowning, leaving only those events that were presumed to have cardiac etiology. Air pollution concentrations obtained from a central monitoring site were used for day of the arrest and for lag 1, lag 2, and lag 3, including the average lag 0–1. Results: An interquartile range increase of 4.26 &mgr;g/m3 in PM2.5 over 2 days (lag 0–1) was associated with an increase in risk for an out-of-hospital cardiac arrest of 3.6% (95% confidence interval = 1.3% to 6.0%). PM10 and carbon monoxide also showed associations, but not as strong as for PM2.5. Longer lag periods did not show such strong relationships. There was no association of these cardiac events with ozone, sulfur dioxide, or nitrogen dioxide in any lag period. Individuals age 65–74 years old were most susceptible to PM2.5 exposure, while those 75 years and older had the lowest risk. Conclusion: These findings support an association between daily average PM2.5 concentrations and an increased risk of out-of-hospital cardiac arrests.

Systematic Review of Guidelines for the Management of Asymptomatic and Symptomatic Carotid Stenosis.

Background and Purpose— We systematically compared and appraised contemporary guidelines on management of asymptomatic and symptomatic carotid artery stenosis. Methods— We systematically searched for guideline recommendations on carotid endarterectomy (CEA) or carotid angioplasty/stenting (CAS) published in any language between January 1, 2008, and January 28, 2015. Only the latest guideline per writing group was selected. Each guideline was analyzed independently by 2 to 6 authors to determine clinical scenarios covered, recommendations given, and scientific evidence used. Results— Thirty-four eligible guidelines were identified from 23 different regions/countries in 6 languages. Of 28 guidelines with asymptomatic carotid artery stenosis procedural recommendations, 24 (86%) endorsed CEA (recommended it should or may be provided) for ≈50% to 99% average-surgical-risk asymptomatic carotid artery stenosis, 17 (61%) endorsed CAS, 8 (29%) opposed CAS, and 1 (4%) endorsed medical treatment alone. For asymptomatic carotid artery stenosis patients considered high-CEA-risk because of comorbidities, vascular anatomy, or undefined reasons, CAS was endorsed in 13 guidelines (46%). Thirty-one of 33 guidelines (94%) with symptomatic carotid artery stenosis procedural recommendations endorsed CEA for patients with ≈50% to 99% average-CEA-risk symptomatic carotid artery stenosis, 19 (58%) endorsed CAS and 9 (27%) opposed CAS. For high-CEA-risk symptomatic carotid artery stenosis because of comorbidities, vascular anatomy, or undefined reasons, CAS was endorsed in 27 guidelines (82%). Guideline procedural recommendations were based only on results of trials in which patients were randomized 12 to 34 years ago, rarely reflected medical treatment improvements and often understated potential CAS hazards. Qualifying terminology summarizing recommendations or evidence lacked standardization, impeding guideline interpretation, and comparison. Conclusions— This systematic review has identified many opportunities to modernize and otherwise improve carotid stenosis management guidelines.

The impact of smoke on respiratory hospital outcomes during the 2002-2003 bushfire season, Victoria, Australia.

Background and objective:  Uncontrolled bushfires produce copious amounts of smoke that can result in adverse effects on human health and so are important considerations for emergency, public health and environmental protection agencies. During January to March 2003, the north‐east and Alpine regions of the state of Victoria experienced major bushfires that created a blanket of smoke over the entire state for extended periods of time. This study aimed to explore the daily trends in air pollutants and temporal correlations with changes in respiratory outcomes and to determine whether variation in particulate matter < 10 µm (PM10), visibility‐reducing particles and ozone produced by bushfires could explain variation in respiratory outcomes.

A panel study of air pollution in subjects with heart failure: negative results in treated patients

Objectives: To investigate preclinical adverse effects of ambient particulate air pollution and nitrogen oxides in patients with heart failure. Methods: A cohort of 132 non-smoking patients living in Aberdeen, Scotland, with stable chronic heart failure were enrolled in a repeated-measures panel study. Patients with atrial fibrillation or pacemakers were excluded. Participants were studied for 3 days every 2 months for up to 1 year with monitoring of pollutant exposure and concurrent measurements of pathophysiological responses. Measurements included daily area concentration of particulate matter with a median aerodynamic diameter of <10 micrometres (PM10), particle number concentration (PNC) and nitrogen oxides; daily estimated personal concentration of particulate matter with a median aerodynamic diameter of <2.5 micrometres (PM2.5) and PNC exposures; and 3-day cumulative personal nitrogen dioxide (NO2). Concurrent meteorological data were recorded. Blood was taken at the end of each 3-day block for assays of markers of endothelial activation, inflammation and coagulation. Cardiac rhythm was monitored by ambulatory Holter monitor during the final 24 h of each block. Results: The average 24 h background ambient PM10 ranged from 7.4 to 68 μg.m−3 and PNC from 454 to 11 283 particles.cm−3. No associations were demonstrated between the incidence of arrhythmias, heart rate variability or haematological/biochemical measures and any variations in pollutant exposures at any lags. Conclusion: Assuming that low-level pollution affects the parameters measured, these findings may suggest a beneficial effect of modern cardioprotective therapy, which may modify responses to external risk factors. Widespread use of such drugs in susceptible populations may in future reduce the adverse effects of air pollution on the heart.

Traffic-related air pollution exposure is associated with allergic sensitization, asthma, and poor lung function in middle age

Background: Traffic‐related air pollution (TRAP) exposure is associated with allergic airway diseases and reduced lung function in children, but evidence concerning adults, especially in low‐pollution settings, is scarce and inconsistent. Objectives: We sought to determine whether exposure to TRAP in middle age is associated with allergic sensitization, current asthma, and reduced lung function in adults, and whether these associations are modified by variants in Glutathione S‐Transferase genes. Methods: The study sample comprised the proband 2002 laboratory study of the Tasmanian Longitudinal Health Study. Mean annual residential nitrogen dioxide (NO2) exposure was estimated for current residential addresses using a validated land‐use regression model. Associations between TRAP exposure and allergic sensitization, lung function, current wheeze, and asthma (n = 1405) were investigated using regression models. Results: Increased mean annual NO2 exposure was associated with increased risk of atopy (adjusted odds ratio [aOR], 1.14; 95% CI, 1.02‐1.28 per 1 interquartile range increase in NO2 [2.2 ppb]) and current wheeze (aOR, 1.14; 1.02‐1.28). Similarly, living less than 200 m from a major road was associated with current wheeze (aOR, 1.38; 95% CI, 1.06‐1.80) and atopy (aOR, 1.26; 95% CI, 0.99‐1.62), and was also associated with having significantly lower prebronchodilator and postbronchodilator FEV1 and prebronchodilator forced expiratory flow at 25% to 75% of forced vital capacity. We found evidence of interactions between living less than 200 m from a major road and GSTT1 polymorphism for atopy, asthma, and atopic asthma. Overall, carriers of the GSTT1 null genotype had an increased risk of asthma and allergic outcomes if exposed to TRAP. Conclusions: Even relatively low TRAP exposures confer an increased risk of adverse respiratory and allergic outcomes in genetically susceptible individuals.